thesis.bib~

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@Article{Hanahan2000,
   Author="Hanahan, D.  and Weinberg, R. A. ",
   Title="{{T}he hallmarks of cancer}",
   Journal="Cell",
   Year="2000",
   Volume="100",
   Number="1",
   Pages="57--70",
   Month="Jan"
}

@Article{Hanahan2011,
   Author="Hanahan, D.  and Weinberg, R. A. ",
   Title="{{H}allmarks of cancer: the next generation}",
   Journal="Cell",
   Year="2011",
   Volume="144",
   Number="5",
   Pages="646--674",
   Month="Mar"
}


@Article{Wadman2008,
   Author="Wadman, M.  and Watson, J. ",
   Title="{{J}ames {W}atson's genome sequenced at high speed}",
   Journal="Nature",
   Year="2008",
   Volume="452",
   Number="7189",
   Pages="788",
   Month="Apr"
}


@Article{Wheeler2008,
   Author="Wheeler, D. A.  and Srinivasan, M.  and Egholm, M.  and Shen, Y.  and Chen, L.  and McGuire, A.  and He, W.  and Chen, Y. J.  and Makhijani, V.  and Roth, G. T.  and Gomes, X.  and Tartaro, K.  and Niazi, F.  and Turcotte, C. L.  and Irzyk, G. P.  and Lupski, J. R.  and Chinault, C.  and Song, X. Z.  and Liu, Y.  and Yuan, Y.  and Nazareth, L.  and Qin, X.  and Muzny, D. M.  and Margulies, M.  and Weinstock, G. M.  and Gibbs, R. A.  and Rothberg, J. M. ",
   Title="{{T}he complete genome of an individual by massively parallel {D}{N}{A} sequencing}",
   Journal="Nature",
   Year="2008",
   Volume="452",
   Number="7189",
   Pages="872--876",
   Month="Apr"
}



@Article{Collins2007,
   Author="Collins, F. S.  and Barker, A. D. ",
   Title="{{M}apping the cancer genome. {P}inpointing the genes involved in cancer will help chart a new course across the complex landscape of human malignancies}",
   Journal="Sci. Am.",
   Year="2007",
   Volume="296",
   Number="3",
   Pages="50--57",
   Month="Mar"
}


@Article{Bamford2004,
   Author="Bamford, S.  and Dawson, E.  and Forbes, S.  and Clements, J.  and Pettett, R.  and Dogan, A.  and Flanagan, A.  and Teague, J.  and Futreal, P. A.  and Stratton, M. R.  and Wooster, R. ",
   Title="{{T}he {C}{O}{S}{M}{I}{C} ({C}atalogue of {S}omatic {M}utations in {C}ancer) database and website}",
   Journal="Br. J. Cancer",
   Year="2004",
   Volume="91",
   Number="2",
   Pages="355--358",
   Month="Jul"
 }

@Article{Dickson1999,
   Author="Dickson, D. ",
   Title="{{W}ellcome funds cancer database}",
   Journal="Nature",
   Year="1999",
   Volume="401",
   Number="6755",
   Pages="729",
   Month="Oct"
}


@Article{Paabo2009,
   Author={Green, R. E.  and Briggs, A. W.  and Krause, J.  and Prufer, K.  and Burbano, H. A.  and Siebauer, M.  and Lachmann, M.  and P\"a\"abo, S.},
   Title="{{T}he {N}eandertal genome and ancient {D}{N}{A} authenticity}",
   Journal="EMBO J.",
   Year="2009",
   Volume="28",
   Number="17",
   Pages="2494--2502",
   Month="Sep"
}

@Article{Paabo2006,
   Author={Noonan, J. P.  and Coop, G.  and Kudaravalli, S.  and Smith, D.  and Krause, J.  and Alessi, J.  and Chen, F.  and Platt, D.  and P\"a\"abo, S.  and Pritchard, J. K.  and Rubin, E. M.},
   Title="{{S}equencing and analysis of {N}eanderthal genomic {D}{N}{A}}",
   Journal="Science",
   Year="2006",
   Volume="314",
   Number="5802",
   Pages="1113--1118",
   Month="Nov"
}



@Article{Venter2001,
   Author={Venter, J. C.  and Adams, M. D.  and Myers, E. W.  and Li, P. W.  and Mural, R. J.  and Sutton, G. G.  and Smith, H. O.  and Yandell, M.  and Evans, C. A.  and Holt, R. A.  and Gocayne, J. D.  and Amanatides, P.  and Ballew, R. M.  and Huson, D. H.  and Wortman, J. R.  and Zhang, Q.  and Kodira, C. D.  and Zheng, X. H.  and Chen, L.  and Skupski, M.  and Subramanian, G.  and Thomas, P. D.  and Zhang, J.  and Gabor Miklos, G. L.  and Nelson, C.  and Broder, S.  and Clark, A. G.  and Nadeau, J.  and McKusick, V. A.  and Zinder, N.  and Levine, A. J.  and Roberts, R. J.  and Simon, M.  and Slayman, C.  and Hunkapiller, M.  and Bolanos, R.  and Delcher, A.  and Dew, I.  and Fasulo, D.  and Flanigan, M.  and Florea, L.  and Halpern, A.  and Hannenhalli, S.  and Kravitz, S.  and Levy, S.  and Mobarry, C.  and Reinert, K.  and Remington, K.  and Abu-Threideh, J.  and Beasley, E.  and Biddick, K.  and Bonazzi, V.  and Brandon, R.  and Cargill, M.  and Chandramouliswaran, I.  and Charlab, R.  and Chaturvedi, K.  and Deng, Z.  and Di Francesco, V.  and Dunn, P.  and Eilbeck, K.  and Evangelista, C.  and Gabrielian, A. E.  and Gan, W.  and Ge, W.  and Gong, F.  and Gu, Z.  and Guan, P.  and Heiman, T. J.  and Higgins, M. E.  and Ji, R. R.  and Ke, Z.  and Ketchum, K. A.  and Lai, Z.  and Lei, Y.  and Li, Z.  and Li, J.  and Liang, Y.  and Lin, X.  and Lu, F.  and Merkulov, G. V.  and Milshina, N.  and Moore, H. M.  and Naik, A. K.  and Narayan, V. A.  and Neelam, B.  and Nusskern, D.  and Rusch, D. B.  and Salzberg, S.  and Shao, W.  and Shue, B.  and Sun, J.  and Wang, Z.  and Wang, A.  and Wang, X.  and Wang, J.  and Wei, M.  and Wides, R.  and Xiao, C.  and Yan, C.  and Yao, A.  and Ye, J.  and Zhan, M.  and Zhang, W.  and Zhang, H.  and Zhao, Q.  and Zheng, L.  and Zhong, F.  and Zhong, W.  and Zhu, S.  and Zhao, S.  and Gilbert, D.  and Baumhueter, S.  and Spier, G.  and Carter, C.  and Cravchik, A.  and Woodage, T.  and Ali, F.  and An, H.  and Awe, A.  and Baldwin, D.  and Baden, H.  and Barnstead, M.  and Barrow, I.  and Beeson, K.  and Busam, D.  and Carver, A.  and Center, A.  and Cheng, M. L.  and Curry, L.  and Danaher, S.  and Davenport, L.  and Desilets, R.  and Dietz, S.  and Dodson, K.  and Doup, L.  and Ferriera, S.  and Garg, N.  and Gluecksmann, A.  and Hart, B.  and Haynes, J.  and Haynes, C.  and Heiner, C.  and Hladun, S.  and Hostin, D.  and Houck, J.  and Howland, T.  and Ibegwam, C.  and Johnson, J.  and Kalush, F.  and Kline, L.  and Koduru, S.  and Love, A.  and Mann, F.  and May, D.  and McCawley, S.  and McIntosh, T.  and McMullen, I.  and Moy, M.  and Moy, L.  and Murphy, B.  and Nelson, K.  and Pfannkoch, C.  and Pratts, E.  and Puri, V.  and Qureshi, H.  and Reardon, M. 
           and Rodriguez, R.  and Rogers, Y. H.  and Romblad, D.  and Ruhfel, B.  and Scott, R.  and Sitter, C.  and Smallwood, M.  and Stewart, E.  and Strong, R.  and Suh, E.  and Thomas, R.  and Tint, N. N.  and Tse, S.  and Vech, C.  and Wang, G.  and Wetter, J.  and Williams, S.  and Williams, M.  and Windsor, S.  and Winn-Deen, E.  and Wolfe, K.  and Zaveri, J.  and Zaveri, K.  and Abril, J. F.  and Guigo, R.  and Campbell, M. J.  and Sjolander, K. V.  and Karlak, B.  and Kejariwal, A.  and Mi, H.  and Lazareva, B.  and Hatton, T.  and Narechania, A.  and Diemer, K.  and Muruganujan, A.  and Guo, N.  and Sato, S.  and Bafna, V.  and Istrail, S.  and Lippert, R.  and Schwartz, R.  and Walenz, B.  and Yooseph, S.  and Allen, D.  and Basu, A.  and Baxendale, J.  and Blick, L.  and Caminha, M.  and Carnes-Stine, J.  and Caulk, P.  and Chiang, Y. H.  and Coyne, M.  and Dahlke, C.  and Mays, A.  and Dombroski, M.  and Donnelly, M.  and Ely, D.  and Esparham, S.  and Fosler, C.  and Gire, H.  and Glanowski, S.  and Glasser, K.  and Glodek, A.  and Gorokhov, M.  and Graham, K.  and Gropman, B.  and Harris, M.  and Heil, J.  and Henderson, S.  and Hoover, J.  and Jennings, D.  and Jordan, C.  and Jordan, J.  and Kasha, J.  and Kagan, L.  and Kraft, C.  and Levitsky, A.  and Lewis, M.  and Liu, X.  and Lopez, J.  and Ma, D.  and Majoros, W.  and McDaniel, J.  and Murphy, S.  and Newman, M.  and Nguyen, T.  and Nguyen, N.  and Nodell, M.  and Pan, S.  and Peck, J.  and Peterson, M.  and Rowe, W.  and Sanders, R.  and Scott, J.  and Simpson, M.  and Smith, T.  and Sprague, A.  and Stockwell, T.  and Turner, R.  and Venter, E.  and Wang, M.  and Wen, M.  and Wu, D.  and Wu, M.  and Xia, A.  and Zandieh, A.  and Zhu, X. },
   Title="{{T}he sequence of the human genome}",
   Journal="Science",
   Year="2001",
   Volume="291",
   Number="5507",
   Pages="1304--1351",
   Month="Feb"
}

@article{Lander2001,
   Author={Lander, E. S.  and Linton, L. M.  and Birren, B.  and Nusbaum, C.  and Zody, M. C.  and Baldwin, J.  and Devon, K.  and Dewar, K.  and Doyle, M.  and FitzHugh, W.  and Funke, R.  and Gage, D.  and Harris, K.  and Heaford, A.  and Howland, J.  and Kann, L.  and Lehoczky, J.  and LeVine, R.  and McEwan, P.  and McKernan, K.  and Meldrim, J.  and Mesirov, J. P.  and Miranda, C.  and Morris, W.  and Naylor, J.  and Raymond, C.  and Rosetti, M.  and Santos, R.  and Sheridan, A.  and Sougnez, C.  and Stange-Thomann, Y.  and Stojanovic, N.  and Subramanian, A.  and Wyman, D.  and Rogers, J.  and Sulston, J.  and Ainscough, R.  and Beck, S.  and Bentley, D.  and Burton, J.  and Clee, C.  and Carter, N.  and Coulson, A.  and Deadman, R.  and Deloukas, P.  and Dunham, A.  and Dunham, I.  and Durbin, R.  and French, L.  and Grafham, D.  and Gregory, S.  and Hubbard, T.  and Humphray, S.  and Hunt, A.  and Jones, M.  and Lloyd, C.  and McMurray, A.  and Matthews, L.  and Mercer, S.  and Milne, S.  and Mullikin, J. C.  and Mungall, A.  and Plumb, R.  and Ross, M.  and Shownkeen, R.  and Sims, S.  and Waterston, R. H.  and Wilson, R. K.  and Hillier, L. W.  and McPherson, J. D.  and Marra, M. A.  and Mardis, E. R.  and Fulton, L. A.  and Chinwalla, A. T.  and Pepin, K. H.  and Gish, W. R.  and Chissoe, S. L.  and Wendl, M. C.  and Delehaunty, K. D.  and Miner, T. L.  and Delehaunty, A.  and Kramer, J. B.  and Cook, L. L.  and Fulton, R. S.  and Johnson, D. L.  and Minx, P. J.  and Clifton, S. W.  and Hawkins, T.  and Branscomb, E.  and Predki, P.  and Richardson, P.  and Wenning, S.  and Slezak, T.  and Doggett, N.  and Cheng, J. F.  and Olsen, A.  and Lucas, S.  and Elkin, C.  and Uberbacher, E.  and Frazier, M.  and Gibbs, R. A.  and Muzny, D. M.  and Scherer, S. E.  and Bouck, J. B.  and Sodergren, E. J.  and Worley, K. C.  and Rives, C. M.  and Gorrell, J. H.  and Metzker, M. L.  and Naylor, S. L.  and Kucherlapati, R. S.  and Nelson, D. L.  and Weinstock, G. M.  and Sakaki, Y.  and Fujiyama, A.  and Hattori, M.  and Yada, T.  and Toyoda, A.  and Itoh, T.  and Kawagoe, C.  and Watanabe, H.  and Totoki, Y.  and Taylor, T.  and Weissenbach, J.  and Heilig, R.  and Saurin, W.  and Artiguenave, F.  and Brottier, P.  and Bruls, T.  and Pelletier, E.  and Robert, C.  and Wincker, P.  and Smith, D. R.  and Doucette-Stamm, L.  and Rubenfield, M.  and Weinstock, K.  and Lee, H. M.  and Dubois, J.  and Rosenthal, A.  and Platzer, M.  and Nyakatura, G.  and Taudien, S.  and Rump, A.  and Yang, H.  and Yu, J.  and Wang, J.  and Huang, G.  and Gu, J.  and Hood, L.  and Rowen, L.  and Madan, A.  and Qin, S.  and Davis, R. W.  and Federspiel, N. A.  and Abola, A. P.  and Proctor, M. J.  and Myers, R. M.
   and Schmutz, J.  and Dickson, M.  and Grimwood, J.  and Cox, D. R.  and Olson, M. V.  and Kaul, R.  and Raymond, C.  and Shimizu, N.  and Kawasaki, K.  and Minoshima, S.  and Evans, G. A.  and Athanasiou, M.  and Schultz, R.  and Roe, B. A.  and Chen, F.  and Pan, H.  and Ramser, J.  and Lehrach, H.  and Reinhardt, R.  and McCombie, W. R.  and de la Bastide, M.  and Dedhia, N.  and Blocker, H.  and Hornischer, K.  and Nordsiek, G.  and Agarwala, R.  and Aravind, L.  and Bailey, J. A.  and Bateman, A.  and Batzoglou, S.  and Birney, E.  and Bork, P.  and Brown, D. G.  and Burge, C. B.  and Cerutti, L.  and Chen, H. C.  and Church, D.  and Clamp, M.  and Copley, R. R.  and Doerks, T.  and Eddy, S. R.  and Eichler, E. E.  and Furey, T. S.  and Galagan, J.  and Gilbert, J. G.  and Harmon, C.  and Hayashizaki, Y.  and Haussler, D.  and Hermjakob, H.  and Hokamp, K.  and Jang, W.  and Johnson, L. S.  and Jones, T. A.  and Kasif, S.  and Kaspryzk, A.  and Kennedy, S.  and Kent, W. J.  and Kitts, P.  and Koonin, E. V.  and Korf, I.  and Kulp, D.  and Lancet, D.  and Lowe, T. M.  and McLysaght, A.  and Mikkelsen, T.  and Moran, J. V.  and Mulder, N.  and Pollara, V. J.  and Ponting, C. P.  and Schuler, G.  and Schultz, J.  and Slater, G.  and Smit, A. F.  and Stupka, E.  and Szustakowki, J.  and Thierry-Mieg, D.  and Thierry-Mieg, J.  and Wagner, L.  and Wallis, J.  and Wheeler, R.  and Williams, A.  and Wolf, Y. I.  and Wolfe, K. H.  and Yang, S. P.  and Yeh, R. F.  and Collins, F.  and Guyer, M. S.  and Peterson, J.  and Felsenfeld, A.  and Wetterstrand, K. A.  and Patrinos, A.  and Morgan, M. J.  and de Jong, P.  and Catanese, J. J.  and Osoegawa, K.  and Shizuya, H.  and Choi, S.  and Chen, Y. J.  and Szustakowki, J. },
   Title={{I}nitial sequencing and analysis of the human genome},
   Journal={Nature},
   Year={2001},
   Volume={409},
   Number={6822},
   Pages={860--921},
   Month={Feb},
}



@article{Clark2004,
  doi = {10.1124/jpet.103.064824},
  year = {2004},
  month = {apr},
  publisher = {American Society for Pharmacology {\&} Experimental Therapeutics ({ASPET})},
  volume = {310},
  number = {1},
  pages = {215--222},
  author = {M. J. Clark},
  title = {{Endogenous Regulator of G Protein Signaling Proteins Suppress G~o-Dependent ~-Opioid Agonist-Mediated Adenylyl Cyclase Supersensitization}},
  journal = {Journal of Pharmacology and Experimental Therapeutics},
}

@article{Aarts2015,
   Author = {Aarts, M. and Bajrami, I. and Herrera-Abreu, M. T. and Elliott, R. and Brough, R. and Ashworth, A. and Lord, C. J. and Turner, N. C.},
   Title = {Functional Genetic Screen Identifies Increased Sensitivity to WEE1 Inhibition in Cells with Defects in Fanconi Anemia and HR Pathways},
   Journal = {Mol Cancer Ther},
   Volume = {14},
   Number = {4},
   Pages = {865-76},
      Year = {2015} }




@article{Agarwal2010,
   Author = {Agarwal, Sumeet and Deane, Charlotte M. and Porter, Mason A. and Jones, Nick S.},
   Title = {Revisiting Date and Party Hubs: Novel Approaches to Role Assignment in Protein Interaction Networks},
   Journal = {PLoS Comput Biol},
   Volume = {6},
   Number = {6},
   Pages = {e1000817},
      Year = {2010} }




@article{Ashworth2008,
   Author = {Ashworth, A.},
   Title = {A synthetic lethal therapeutic approach: poly(ADP) ribose polymerase inhibitors for the treatment of cancers deficient in DNA double-strand break repair},
   Journal = {J Clin Oncol},
   Volume = {26},
   Number = {22},
   Pages = {3785-90},
   Year = {2008} }




@article{Audeh2010,
   Author = {Audeh, M. W. and Carmichael, J. and Penson, R. T. and Friedlander, M. and Powell, B. and Bell-McGuinn, K. M. and Scott, C. and Weitzel, J. N. and Oaknin, A. and Loman, N. and Lu, K. and Schmutzler, R. K. and Matulonis, U. and Wickens, M. and Tutt, A.},
   Title = {Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and recurrent ovarian cancer: a proof-of-concept trial},
   Journal = {Lancet},
   Volume = {376},
   Number = {9737},
   Pages = {245-51},
   Keywords = {Adult
Aged
Antineoplastic Agents/*therapeutic use
Female
Genes, BRCA1
Genes, BRCA2
Germ-Line Mutation
Humans
Maximum Tolerated Dose
Middle Aged
Neoplasm Recurrence, Local/*drug therapy
Ovarian Neoplasms/*drug therapy/*genetics/pathology
Phthalazines/*therapeutic use
Piperazines/*therapeutic use
Poly(ADP-ribose) Polymerases/*antagonists & inhibitors
Prospective Studies},
   Year = {2010} }




@article{Babu2010,
   Author = {Babu, M. and Arnold, R. and Bundalovic-Torma, C. and Gagarinova, A. and Wong, K. S. and Kumar, A. and Stewart, G. and Samanfar, B. and Aoki, H. and Wagih, O. and Vlasblom, J. and Phanse, S. and Lad, K. and Yeou Hsiung Yu, A. and Graham, C. and Jin, K. and Brown, E. and Golshani, A. and Kim, P. and Moreno-Hagelsieb, G. and Greenblatt, J. and Houry, W. A. and Parkinson, J. and Emili, A.},
   Title = {Quantitative genome-wide genetic interaction screens reveal global epistatic relationships of protein complexes in Escherichia coli},
   Journal = {PLoS Genet},
   Volume = {10},
   Number = {2},
   Pages = {e1004120},
      Year = {2014} }




@article{Babyak2004,
   Author = {Babyak, M. A.},
   Title = {What you see may not be what you get: a brief, nontechnical introduction to overfitting in regression-type models},
   Journal = {Psychosom Med},
   Volume = {66},
   Number = {3},
   Pages = {411-21},
   Keywords = {Computer Simulation
Data Interpretation, Statistical
Humans
Models, Statistical
Psychophysiology/statistics & numerical data
Psychosomatic Medicine/statistics & numerical data
Regression Analysis
Research Design
Statistics as Topic/education/*methods},
   Year = {2004} }






@article{Barrat2000,
   Author = {Barrat, A. and Weigt, M.},
   Title = {On the properties of small-world network models},
   Journal = {The European Physical Journal B - Condensed Matter and Complex Systems},
   Volume = {13},
   Number = {3},
   Pages = {547-560},
   Keywords = {PACS. 05.50.+q Lattice theory and statistics (Ising, Potts, etc.) - 64.60.Cn Order-disorder transformations
statistical mechanics of model systems - 05.70.Fh Phase transitions: general studies},
   Year = {2000} }




@article{Baryshnikova2010a,
   Author = {Baryshnikova, A. and Costanzo, M. and Dixon, S. and Vizeacoumar, F. J. and Myers, C. L. and Andrews, B. and Boone, C.},
   Title = {Synthetic genetic array (SGA) analysis in Saccharomyces cerevisiae and Schizosaccharomyces pombe},
   Journal = {Methods Enzymol},
   Volume = {470},
   Pages = {145-79},
   Keywords = {Gene Expression Regulation, Fungal/genetics
Genes, Fungal/*genetics
Oligonucleotide Array Sequence Analysis/*methods
Saccharomyces cerevisiae/*genetics
Schizosaccharomyces/*genetics},
   Year = {2010} }




@article{Baryshnikova2010b,
   Author = {Baryshnikova, Anastasia and Costanzo, Michael and Kim, Yungil and Ding, Huiming and Koh, Judice and Toufighi, Kiana and Youn, Ji-Young and Ou, Jiongwen and San Luis, Bryan-Joseph and Bandyopadhyay, Sunayan and Hibbs, Matthew and Hess, David and Gingras, Anne-Claude and Bader, Gary D. and Troyanskaya, Olga G. and Brown, Grant W. and Andrews, Brenda and Boone, Charles and Myers, Chad L.},
   Title = {Quantitative analysis of fitness and genetic interactions in yeast on a genome scale},
   Journal = {Nat Meth},
   Volume = {7},
   Number = {12},
   Pages = {1017-1024},
      Year = {2010} }




@book{Bateson1909,
   Author = {Bateson, William and Mendel, Gregor},
   Title = {Mendel's principles of heredity, by W. Bateson},
   Publisher = {University Press},
   Address = {Cambridge [Eng.]},
   Keywords = {Biography
Evolution
Genetics
Heredity
Hybridization
Mendel's law
Science},
   Year = {1909} }




@article{Bitler2015,
   Author = {Bitler, B. G. and Aird, K. M. and Garipov, A. and Li, H. and Amatangelo, M. and Kossenkov, A. V. and Schultz, D. C. and Liu, Q. and Shih Ie, M. and Conejo-Garcia, J. R. and Speicher, D. W. and Zhang, R.},
   Title = {Synthetic lethality by targeting EZH2 methyltransferase activity in ARID1A-mutated cancers},
   Journal = {Nat Med},
   Volume = {21},
   Number = {3},
   Pages = {231-8},
      Year = {2015} }




@article{Boettcher2014,
   Author = {Boettcher, Michael and Lawson, Andrew and Ladenburger, Viola and Fredebohm, Johannes and Wolf, Jonas and Hoheisel, Jörg D and Frezza, Christian and Shlomi, Tomer},
   Title = {High throughput synthetic lethality screen reveals a tumorigenic role of adenylate cyclase in fumarate hydratase-deficient cancer cells},
   Journal = {BMC Genomics},
   Volume = {15},
   Pages = {158},
      Year = {2014} }




@article{Boone2007,
   Author = {Boone, C. and Bussey, H. and Andrews, B. J.},
   Title = {Exploring genetic interactions and networks with yeast},
   Journal = {Nat Rev Genet},
   Volume = {8},
   Number = {6},
   Pages = {437-49},
   Keywords = {Algorithms
Chromosome Mapping
Diploidy
Epistasis, Genetic
Gene Deletion
Genes, Lethal
Genome, Fungal
Genomics
Models, Genetic
Mutation
Oligonucleotide Array Sequence Analysis
Phenotype
Saccharomyces cerevisiae/*genetics/metabolism
Saccharomyces cerevisiae Proteins/genetics/metabolism},
   Year = {2007} }




@article{Boucher2013,
   Author = {Boucher, B. and Jenna, S.},
   Title = {Genetic interaction networks: better understand to better predict},
   Journal = {Front Genet},
   Volume = {4},
   Pages = {290},
      Year = {2013} }




@article{Bozovic-Spasojevic2012,
   Author = {Bozovic-Spasojevic, I. and Azambuja, E. and McCaskill-Stevens, Worta and Dinh, P. and Cardoso, F.},
   Title = {Chemoprevention for breast cancer},
   Journal = {Cancer treatment reviews},
   Volume = {38},
   Number = {5},
   Pages = {329-339},
   Keywords = {Breast cancer
Prevention
Tamoxifen
Raloxifene
Aromatase inhibitors},
   Year = {2012} }




@article{Breiman2001,
   Author = {Breiman, Leo},
   Title = {Random Forests},
   Journal = {Machine Learning},
   Volume = {45},
   Number = {1},
   Pages = {5-32},
   Keywords = {classification
regression
ensemble},
   Year = {2001} }




@article{Bryant2005,
   Author = {Bryant, H. E. and Schultz, N. and Thomas, H. D. and Parker, K. M. and Flower, D. and Lopez, E. and Kyle, S. and Meuth, M. and Curtin, N. J. and Helleday, T.},
   Title = {Specific killing of BRCA2\-deficient tumours with inhibitors of poly\(ADP\-ribose\) polymerase},
   Journal = {Nature},
   Volume = {434},
   Number = {7035},
   Pages = {913-7},
   Year = {2005} }




@article{Bussey2006,
   Author = {Bussey, H. and Andrews, B. and Boone, C.},
   Title = {From worm genetic networks to complex human diseases},
   Journal = {Nat Genet},
   Volume = {38},
   Number = {8},
   Pages = {862-3},
   Keywords = {Animals
Caenorhabditis elegans/*genetics/metabolism
Chromosome Mapping
Genetic Diseases, Inborn/genetics
Humans
Phenotype
RNA Interference
Saccharomyces cerevisiae/genetics
Signal Transduction},
   Year = {2006} }




@article{Butland2008,
   Author = {Butland, G. and Babu, M. and Diaz-Mejia, J. J. and Bohdana, F. and Phanse, S. and Gold, B. and Yang, W. and Li, J. and Gagarinova, A. G. and Pogoutse, O. and Mori, H. and Wanner, B. L. and Lo, H. and Wasniewski, J. and Christopolous, C. and Ali, M. and Venn, P. and Safavi-Naini, A. and Sourour, N. and Caron, S. and Choi, J. Y. and Laigle, L. and Nazarians-Armavil, A. and Deshpande, A. and Joe, S. and Datsenko, K. A. and Yamamoto, N. and Andrews, B. J. and Boone, C. and Ding, H. and Sheikh, B. and Moreno-Hagelseib, G. and Greenblatt, J. F. and Emili, A.},
   Title = {eSGA: E. coli synthetic genetic array analysis},
   Journal = {Nat Methods},
   Volume = {5},
   Number = {9},
   Pages = {789-95},
   Keywords = {Conjugation, Genetic
Escherichia coli/*genetics
Genome, Bacterial
Mutation
*Oligonucleotide Array Sequence Analysis},
   Year = {2008} }




@article{Chipman2009,
   Author = {Chipman, Kyle and Singh, Ambuj},
   Title = {Predicting genetic interactions with random walks on biological networks},
   Journal = {BMC Bioinformatics},
   Volume = {10},
   Number = {1},
   Pages = {17},
      Year = {2009} }




@article{Collins2006,
   Author = {Collins, Sean and Schuldiner, Maya and Krogan, Nevan and Weissman, Jonathan},
   Title = {A strategy for extracting and analyzing large-scale quantitative epistatic interaction data},
   Journal = {Genome Biology},
   Volume = {7},
   Number = {7},
   Pages = {R63},
      Year = {2006} }




@article{Corcoran2012,
   Author = {Corcoran, Ryan B. and Ebi, Hiromichi and Turke, Alexa B. and Coffee, Erin M. and Nishino, Michiya and Cogdill, Alexandria P. and Brown, Ronald D. and Della Pelle, Patricia and Dias-Santagata, Dora and Hung, Kenneth E. and Flaherty, Keith T. and Piris, Adriano and Wargo, Jennifer A. and Settleman, Jeffrey and Mino-Kenudson, Mari and Engelman, Jeffrey A.},
   Title = {EGFR-Mediated Reactivation of MAPK Signaling Contributes to Insensitivity of BRAF-Mutant Colorectal Cancers to RAF Inhibition with Vemurafenib},
   Journal = {Cancer Discovery},
   Volume = {2},
   Number = {3},
   Pages = {227-235},
      Year = {2012} }




@article{Costanzo2010,
   Author = {Costanzo, M. and Baryshnikova, A. and Bellay, J. and Kim, Y. and Spear, E. D. and Sevier, C. S. and Ding, H. and Koh, J. L. and Toufighi, K. and Mostafavi, S. and Prinz, J. and St Onge, R. P. and van der Sluis, B. and Makhnevych, T. and Vizeacoumar, F. J. and Alizadeh, S. and Bahr, S. and Brost, R. L. and Chen, Y. and Cokol, M. and Deshpande, R. and Li, Z. and Lin, Z. Y. and Liang, W. and Marback, M. and Paw, J. and San Luis, B. J. and Shuteriqi, E. and Tong, A. H. and van Dyk, N. and Wallace, I. M. and Whitney, J. A. and Weirauch, M. T. and Zhong, G. and Zhu, H. and Houry, W. A. and Brudno, M. and Ragibizadeh, S. and Papp, B. and Pal, C. and Roth, F. P. and Giaever, G. and Nislow, C. and Troyanskaya, O. G. and Bussey, H. and Bader, G. D. and Gingras, A. C. and Morris, Q. D. and Kim, P. M. and Kaiser, C. A. and Myers, C. L. and Andrews, B. J. and Boone, C.},
   Title = {The genetic landscape of a cell},
   Journal = {Science},
   Volume = {327},
   Number = {5964},
   Pages = {425-31},
   Keywords = {Computational Biology
Gene Duplication
Gene Expression Regulation, Fungal
*Gene Regulatory Networks
Genes, Fungal
Genetic Fitness
*Genome, Fungal
Metabolic Networks and Pathways
Mutation
Protein Interaction Mapping
Saccharomyces cerevisiae/*genetics/*metabolism/physiology
Saccharomyces cerevisiae Proteins/genetics/*metabolism},
   Year = {2010} }




@article{Costanzo2011,
   Author = {Costanzo, M. and Baryshnikova, A. and Myers, C. L. and Andrews, B. and Boone, C.},
   Title = {Charting the genetic interaction map of a cell},
   Journal = {Curr Opin Biotechnol},
   Volume = {22},
   Number = {1},
   Pages = {66-74},
   Keywords = {Animals
Cells/*metabolism
Epistasis, Genetic
*Gene Regulatory Networks
Genome
*Genome-Wide Association Study
Genomics/methods
Genotype
Humans
Phenotype
Protein Interaction Mapping
Proteomics/methods
Saccharomyces cerevisiae},
   Year = {2011} }



@article{Davierwala2005,
   Author = {Davierwala, Armaity P. and Haynes, Jennifer and Li, Zhijian and Brost, Renee L. and Robinson, Mark D. and Yu, Lisa and Mnaimneh, Sanie and Ding, Huiming and Zhu, Hongwei and Chen, Yiqun and Cheng, Xin and Brown, Grant W. and Boone, Charles and Andrews, Brenda J. and Hughes, Timothy R.},
   Title = {The synthetic genetic interaction spectrum of essential genes},
   Journal = {Nat Genet},
   Volume = {37},
   Number = {10},
   Pages = {1147-1152},
      Year = {2005} }




@article{Davies2002,
   Author = {Davies, H. and Bignell, G. R. and Cox, C. and Stephens, P. and Edkins, S. and Clegg, S. and Teague, J. and Woffendin, H. and Garnett, M. J. and Bottomley, W. and Davis, N. and Dicks, E. and Ewing, R. and Floyd, Y. and Gray, K. and Hall, S. and Hawes, R. and Hughes, J. and Kosmidou, V. and Menzies, A. and Mould, C. and Parker, A. and Stevens, C. and Watt, S. and Hooper, S. and Wilson, R. and Jayatilake, H. and Gusterson, B. A. and Cooper, C. and Shipley, J. and Hargrave, D. and Pritchard-Jones, K. and Maitland, N. and Chenevix-Trench, G. and Riggins, G. J. and Bigner, D. D. and Palmieri, G. and Cossu, A. and Flanagan, A. and Nicholson, A. and Ho, J. W. and Leung, S. Y. and Yuen, S. T. and Weber, B. L. and Seigler, H. F. and Darrow, T. L. and Paterson, H. and Marais, R. and Marshall, C. J. and Wooster, R. and Stratton, M. R. and Futreal, P. A.},
   Title = {Mutations of the BRAF gene in human cancer},
   Journal = {Nature},
   Volume = {417},
   Number = {6892},
   Pages = {949-54},
   Keywords = {3T3 Cells
Amino Acid Sequence
Animals
Base Sequence
Cell Division
Cell Transformation, Neoplastic/genetics
DNA Mutational Analysis
Enzyme Activation
Humans
MAP Kinase Signaling System
Melanoma/enzymology/*genetics/metabolism/pathology
Mice
Mitogen-Activated Protein Kinases/metabolism
Molecular Sequence Data
Mutation, Missense/*genetics
Neoplasms/enzymology/*genetics/metabolism/pathology
Protein Structure, Tertiary
Proto-Oncogene Proteins B-raf
Proto-Oncogene Proteins c-raf/chemistry/*genetics/metabolism
Tumor Cells, Cultured
ras Proteins/immunology/metabolism},
   Year = {2002} }




@article{Deshpande2013,
   Author = {Deshpande, R. and Asiedu, M. K. and Klebig, M. and Sutor, S. and Kuzmin, E. and Nelson, J. and Piotrowski, J. and Shin, S. H. and Yoshida, M. and Costanzo, M. and Boone, C. and Wigle, D. A. and Myers, C. L.},
   Title = {A comparative genomic approach for identifying synthetic lethal interactions in human cancer},
   Journal = {Cancer Res},
   Volume = {73},
   Number = {20},
   Pages = {6128-36},
      Year = {2013} }




@article{DiNicolantonio2008,
   Author = {Di Nicolantonio, F. and Martini, M. and Molinari, F. and Sartore-Bianchi, A. and Arena, S. and Saletti, P. and De Dosso, S. and Mazzucchelli, L. and Frattini, M. and Siena, S. and Bardelli, A.},
   Title = {Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer},
   Journal = {J Clin Oncol},
   Volume = {26},
   Number = {35},
   Pages = {5705-12},
   Keywords = {Adult
Aged
Aged, 80 and over
Antibodies, Monoclonal/*therapeutic use
Antibodies, Monoclonal, Humanized
Antineoplastic Agents/*therapeutic use
Benzenesulfonates/pharmacology
Cell Survival/drug effects
Colorectal Neoplasms/*drug therapy/enzymology/genetics/pathology
Disease-Free Survival
Dose-Response Relationship, Drug
Drug Resistance, Neoplasm/genetics
Female
Gene Expression Profiling
*Gene Expression Regulation, Neoplastic
HT29 Cells
Humans
Italy
Male
Middle Aged
Mutation
Neoplasm Metastasis
Niacinamide/analogs & derivatives
*Patient Selection
Phenylurea Compounds
Protein Kinase Inhibitors/pharmacology
Proto-Oncogene Proteins/genetics
Proto-Oncogene Proteins B-raf/antagonists & inhibitors/*genetics
Pyridines/pharmacology
Receptor, Epidermal Growth Factor/*antagonists & inhibitors
Retrospective Studies
Switzerland
Time Factors
Treatment Outcome
Tumor Markers, Biological/*genetics
ras Proteins/genetics},
   Year = {2008} }




@article{Dienstmann2011,
   Author = {Dienstmann, R. and Tabernero, J.},
   Title = {BRAF as a target for cancer therapy},
   Journal = {Anticancer Agents Med Chem},
   Volume = {11},
   Number = {3},
   Pages = {285-95},
   Keywords = {Adenocarcinoma/*drug therapy/mortality/pathology
Animals
Antineoplastic Agents/chemical synthesis/pharmacology/*therapeutic use
Carcinoma
Cell Line, Tumor
Cell Proliferation/drug effects
Clinical Trials as Topic
Colorectal Neoplasms/*drug therapy/mortality/pathology
Disease Models, Animal
Disease-Free Survival
Drug Evaluation, Preclinical
Drug Resistance, Neoplasm/drug effects/genetics
Humans
Indoles/chemical synthesis/pharmacology/*therapeutic use
Melanoma/drug therapy/genetics/mortality/pathology
Mice
Molecular Targeted Therapy/methods
Mutation
Phosphorylation/drug effects
Protein Kinase Inhibitors/chemical synthesis/pharmacology/*therapeutic use
*Proto-Oncogene Proteins B-raf/antagonists & inhibitors/genetics/metabolism
Rats
Signal Transduction/drug effects/genetics
Sulfonamides/chemical synthesis/pharmacology/*therapeutic use
Thyroid Neoplasms/drug therapy/mortality/pathology
Xenograft Model Antitumor Assays},
   Year = {2011} }




@article{Dixon2009a,
   Author = {Dixon, S. J. and Andrews, B. J. and Boone, C.},
   Title = {Exploring the conservation of synthetic lethal genetic interaction networks},
   Journal = {Commun Integr Biol},
   Volume = {2},
   Number = {2},
   Pages = {78-81},
      Year = {2009} }




@article{Dixon2009b,
   Author = {Dixon, S. J. and Costanzo, M. and Baryshnikova, A. and Andrews, B. and Boone, C.},
   Title = {Systematic mapping of genetic interaction networks},
   Journal = {Annu Rev Genet},
   Volume = {43},
   Pages = {601-25},
   Keywords = {Animals
*Gene Regulatory Networks
Genetic Techniques
Humans
Phenotype
Saccharomyces cerevisiae/genetics
Signal Transduction},
   Year = {2009} }




@article{Dixon2008,
   Author = {Dixon, S. J. and Fedyshyn, Y. and Koh, J. L. and Prasad, T. S. and Chahwan, C. and Chua, G. and Toufighi, K. and Baryshnikova, A. and Hayles, J. and Hoe, K. L. and Kim, D. U. and Park, H. O. and Myers, C. L. and Pandey, A. and Durocher, D. and Andrews, B. J. and Boone, C.},
   Title = {Significant conservation of synthetic lethal genetic interaction networks between distantly related eukaryotes},
   Journal = {Proc Natl Acad Sci U S A},
   Volume = {105},
   Number = {43},
   Pages = {16653-8},
   Keywords = {*Gene Regulatory Networks
*Genes, Fungal
Genes, Lethal
*Phylogeny
Saccharomyces cerevisiae/genetics
Schizosaccharomyces/genetics},
   Year = {2008} }




@book{Dorogovtsev2003,
   Author = {Dorogovtsev, Sergey N and Mendes, Jos\'e FF},
   Title = {Evolution of networks: From biological nets to the Internet and WWW},
   Publisher = {Oxford University Press, USA},
      Year = {2003} }




@article{Erdos1959,
   Author = {Erd\"os, P. and R\'enyi, A},
   Title = {On Random Graphs I},
   Journal = {Publ. Math.  Debrecen},
   Volume = {6},
   Pages = {290-297},
      Year = {1959} }




@inproceedings{Erdos1960,
   Author = {Erd\"os, P. and R\'enyi, A.},
   Title = {On the Evolution of Random Graphs},
   BookTitle = {PUBLICATION OF THE MATHEMATICAL INSTITUTE OF THE HUNGARIAN ACADEMY OF SCIENCES},
   Pages = {17-61},
      Year = {1960} }




@article{Farmer2005,
   Author = {Farmer, H. and McCabe, N. and Lord, C. J. and Tutt, A. N. and Johnson, D. A. and Richardson, T. B. and Santarosa, M. and Dillon, K. J. and Hickson, I. and Knights, C. and Martin, N. M. and Jackson, S. P. and Smith, G. C. and Ashworth, A.},
   Title = {Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy},
   Journal = {Nature},
   Volume = {434},
   Number = {7035},
   Pages = {917-21},
   Keywords = {Animals
Antineoplastic Agents/pharmacology
Apoptosis/drug effects
Cell Survival/drug effects
DNA Damage
*DNA Repair
*Genes, BRCA1
*Genes, BRCA2
Mice
Mice, Nude
Models, Biological
Mutation/*genetics
Neoplasms/*drug therapy/enzymology/*genetics/pathology
Poly(ADP-ribose) Polymerases/*antagonists &
inhibitors/deficiency/genetics/metabolism
Substrate Specificity
Xenograft Model Antitumor Assays},
   Year = {2005} }




@article{Fece2015,
   Author = {Fece de la Cruz, F. and Gapp, B. V. and Nijman, S. M.},
   Title = {Synthetic Lethal Vulnerabilities of Cancer},
   Journal = {Annu Rev Pharmacol Toxicol},
   Volume = {55},
   Pages = {513-531},
      Year = {2015} }




@article{Fisher1919,
   Author = {Fisher, R. A.},
   Title = {XV.—The Correlation between Relatives on the Supposition of Mendelian Inheritance},
   Journal = {Earth and Environmental Science Transactions of the Royal Society of Edinburgh},
   Volume = {52},
   Number = {02},
   Pages = {399-433},
      Year = {1919} }




@article{Fong2009,
   Author = {Fong, P. C. and Boss, D. S. and Yap, T. A. and Tutt, A. and Wu, P. and Mergui-Roelvink, M. and Mortimer, P. and Swaisland, H. and Lau, A. and O'Connor, M. J. and Ashworth, A. and Carmichael, J. and Kaye, S. B. and Schellens, J. H. and de Bono, J. S.},
   Title = {Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers},
   Journal = {N Engl J Med},
   Volume = {361},
   Number = {2},
   Pages = {123-34},
   Keywords = {Adult
Aged
Aged, 80 and over
Dose-Response Relationship, Drug
Drug Design
Female
*Genes, BRCA1
*Genes, BRCA2
Germ-Line Mutation
Heterozygote
Humans
Male
Middle Aged
Neoplasms/*drug therapy/genetics
Phthalazines/adverse effects/pharmacokinetics/*therapeutic use
Piperazines/adverse effects/pharmacokinetics/*therapeutic use
Poly(ADP-ribose) Polymerases/*antagonists & inhibitors
Young Adult},
   Year = {2009} }




@article{Fong2010,
   Author = {Fong, P. C. and Yap, T. A. and Boss, D. S. and Carden, C. P. and Mergui-Roelvink, M. and Gourley, C. and De Greve, J. and Lubinski, J. and Shanley, S. and Messiou, C. and A'Hern, R. and Tutt, A. and Ashworth, A. and Stone, J. and Carmichael, J. and Schellens, J. H. and de Bono, J. S. and Kaye, S. B.},
   Title = {Poly(ADP)-ribose polymerase inhibition: frequent durable responses in BRCA carrier ovarian cancer correlating with platinum-free interval},
   Journal = {J Clin Oncol},
   Volume = {28},
   Number = {15},
   Pages = {2512-9},
   Keywords = {Adult
Aged
Aged, 80 and over
Cell Line, Tumor
Cohort Studies
Dose-Response Relationship, Drug
Drug Resistance, Neoplasm
Fallopian Tube Neoplasms/drug therapy/enzymology/genetics/pathology
Female
Genes, BRCA1
Genes, BRCA2
Germ-Line Mutation
Humans
Middle Aged
Neoplasm Staging
Ovarian Neoplasms/*drug therapy/enzymology/*genetics/pathology
Peritoneal Neoplasms/drug therapy/enzymology/genetics/pathology
Pharmacogenetics
Phthalazines/adverse effects/*therapeutic use
Piperazines/adverse effects/*therapeutic use
Poly(ADP-ribose) Polymerases/*antagonists & inhibitors/genetics},
   Year = {2010} }




@article{Fraser2004,
   Author = {Fraser, A.},
   Title = {Towards full employment: using RNAi to find roles for the redundant},
   Journal = {Oncogene},
   Volume = {23},
   Number = {51},
   Pages = {8346-52},
   Keywords = {Animals
Caenorhabditis elegans/genetics/physiology
Gene Expression Regulation/physiology
Genes, Lethal
Mutation
Neoplasms/genetics/metabolism
RNA Interference/*physiology
Saccharomyces cerevisiae/genetics/physiology},
   Year = {2004} }







@article{Hall2009,
   Author = {Hall, Mark and Frank, Eibe and Holmes, Geoffrey and Pfahringer, Bernhard and Reutemann, Peter and Witten, Ian H.},
   Title = {The WEKA data mining software: an update},
   Journal = {SIGKDD Explor. Newsl.},
   Volume = {11},
   Number = {1},
   Pages = {10-18},
      Year = {2009} }









@article{Heiskanen2012,
   Author = {Heiskanen, Marja A. and Aittokallio, Tero},
   Title = {Mining high-throughput screens for cancer drug targets-lessons from yeast chemical-genomic profiling and synthetic lethality},
   Journal = {Wiley Interdisciplinary Reviews: Data Mining and Knowledge Discovery},
   Volume = {2},
   Number = {3},
   Pages = {263-272},
      Year = {2012} }




@article{Hillenmeyer2008,
   Author = {Hillenmeyer, M. E.},
   Title = {The chemical genomic portrait of yeast: uncovering a phenotype for all genes},
   Journal = {Science},
   Volume = {320},
   Pages = {362-365},
      Year = {2008} }




@article{Hoehndorf2013,
   Author = {Hoehndorf, Robert and Hardy, Nigel W. and Osumi-Sutherland, David and Tweedie, Susan and Schofield, Paul N. and Gkoutos, Georgios V.},
   Title = {Systematic Analysis of Experimental Phenotype Data Reveals Gene Functions},
   Journal = {PLoS ONE},
   Volume = {8},
   Number = {4},
   Pages = {e60847},
      Year = {2013} }




@article{Holme2002,
   Author = {Holme, Petter and Kim, Beom Jun},
   Title = {Growing scale-free networks with tunable clustering},
   Journal = {Physical Review E},
   Volume = {65},
   Number = {2},
   Pages = {026107},
      Year = {2002} }




@article{Hopkins2008,
   Author = {Hopkins, Andrew L.},
   Title = {Network pharmacology: the next paradigm in drug discovery},
   Journal = {Nat Chem Biol},
   Volume = {4},
   Number = {11},
   Pages = {682-690},
      Year = {2008} }




@article{Jerby2014,
   Author = {Jerby-Arnon, Livnat and Pfetzer, Nadja and Waldman, Yedael Y and McGarry, Lynn and James, Daniel and Shanks, Emma and Seashore-Ludlow, Brinton and Weinstock, Adam and Geiger, Tamar and Clemons, Paul A and Gottlieb, Eyal and Ruppin, Eytan},
   Title = {Predicting Cancer-Specific Vulnerability via Data-Driven Detection of Synthetic Lethality},
   Journal = {Cell},
   Volume = {158},
   Number = {5},
   Pages = {1199-1209},
      Year = {2014} }




@incollection{Joachims1999,
   Author = {Joachims, Thorsten},
   Title = {Making large-scale support vector machine learning practical},
   BookTitle = {Advances in kernel methods},
   Editor = {Bernhard, Sch and lkopf and Christopher, J. C. Burges and Alexander, J. Smola},
   Publisher = {MIT Press},
   Pages = {169-184},
      Year = {1999} }


@article{Kelley2005,
   Author = {Kelley, Ryan and Ideker, Trey},
   Title = {Systematic interpretation of genetic interactions using protein networks},
   Journal = {Nat Biotech},
   Volume = {23},
   Number = {5},
   Pages = {561-566},
      Year = {2005} }




@phdthesis{Kelly2013,
   Author = {Kelly, S. T.},
   Title = {Statistical Predictions of Synthetic Lethal Interactions in Cancer},
   School = {University of Otago},
   Type = {Dissertation},
      Year = {2013} }




@article{Kozlov2015,
   Author = {Kozlov, Konstantin N. and Gursky, Vitaly V. and Kulakovskiy, Ivan V. and Samsonova, Maria G.},
   Title = {Sequence-based model of gap gene regulation network},
   Journal = {BMC Genomics},
   Volume = {15},
   Number = {Suppl 12},
   Pages = {S6},
      Year = {2015} }






@article{Laufer2013,
   Author = {Laufer, C. and Fischer, B. and Billmann, M. and Huber, W. and Boutros, M.},
   Title = {Mapping genetic interactions in human cancer cells with RNAi and multiparametric phenotyping},
   Journal = {Nat Methods},
   Volume = {10},
   Number = {5},
   Pages = {427-31},
   Keywords = {Automation
Colonic Neoplasms/genetics/pathology
Humans
Phenotype
Quality Control
*RNA Interference},
   Year = {2013} }




@article{LeMeur2008,
   Author = {Le Meur, N. and Gentleman, R.},
   Title = {Modeling synthetic lethality},
   Journal = {Genome Biol},
   Volume = {9},
   Number = {9},
   Pages = {R135},
   Keywords = {Computational Biology/methods
*Epistasis, Genetic
*Genes, Lethal
Models, Genetic
Molecular Chaperones/metabolism
Multiprotein Complexes/genetics/metabolism
Saccharomyces cerevisiae/*genetics
Saccharomyces cerevisiae Proteins/*genetics/metabolism},
   Year = {2008} }




@article{Lee2010a,
   Author = {Lee, Anna Y. and Perreault, Richard and Harel, Sharon and Boulier, Elodie L. and Suderman, Matthew and Hallett, Michael and Jenna, Sarah},
   Title = {Searching for Signaling Balance through the Identification of Genetic Interactors of the Rab Guanine-Nucleotide Dissociation Inhibitor gdi-1},
   Journal = {PLoS ONE},
   Volume = {5},
   Number = {5},
   Pages = {e10624},
      Year = {2010} }




@article{Lee2010b,
   Author = {Lee, Insuk and Lehner, Ben and Vavouri, Tanya and Shin, Junha and Fraser, Andrew G. and Marcotte, Edward M.},
   Title = {Predicting genetic modifier loci using functional gene networks},
   Journal = {Genome Research},
   Volume = {20},
   Number = {8},
   Pages = {1143-1153},
      Year = {2010} }




@article{Lee2009,
   Author = {Lee, I. and Marcotte, E. M.},
   Title = {Effects of functional bias on supervised learning of a gene network model},
   Journal = {Methods Mol Biol},
   Volume = {541},
   Pages = {463-75},
   Keywords = {*Artificial Intelligence
Bias (Epidemiology)
Computational Biology/*methods
Databases, Genetic/*statistics & numerical data
Gene Regulatory Networks/*physiology
Models, Biological
Pattern Recognition, Automated/methods/*statistics & numerical data
Saccharomyces cerevisiae/genetics},
   Year = {2009} }




@article{Lee2012,
   Author = {Lee, M. J. and Ye, A. S. and Gardino, A. K. and Heijink, A. M. and Sorger, P. K. and MacBeath, G. and Yaffe, M. B.},
   Title = {Sequential application of anticancer drugs enhances cell death by rewiring apoptotic signaling networks},
   Journal = {Cell},
   Volume = {149},
   Number = {4},
   Pages = {780-94},
   Keywords = {Antineoplastic Agents/*administration & dosage
*Apoptosis
Breast Neoplasms/*drug therapy/metabolism/pathology
Caspase 8
Cell Line, Tumor
DNA Damage
Drug Therapy, Combination/*methods
Female
Humans
Metabolic Networks and Pathways
Models, Biological
Receptor, Epidermal Growth Factor/*antagonists & inhibitors/metabolism
*Signal Transduction},
   Year = {2012} }


@misc{LeMeur2014,
   Author = {Le Meur, N. and Jiang, Z. and Liu, T. and Mar, J. and Gentleman, R. C.},
   Title = {SLGI: Synthetic Lethal Genetic Interaction. R package version 1.26.0},
         Year = {2014} }




@article{Li2011,
   Author = {Li, B. and Cao, W. and Zhou, J. and Luo, F.},
   Title = {Understanding and predicting synthetic lethal genetic interactions in Saccharomyces cerevisiae using domain genetic interactions},
   Journal = {BMC Syst Biol},
   Volume = {5},
   Pages = {73},
   Keywords = {Algorithms
Computational Biology/*methods
Databases, Protein
Fungal Proteins/chemistry
Genes, Fungal
Likelihood Functions
Models, Biological
Models, Genetic
Models, Statistical
Probability
Protein Structure, Tertiary
Saccharomyces cerevisiae/*genetics
Saccharomyces cerevisiae Proteins/genetics
Systems Biology},
   Year = {2011} }




@article{Li2014,
   Author = {Li, X. J. and Mishra, S. K. and Wu, M. and Zhang, F. and Zheng, J.},
   Title = {Syn-Lethality: An Integrative Knowledge Base of Synthetic Lethality towards Discovery of Selective Anticancer Therapies},
   Journal = {Biomed Res Int},
   Volume = {2014},
   Pages = {196034},
      Year = {2014} }




@article{Lokody2014,
   Author = {Lokody, Isabel},
   Title = {Computational modelling: A computational crystal ball},
   Journal = {Nature Reviews Cancer},
   Volume = {14},
   Number = {10},
   Pages = {649-649},
      Year = {2014} }

@article{Loupakis2009,
   Author = {Loupakis, F. and Ruzzo, A. and Cremolini, C. and Vincenzi, B. and Salvatore, L. and Santini, D. and Masi, G. and Stasi, I. and Canestrari, E. and Rulli, E. and Floriani, I. and Bencardino, K. and Galluccio, N. and Catalano, V. and Tonini, G. and Magnani, M. and Fontanini, G. and Basolo, F. and Falcone, A. and Graziano, F.},
   Title = {KRAS codon 61, 146 and BRAF mutations predict resistance to cetuximab plus irinotecan in KRAS codon 12 and 13 wild-type metastatic colorectal cancer},
   Journal = {Br J Cancer},
   Volume = {101},
   Number = {4},
   Pages = {715-21},
   Keywords = {Adenocarcinoma/*genetics/pathology
Adult
Aged
Antibodies, Monoclonal/administration & dosage
Antibodies, Monoclonal, Humanized
Antineoplastic Combined Chemotherapy Protocols/therapeutic use
Camptothecin/administration & dosage/analogs & derivatives
Codon
Colorectal Neoplasms/drug therapy/*genetics/pathology
DNA Mutational Analysis
Disease-Free Survival
Drug Resistance, Neoplasm/*genetics
Female
Humans
Kaplan-Meier Estimate
Male
Middle Aged
Mutation
Proto-Oncogene Proteins/*genetics
Proto-Oncogene Proteins B-raf/*genetics
Receptor, Epidermal Growth Factor/metabolism
Tumor Markers, Biological/*genetics
ras Proteins/*genetics},
   Year = {2009} }




@article{Lu2013,
   Author = {Lu, Xiaowen and Kensche, Philip R. and Huynen, Martijn A. and Notebaart, Richard A.},
   Title = {Genome evolution predicts genetic interactions in protein complexes and reveals cancer drug targets},
   Journal = {Nat Commun},
   Volume = {4},
      Year = {2013} }



@article{Lum2004,
   Author = {Lum, PY and Armour, CD and Stepaniants, SB and Cavet, G and Wolf, MK and Butler, JS and Hinshaw, JC and Garnier, P and Prestwich, GD and Leonardson, A and Garrett-Engele, P and Rush, CM and Bard, M and Schimmack, G and Phillips, JW and Roberts, CJ and Shoemaker, DD},
   Title = {Discovering modes of action for therapeutic compounds using a genome-wide screen of yeast heterozygotes},
   Volume = {116},
   Pages = {121-137},
      Year = {2004} }




@article{Milgram1967,
   Author = {Milgram, Stanley},
   Title = {The Small World Problem},
   Journal = {Psychology Today},
   Volume = {2},
   Pages = {60-67},
   Keywords = {bibtex-import
networks},
   Year = {1967} }




@article{Ooi2003,
   Author = {Ooi, S. L. and Shoemaker, D. D. and Boeke, J. D.},
   Title = {DNA helicase gene interaction network defined using synthetic lethality analyzed by microarray},
   Journal = {Nat Genet},
   Volume = {35},
   Number = {3},
   Pages = {277-86},
   Keywords = {DNA Helicases/*genetics/metabolism
DNA Replication
*Genes, Lethal
*Oligonucleotide Array Sequence Analysis
Recombination, Genetic
Saccharomyces cerevisiae/enzymology/*genetics},
   Year = {2003} }




@article{Paladugu2008,
   Author = {Paladugu, Sri and Zhao, Shan and Ray, Animesh and Raval, Alpan},
   Title = {Mining protein networks for synthetic genetic interactions},
   Journal = {BMC Bioinformatics},
   Volume = {9},
   Number = {1},
   Pages = {426},
      Year = {2008} }




@article{Pandey2010,
   Author = {Pandey, G. and Zhang, B. and Chang, A. N. and Myers, C. L. and Zhu, J. and Kumar, V. and Schadt, E. E.},
   Title = {An integrative multi-network and multi-classifier approach to predict genetic interactions},
   Journal = {PLoS Comput Biol},
   Volume = {6},
   Number = {9},
   Keywords = {Area Under Curve
Computational Biology/*methods
Databases, Genetic
*Gene Regulatory Networks
*Genes, Fungal
Phenotype
ROC Curve
Reproducibility of Results
Saccharomyces cerevisiae Proteins/chemistry/classification/*genetics
Statistics, Nonparametric
Transcription Factors/chemistry/classification/*genetics},
   Year = {2010} }




@article{Prahallad2012,
   Author = {Prahallad, A. and Sun, C. and Huang, S. and Di Nicolantonio, F. and Salazar, R. and Zecchin, D. and Beijersbergen, R. L. and Bardelli, A. and Bernards, R.},
   Title = {Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR},
   Journal = {Nature},
   Volume = {483},
   Number = {7387},
   Pages = {100-3},
   Keywords = {Animals
Antibodies, Monoclonal/pharmacology
Antibodies, Monoclonal, Humanized
Antineoplastic Agents/pharmacology/therapeutic use
Apoptosis/drug effects
Cell Line, Tumor
Cell Proliferation/drug effects
Colorectal Neoplasms/*drug therapy/*enzymology/genetics/pathology
Drug Resistance, Neoplasm/*drug effects
Drug Synergism
Enzyme Activation/drug effects
Feedback, Physiological/*drug effects
Female
HEK293 Cells
Humans
Indoles/pharmacology/therapeutic use
Melanoma/drug therapy/metabolism
Mice
Protein Kinase Inhibitors/pharmacology/therapeutic use
Proto-Oncogene Proteins B-raf/*antagonists &
inhibitors/chemistry/*genetics/metabolism
Quinazolines/pharmacology/therapeutic use
RNA Interference
Receptor, Epidermal Growth Factor/*agonists/antagonists & inhibitors/metabolism
Sulfonamides/pharmacology/therapeutic use
Xenograft Model Antitumor Assays},
   Year = {2012} }




@article{Qi2008,
   Author = {Qi, Yan and Suhail, Yasir and Lin, Yu-yi and Boeke, Jef D. and Bader, Joel S.},
   Title = {Finding friends and enemies in an enemies-only network: A graph diffusion kernel for predicting novel genetic interactions and co-complex membership from yeast genetic interactions},
   Journal = {Genome Research},
   Volume = {18},
   Number = {12},
   Pages = {1991-2004},
      Year = {2008} }

@article{Roguev2008,
   Author = {Roguev, A. and Bandyopadhyay, S. and Zofall, M. and Zhang, K. and Fischer, T. and Collins, S. R. and Qu, H. and Shales, M. and Park, H. O. and Hayles, J. and Hoe, K. L. and Kim, D. U. and Ideker, T. and Grewal, S. I. and Weissman, J. S. and Krogan, N. J.},
   Title = {Conservation and rewiring of functional modules revealed by an epistasis map in fission yeast},
   Journal = {Science},
   Volume = {322},
   Number = {5900},
   Pages = {405-10},
   Keywords = {DNA Repair
DNA Replication
*Epistasis, Genetic
Gene Expression Regulation, Fungal
Gene Regulatory Networks
*Genes, Fungal
Histones/metabolism
Mutation
RNA Interference
Saccharomyces cerevisiae/genetics/metabolism
Schizosaccharomyces/*genetics/metabolism
Schizosaccharomyces pombe Proteins/genetics/metabolism},
   Year = {2008} }




@article{Roguev2007,
   Author = {Roguev, Assen and Wiren, Marianna and Weissman, Jonathan S. and Krogan, Nevan J.},
   Title = {High-throughput genetic interaction mapping in the fission yeast Schizosaccharomyces pombe},
   Journal = {Nat Meth},
   Volume = {4},
   Number = {10},
   Pages = {861-866},
      Year = {2007} }


@article{Sander2014,
   Author = {Sander, J. D. and Joung, J. K.},
   Title = {CRISPR-Cas systems for editing, regulating and targeting genomes},
   Journal = {Nat Biotechnol},
   Volume = {32},
   Number = {4},
   Pages = {347-55},
   Keywords = {Animals
*CRISPR-Cas Systems
*Clustered Regularly Interspaced Short Palindromic Repeats
Genetic Engineering/*methods
Genomics/*methods
Humans
Mice
Rabbits
Rats},
   Year = {2014} }




@article{Schuldiner2005,
   Author = {Schuldiner, M. and Collins, S. R. and Thompson, N. J. and Denic, V. and Bhamidipati, A. and Punna, T. and Ihmels, J. and Andrews, B. and Boone, C. and Greenblatt, J. F. and Weissman, J. S. and Krogan, N. J.},
   Title = {Exploration of the function and organization of the yeast early secretory pathway through an epistatic miniarray profile},
   Journal = {Cell},
   Volume = {123},
   Number = {3},
   Pages = {507-19},
   Keywords = {Cluster Analysis
Computational Biology
Endoplasmic Reticulum/genetics/metabolism
*Epistasis, Genetic
*Gene Expression Profiling
Glycosylation
Membrane Proteins/genetics
Mutation
*Protein Interaction Mapping
Protein Transport/genetics
Receptors, Peptide/genetics
Saccharomyces cerevisiae/genetics/*metabolism
Saccharomyces cerevisiae Proteins/genetics/*metabolism},
   Year = {2005} }




@article{Schuldiner2006,
   Author = {Schuldiner, M. and Collins, S. R. and Weissman, J. S. and Krogan, N. J.},
   Title = {Quantitative genetic analysis in Saccharomyces cerevisiae using epistatic miniarray profiles (E-MAPs) and its application to chromatin functions},
   Journal = {Methods},
   Volume = {40},
   Number = {4},
   Pages = {344-52},
   Keywords = {Chromatin/genetics/*metabolism
Chromatin Assembly and Disassembly
Computational Biology
*Epistasis, Genetic
Oligonucleotide Array Sequence Analysis
*Protein Interaction Mapping
Saccharomyces cerevisiae/*genetics/metabolism
Saccharomyces cerevisiae Proteins/*genetics},
   Year = {2006} }




@article{Shaib2013,
   Author = {Shaib, W. and Mahajan, R. and El-Rayes, B.},
   Title = {Markers of resistance to anti-EGFR therapy in colorectal cancer},
   Journal = {J Gastrointest Oncol},
   Volume = {4},
   Number = {3},
   Pages = {308-18},
      Year = {2013} }




@article{Siena2009,
   Author = {Siena, S. and Sartore-Bianchi, A. and Di Nicolantonio, F. and Balfour, J. and Bardelli, A.},
   Title = {Biomarkers predicting clinical outcome of epidermal growth factor receptor-targeted therapy in metastatic colorectal cancer},
   Journal = {J Natl Cancer Inst},
   Volume = {101},
   Number = {19},
   Pages = {1308-24},
   Keywords = {Animals
Antibodies, Monoclonal/*pharmacology/therapeutic use
Antibodies, Monoclonal, Humanized
Antineoplastic Agents/*pharmacology
Colorectal Neoplasms/*drug therapy/genetics/pathology
Disease-Free Survival
Gene Expression Regulation, Neoplastic/drug effects
Humans
*Mutation/drug effects
Neoplasm Staging
Odds Ratio
PTEN Phosphohydrolase/drug effects/genetics
Phosphatidylinositol 3-Kinases/drug effects/genetics
Predictive Value of Tests
Proto-Oncogene Proteins/*drug effects/*genetics
Proto-Oncogene Proteins B-raf/drug effects/genetics
Proto-Oncogene Proteins p21(ras)/drug effects/genetics
Randomized Controlled Trials as Topic
Receptor, Epidermal Growth Factor/*antagonists & inhibitors/metabolism
Research Design
Tumor Markers, Biological/*metabolism},
   Year = {2009} }







@article{Sun2014,
   Author = {Sun, Chong and Wang, Liqin and Huang, Sidong and Heynen, Guus J. J. E. and Prahallad, Anirudh and Robert, Caroline and Haanen, John and Blank, Christian and Wesseling, Jelle and Willems, Stefan M. and Zecchin, Davide and Hobor, Sebastijan and Bajpe, Prashanth K. and Lieftink, Cor and Mateus, Christina and Vagner, Stephan and Grernrum, Wipawadee and Hofland, Ingrid and Schlicker, Andreas and Wessels, Lodewyk F. A. and Beijersbergen, Roderick L. and Bardelli, Alberto and Di Nicolantonio, Federica and Eggermont, Alexander M. M. and Bernards, Rene},
   Title = {Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma},
   Journal = {Nature},
   Volume = {508},
   Number = {7494},
   Pages = {118-122},
      Year = {2014} }




@article{Taylor2009,
   Author = {Taylor, I. W. and Linding, R. and Warde-Farley, D. and Liu, Y. and Pesquita, C. and Faria, D. and Bull, S. and Pawson, T. and Morris, Q. and Wrana, J. L.},
   Title = {Dynamic modularity in protein interaction networks predicts breast cancer outcome},
   Journal = {Nat Biotechnol},
   Volume = {27},
   Number = {2},
   Pages = {199-204},
   Keywords = {Algorithms
Breast Neoplasms/*diagnosis/*metabolism
Computational Biology
Computer Simulation
Data Interpretation, Statistical
Female
Gene Regulatory Networks/*physiology
Humans
Kaplan-Meier Estimate
Neoplasm Proteins/genetics/metabolism
Prognosis
Protein Interaction Mapping/*methods
ROC Curve
Reproducibility of Results
Signal Transduction/*physiology
Statistics, Nonparametric
Ubiquitin-Protein Ligases/genetics/metabolism},
   Year = {2009} }


@article{Tiong2013,
   Author = {Tiong, K. L. and Chang, K. C. and Yeh, K. T. and Liu, T. Y. and Wu, J. H. and Hsieh, P. H. and Lin, S. H. and Lai, W. Y. and Hsu, Y. C. and Chen, J. Y. and Chang, J. G. and Shieh, G. S.},
   Title = {CSNK1E/CTNNB1 are synthetic lethal to TP53 in colorectal cancer and are markers for prognosis},
   Journal = {Neoplasia},
   Volume = {16},
   Number = {5},
   Pages = {441-50},
      Year = {2014} }




@article{Tischler2008,
   Author = {Tischler, Julia and Lehner, Ben and Fraser, Andrew G.},
   Title = {Evolutionary plasticity of genetic interaction networks},
   Journal = {Nat Genet},
   Volume = {40},
   Number = {4},
   Pages = {390-391},
      Year = {2008} }




@article{Tong2001,
   Author = {Tong, A. H. and Evangelista, M. and Parsons, A. B. and Xu, H. and Bader, G. D. and Page, N. and Robinson, M. and Raghibizadeh, S. and Hogue, C. W. and Bussey, H. and Andrews, B. and Tyers, M. and Boone, C.},
   Title = {Systematic genetic analysis with ordered arrays of yeast deletion mutants},
   Journal = {Science},
   Volume = {294},
   Number = {5550},
   Pages = {2364-8},
   Keywords = {Carrier Proteins/genetics/physiology
Cell Cycle Proteins/genetics/physiology
Cell Polarity
Computational Biology
Crosses, Genetic
*Cytoskeletal Proteins
Cytoskeleton/physiology
DNA Helicases/genetics/physiology
DNA Repair
DNA, Fungal/biosynthesis
Databases, Genetic
Endodeoxyribonucleases/genetics/physiology
Flap Endonucleases
Fungal Proteins/genetics/physiology
*Gene Deletion
Genes, Essential
Genes, Fungal/*physiology
Genetic Markers
*Genetic Techniques
Genome, Fungal
*Microfilament Proteins
Microtubule Proteins/genetics/physiology
Mitosis
RecQ Helicases
Recombination, Genetic
Robotics
Saccharomyces cerevisiae/*genetics/growth & development/*physiology
Saccharomyces cerevisiae Proteins/genetics/physiology},
   Year = {2001} }




@article{Tong2004,
   Author = {Tong, A. H. and Lesage, G. and Bader, G. D. and Ding, H. and Xu, H. and Xin, X. and Young, J. and Berriz, G. F. and Brost, R. L. and Chang, M. and Chen, Y. and Cheng, X. and Chua, G. and Friesen, H. and Goldberg, D. S. and Haynes, J. and Humphries, C. and He, G. and Hussein, S. and Ke, L. and Krogan, N. and Li, Z. and Levinson, J. N. and Lu, H. and Menard, P. and Munyana, C. and Parsons, A. B. and Ryan, O. and Tonikian, R. and Roberts, T. and Sdicu, A. M. and Shapiro, J. and Sheikh, B. and Suter, B. and Wong, S. L. and Zhang, L. V. and Zhu, H. and Burd, C. G. and Munro, S. and Sander, C. and Rine, J. and Greenblatt, J. and Peter, M. and Bretscher, A. and Bell, G. and Roth, F. P. and Brown, G. W. and Andrews, B. and Bussey, H. and Boone, C.},
   Title = {Global mapping of the yeast genetic interaction network},
   Journal = {Science},
   Volume = {303},
   Number = {5659},
   Pages = {808-13},
   Keywords = {Amino Acid Sequence
Computational Biology
Cystic Fibrosis/genetics
Gene Deletion
Genes, Essential
*Genes, Fungal
Genetic Diseases, Inborn/genetics
Genotype
Humans
Molecular Sequence Data
Multifactorial Inheritance
Mutation
Phenotype
Polymorphism, Genetic
Retinitis Pigmentosa/genetics
Saccharomyces cerevisiae/*genetics/*metabolism
Saccharomyces cerevisiae Proteins/chemistry/genetics/*metabolism},
   Year = {2004} }




@article{Travers1969,
   Author = {Travers, Jeffrey and Milgram, Stanley},
   Title = {An Experimental Study of the Small World Problem},
   Journal = {Sociometry},
   Volume = {32},
   Number = {4},
   Pages = {425--443},
   Keywords = {small_world social_network_search},
   Year = {1969} }




@article{Tsai2012,
   Author = {Tsai, H. C. and Li, H. and Van Neste, L. and Cai, Y. and Robert, C. and Rassool, F. V. and Shin, J. J. and Harbom, K. M. and Beaty, R. and Pappou, E. and Harris, J. and Yen, R. W. and Ahuja, N. and Brock, M. V. and Stearns, V. and Feller-Kopman, D. and Yarmus, L. B. and Lin, Y. C. and Welm, A. L. and Issa, J. P. and Minn, I. and Matsui, W. and Jang, Y. Y. and Sharkis, S. J. and Baylin, S. B. and Zahnow, C. A.},
   Title = {Transient low doses of DNA-demethylating agents exert durable antitumor effects on hematological and epithelial tumor cells},
   Journal = {Cancer Cell},
   Volume = {21},
   Number = {3},
   Pages = {430-46},
   Keywords = {Animals
Antimetabolites, Antineoplastic/*pharmacology
Apoptosis/drug effects
Azacitidine/*analogs & derivatives/*pharmacology
Bone Marrow Cells/drug effects/pathology
Breast Neoplasms/drug therapy/genetics/pathology
Cell Cycle/drug effects
Cell Line, Tumor
Cell Transformation, Neoplastic/genetics
DNA Damage
DNA Methylation/*drug effects
DNA Modification Methylases/*antagonists & inhibitors
Gene Silencing
Humans
Leukemia/drug therapy/*genetics/pathology
Mice
Molecular Sequence Data
Neoplastic Stem Cells/drug effects/pathology
Promoter Regions, Genetic
Signal Transduction
Tumor Cells, Cultured},
   Year = {2012} }


@article{Typas2008,
   Author = {Typas, A. and Nichols, R. J. and Siegele, D. A. and Shales, M. and Collins, S. R. and Lim, B. and Braberg, H. and Yamamoto, N. and Takeuchi, R. and Wanner, B. L. and Mori, H. and Weissman, J. S. and Krogan, N. J. and Gross, C. A.},
   Title = {High-throughput, quantitative analyses of genetic interactions in E. coli},
   Journal = {Nat Methods},
   Volume = {5},
   Number = {9},
   Pages = {781-7},
   Keywords = {*Conjugation, Genetic
Escherichia coli/*genetics
Genome, Bacterial
*Mutation},
   Year = {2008} }



@book{Vapnik1995,
   Author = {Vapnik, Vladimir N.},
   Title = {The nature of statistical learning theory},
   Publisher = {Springer-Verlag New York, Inc.},
      Year = {1995} }




@article{Vargas2004,
   Author = {Vargas, J. Jr and Gusella, G.L. and Najfeld, V. and Klotman, M.E. and Cara, A.},
   Title = {Novel integrase-defective lentiviral episomal vectors for gene transfer},
   Journal = {Hum Gene Ther},
   Volume = {15},
   Pages = {361-372},
      Year = {2004} }




@article{Vizeacoumar2013,
   Author = {Vizeacoumar, F. J. and Arnold, R. and Vizeacoumar, F. S. and Chandrashekhar, M. and Buzina, A. and Young, J. T. and Kwan, J. H. and Sayad, A. and Mero, P. and Lawo, S. and Tanaka, H. and Brown, K. R. and Baryshnikova, A. and Mak, A. B. and Fedyshyn, Y. and Wang, Y. and Brito, G. C. and Kasimer, D. and Makhnevych, T. and Ketela, T. and Datti, A. and Babu, M. and Emili, A. and Pelletier, L. and Wrana, J. and Wainberg, Z. and Kim, P. M. and Rottapel, R. and O'Brien, C. A. and Andrews, B. and Boone, C. and Moffat, J.},
   Title = {A negative genetic interaction map in isogenic cancer cell lines reveals cancer cell vulnerabilities},
   Journal = {Mol Syst Biol},
   Volume = {9},
   Pages = {696},
   Keywords = {Breast Neoplasms/*genetics/metabolism/pathology
Cell Line, Tumor
Coculture Techniques
*Epistasis, Genetic
Female
Gene Regulatory Networks
*Genes, Essential
Genome, Human
Humans
Mutation
Neoplasm Proteins/*genetics/metabolism
Ovarian Neoplasms/*genetics/metabolism/pathology
PTEN Phosphohydrolase/deficiency/*genetics
Pancreatic Neoplasms/*genetics/metabolism/pathology
RNA, Small Interfering/genetics/metabolism},
   Year = {2013} }


@misc{Wappett2014,
   Author = {Wappett, M.},
   Title = {BiSEp: Toolkit To Identify Candidate Synthetic Lethality. R package version 2.0},
         Year = {2014} }




@article{Warburg1956,
   Author = {Warburg, O.},
   Title = {On the Origin of Cancer Cells},
   Journal = {Science},
   Volume = {123},
   Number = {3191},
   Pages = {390-314},
      Year = {1956} }




@article{Watts1998,
   Author = {Watts, D. J. and Strogatz, S. H.},
   Title = {Collective dynamics of 'small-world' networks},
   Journal = {Nature},
   Volume = {393},
   Number = {6684},
   Pages = {440-2},
   Keywords = {Animals
Caenorhabditis elegans/physiology
Communicable Diseases/*transmission
Games, Experimental
*Models, Biological
Models, Neurological
Models, Theoretical
Nerve Net},
   Year = {1998} }




@article{Wong2004,
   Author = {Wong, Sharyl L. and Zhang, Lan V. and Tong, Amy H. Y. and Li, Zhijian and Goldberg, Debra S. and King, Oliver D. and Lesage, Guillaume and Vidal, Marc and Andrews, Brenda and Bussey, Howard and Boone, Charles and Roth, Frederick P.},
   Title = {Combining biological networks to predict genetic interactions},
   Journal = {Proceedings of the National Academy of Sciences of the United States of America},
   Volume = {101},
   Number = {44},
   Pages = {15682-15687},
      Year = {2004} }




@article{Wu2014,
   Author = {Wu, M. and Li, X. and Zhang, F. and Li, X. and Kwoh, C. K. and Zheng, J.},
   Title = {In silico prediction of synthetic lethality by meta-analysis of genetic interactions, functions, and pathways in yeast and human cancer},
   Journal = {Cancer Inform},
   Volume = {13},
   Number = {Suppl 3},
   Pages = {71-80},
      Year = {2014} }




@article{Yang2012,
   Author = {Yang, H. and Higgins, B. and Kolinsky, K. and Packman, K. and Bradley, W. D. and Lee, R. J. and Schostack, K. and Simcox, M. E. and Kopetz, S. and Heimbrook, D. and Lestini, B. and Bollag, G. and Su, F.},
   Title = {Antitumor activity of BRAF inhibitor vemurafenib in preclinical models of BRAF-mutant colorectal cancer},
   Journal = {Cancer Res},
   Volume = {72},
   Number = {3},
   Pages = {779-89},
   Keywords = {Animals
Antibodies, Monoclonal/administration & dosage
Antibodies, Monoclonal, Humanized/administration & dosage
Antineoplastic Combined Chemotherapy Protocols/therapeutic use
Area Under Curve
Blotting, Western
Camptothecin/administration & dosage/analogs & derivatives
Cell Line, Tumor
Cell Proliferation/drug effects
Colorectal Neoplasms/*drug therapy/genetics/pathology
Deoxycytidine/administration & dosage/analogs & derivatives
Dose-Response Relationship, Drug
Drug Resistance, Neoplasm/drug effects
Fluorouracil/administration & dosage/analogs & derivatives
HCT116 Cells
HT29 Cells
Humans
Indoles/administration & dosage/pharmacokinetics/*pharmacology
Kaplan-Meier Estimate
Mice
Mice, Nude
Mitogen-Activated Protein Kinases/metabolism
Mutation
Phosphorylation/drug effects
Proto-Oncogene Proteins B-raf/*antagonists & inhibitors/genetics/metabolism
Quinazolines/administration & dosage
Sulfonamides/administration & dosage/pharmacokinetics/*pharmacology
*Xenograft Model Antitumor Assays},
   Year = {2012} }




@article{Yuan2013,
   Author = {Yuan, Zi-Xu and Wang, Xiao-Yan and Qin, Qi-Yuan and Chen, De-Feng and Zhong, Qing-Hua and Wang, Lei and Wang, Jian-Ping},
   Title = {The Prognostic Role of BRAF Mutation in Metastatic Colorectal Cancer Receiving Anti-EGFR Monoclonal Antibodies: A Meta-Analysis},
   Journal = {PLoS ONE},
   Volume = {8},
   Number = {6},
   Pages = {e65995},
      Year = {2013} }




@article{Zhang2015,
   Author = {Zhang, F. and Wu, M. and Li, X. J. and Li, X. L. and Kwoh, C. K. and Zheng, J.},
   Title = {Predicting essential genes and synthetic lethality via influence propagation in signaling pathways of cancer cell fates},
   Journal = {J Bioinform Comput Biol},
   Pages = {1541002},
      Year = {2015} }




@article{Zhong2006,
   Author = {Zhong, Weiwei and Sternberg, Paul W.},
   Title = {Genome-Wide Prediction of C. elegans Genetic Interactions},
   Journal = {Science},
   Volume = {311},
   Number = {5766},
   Pages = {1481-1484},
      Year = {2006} }






@article{Guell2014,
   Author = {G\"uell, O. and Sagués, F. and Serrano, M.Á.},
   Title = {Essential Plasticity and Redundancy of Metabolism Unveiled by Synthetic Lethality Analysis},
   Journal = {PLoS Comput Biol},
   Volume = {10},
   Number = {5},
   Pages = {e1003637},
      Year = {2014} }



@article{Strom2012,
   Author = {Str\"om, Cecilia and Helleday, Thomas},
   Title = {Strategies for the Use of Poly(adenosine diphosphate ribose) Polymerase (PARP) Inhibitors in Cancer Therapy},
   Journal = {Biomolecules},
   Volume = {2},
   Number = {4},
   Pages = {635-649},
      Year = {2012} }



@article{Barabasi1999,
   Author = {Barab\'asi, A. L. and Albert, R.},
   Title = {Emergence of scaling in random networks},
   Journal = {Science},
   Volume = {286},
   Number = {5439},
   Pages = {509-12},
      Year = {1999} }




@article{Barabasi2004,
   Author = {Barab\'asi, A. L. and Oltvai, Z. N.},
   Title = {Network biology: understanding the cell's functional organization},
   Journal = {Nat Rev Genet},
   Volume = {5},
   Number = {2},
   Pages = {101-13},
   Keywords = {Animals
Cell Communication
Cell Compartmentation
*Cell Physiological Phenomena
Humans
Metabolism
*Models, Biological},
   Year = {2004} }



@article{Han2004,
   Author = {Han, Jing-Dong J. and Bertin, Nicolas and Hao, Tong and Goldberg, Debra S. and Berriz, Gabriel F. and Zhang, Lan V. and Dupuy, Denis and Walhout, Albertha J. M. and Cusick, Michael E. and Roth, Frederick P. and Vidal, Marc},
   Title = {Evidence for dynamically organized modularity in the yeast protein-protein interaction network},
   Journal = {Nature},
   Volume = {430},
   Number = {6995},
   Pages = {88-93},
      Year = {2004} }

@article{vanSteen2011,
   Author = {van Steen, Kristel},
   Title = {Travelling the world of gene–gene interactions},
   Journal = {Briefings in Bioinformatics},
      Year = {2011} }


@book{vanSteen2010,
   Author = {van Steen, M.},
   Title = {Graph Theory and Complex Networks: An Introduction},
   Publisher = {Maarten van Steen},
   Address = {VU Amsterdam},
      Year = {2010} }

@Article{igraph,
    title = {The igraph software package for complex network research},
    author = {Gabor Csardi and Tamas Nepusz},
    journal = {InterJournal},
    volume = {Complex Systems},
    pages = {1695},
    year = {2006},
    url = {http://igraph.org},
  }



@article{Latora2001,
  title = {Efficient Behavior of Small-World Networks},
  author = {Latora, Vito and Marchiori, Massimo},
  journal = {Phys. Rev. Lett.},
  volume = {87},
  issue = {19},
  pages = {198701},
  numpages = {4},
  year = {2001},
  month = {Oct},
  publisher = {American Physical Society},
  doi = {10.1103/PhysRevLett.87.198701},
  url = {http://link.aps.org/doi/10.1103/PhysRevLett.87.198701},
}

@article{Kranthi2013,
  year = {2013},
  volume = {9},
  number = {8},
  pages = {2163-2167},
  author = {Kranthi, S. and Rao, SB and Manimaran, P},
  title = {Identification of synthetic lethal pairs in biological systems through network information centrality},
  journal = {Mol. BioSyst.},
  publisher  = {The Royal Society of Chemistry},
  doi  = {10.1039/C3MB25589A},
  url  ={http://dx.doi.org/10.1039/C3MB25589A},
  abstract  = {The immense availability of protein interaction data{,} provided with an abstract network approach is valuable for the improved interpretation of biological processes and protein functions globally. The connectivity of a protein and its structure are related to its functional properties. Highly connected proteins are often functionally cardinal and the knockout of such proteins leads to lethality. In this paper{,} we propose a new approach based on graph information centrality measures to identify the synthetic lethal pairs in biological systems. To illustrate the efficacy of our approach{,} we have applied it to a human cancer protein interaction network. It is found that the lethal pairs obtained were analogous to the experimental and computational inferences{,} implying that our approach can serve as a surrogate for predicting the synthetic lethality.},
}



@article{Holm1979,
  year = {1979},
  volume = {6},
  number = {2},
  pages = {65-70},
  author = {Holm, S},
  title = {A simple sequentially rejective multiple test procedure},
  journal = {Scandinavian Journal of Statistics},
}

 
 
@article{Huang2003,
  year = {2003},
  volume = {361},
  pages = {1590-1596},
  author = {Huang, E and Cheng, SH and Dressman, H and Pittman, J and Tsou, MH and Horng, CF and Bild, A and Iversen, ES and Liao, M and Chen, CM and West, M and Nevins, JR and Huang, AT},
  title = {Gene expression predictors of breast cancer outcomes},
  journal = {Lancet},
}



@article{Robinson2010,
  doi = {10.1186/gb-2010-11-3-r25},
  year = {2010},
  publisher = {Springer Nature},
  volume = {11},
  number = {3},
  pages = {R25},
  author = {Mark D Robinson and Alicia Oshlack},
  title = {A scaling normalization method for differential expression analysis of {RNA}-seq data},
  journal = {Genome Biol},
}


@article{Law2014,
  doi = {10.1186/gb-2014-15-2-r29},
  year = {2014},
  publisher = {Springer Nature},
  volume = {15},
  number = {2},
  pages = {R29},
  author = {Charity W Law and Yunshun Chen and Wei Shi and Gordon K Smyth},
  title = {voom: precision weights unlock linear model analysis tools for {RNA}-seq read counts},
  journal = {Genome Biol},
}


@article{ICGC2011,
  author = {Zhang, Junjun and Baran, Joachim and Cros, A and  Guberman, Jonathan M and  Haider, Syed and  Hsu, Jack and  Liang, Yong and  Rivkin, Elena and  Wang, Jianxin and  Whitty, Brett and  Wong-Erasmus, Marie and  Yao, Long and  Kasprzyk, Arek},
  title = {International Cancer Genome Consortium Data Portal—a one-stop shop for cancer genomics data},
  journal = {Database: The Journal of Biological Databases and Curation},
  volume = {2011},
   pages = {bar026},
  year = {2011},
}


@Book{rountree98,
  author = 	 {Nathan Rountree},
  title = 	 {How to do Anything},
  publisher = 	 {Non-existent Publishers},
  year = 	 {1998},
  OPTkey = 	 {},
  OPTeditor = 	 {},
  OPTvolume = 	 {},
  OPTnumber = 	 {},
  OPTseries = 	 {},
  address = 	 {Dunedin, New Zealand},
  OPTedition = 	 {},
  OPTmonth = 	 {},
  OPTnote = 	 {},
  OPTannote = 	 {}
}


@InProceedings{amir97,
  author = 	 {Amihood Amir and Ronen Feldman and Reuven Kashi},
  title = 	 {A New and Versatile Method for Association Generation},
  booktitle = 	 {Principles of Data Mining and Knowledge Engineering;
                   First European Symposium, PKDD'97},
  OPTcrossref =  {},
  OPTkey = 	 {},
  editor = 	 {Jan Komorowsk and Jan Zytkow},
  OPTvolume = 	 {},
  OPTnumber = 	 {},
  OPTseries = 	 {},
  year = 	 {1997},
  OPTorganization = {},
  publisher = {Springer-Verlag},
  address = 	 {Trondheim, Norway},
  month = 	 {June},
  pages = 	 {221--231},
  OPTnote = 	 {},
  OPTannote = 	 {}
}


@Book{goosens94,
  author = 	 {Michael Goosens and Frank Mittelbach and Alexander Samarin},
  title = 	 {The \LaTeX\ Companion},
  publisher = 	 {Addison-Wesley},
  year = 	 {1994},
  OPTkey = 	 {},
  OPTeditor = 	 {},
  OPTvolume = 	 {},
  OPTnumber = 	 {},
  OPTseries = 	 {},
  OPTaddress = 	 {},
  edition = 	 {2},
  month = 	 {May},
  OPTnote = 	 {},
  OPTannote = 	 {}
}


@article{fdr1995,
  author = {Benjamini, Yoav and Hochberg, Yosef},
  title = {Controlling the False Discovery Rate: A Practical and Powerful Approach to Multiple Testing},
  journal = {Journal of the Royal Statistical Society. Series B (Methodological)},
  volume = {57},
  number = {1},
  pages = {289-300},
  abstract = {The common approach to the multiplicity problem calls for controlling the familywise error rate (FWER). This approach, though, has faults, and we point out a few. A different approach to problems of multiple significance testing is presented. It calls for controlling the expected proportion of falsely rejected hypotheses-the false discovery rate. This error rate is equivalent to the FWER when all hypotheses are true but is smaller otherwise. Therefore, in problems where the control of the false discovery rate rather than that of the FWER is desired, there is potential for a gain in power. A simple sequential Bonferroni-type procedure is proved to control the false discovery rate for independent test statistics, and a simulation study shows that the gain in power is substantial. The use of the new procedure and the appropriateness of the criterion are illustrated with examples.},
  keywords = {multiple-testing significance},
  year = {1995},
}



@article{TCGA2012,
  author = {Cancer Genome Atlas Research Network},
  title = {Comprehensive molecular portraits of human breast tumours},
  journal = {Nature},
  volume = {490},
  number = {7418},
  pages = {61-70},
  year = {2012},
}

@article{Guilford1998,
  author = {Guilford, P.J. and Hopkins, J. and Harraway, J. and McLeod, M. and McLeod, N. and Harawira, P. and Taite, H. and Scoular, R. and Miller, A. and Reeve, A. E.},
  title = {E-cadherin germline mutations in familial gastric cancer},
  journal = {Nature},
  volume = {392},
  number = {6674},
  pages = {402-5},
  abstract = {The identification of genes predisposing to familial cancer is an essential step towards understanding the molecular events underlying tumorigenesis and is critical for the clinical management of affected families. Despite a declining incidence, gastric cancer remains a major cause of cancer death worldwide, and about 10% of cases show familial clustering. The relative contributions of inherited susceptibility and environmental effects to familial gastric cancer are poorly understood because little is known of the genetic events that predispose to gastric cancer. Here we describe the identification of the gene responsible for early-onset, histologically poorly differentiated, high grade, diffuse gastric cancer in a large kindred from New Zealand (Aotearoa). Genetic linkage analysis demonstrated significant linkage to markers flanking the gene for the calcium-dependent cell-adhesion protein E-cadherin. Sequencing of the E-cadherin gene revealed a G --> T nucleotide substitution in the donor splice consensus sequence of exon 7, leading to a truncated gene product. Diminished E-cadherin expression is associated with aggressive, poorly differentiated carcinomas. Underexpression of E-cadherin is a prognostic marker of poor clinical outcome in many tumour types, and restored expression of E-cadherin in tumour models can suppress the invasiveness of epithelial tumour cells. The role of E-cadherin in gastric cancer susceptibility was confirmed by identifying inactivating mutations in other gastric cancer families. In one family, a frameshift mutation was identified in exon 15, and in a second family a premature stop codon interrupted exon 13. These results describe, to our knowledge for the first time, a molecular basis for familial gastric cancer, and confirm the important role of E-cadherin mutations in cancer.},
  keywords = {Adolescent Adult Aged Cadherins/*genetics Child Child, Preschool DNA Mutational Analysis Female Genetic Linkage Genetic Markers Genetic Predisposition to Disease *Germ-Line Mutation Humans Infant Infant, Newborn Male Middle Aged Pedigree Polymerase Chain Reaction Polymorphism, Single-Stranded Conformational Stomach Neoplasms/*genetics},
  year = {1998},
}


@article{Johnson2007,
  author = {Johnson, W. E. and Li, C. and Rabinovic, A.},
  title = {Adjusting batch effects in microarray expression data using empirical Bayes methods},
  journal = {Biostatistics},
  volume = {8},
  number = {1},
  pages = {118-27},
  abstract = {Non-biological experimental variation or batch effects are commonly observed across multiple batches of microarray experiments, often rendering the task of combining data from these batches difficult. The ability to combine microarray data sets is advantageous to researchers to increase statistical power to detect biological phenomena from studies where logistical considerations restrict sample size or in studies that require the sequential hybridization of arrays. In general, it is inappropriate to combine data sets without adjusting for batch effects. Methods have been proposed to filter batch effects from data, but these are often complicated and require large batch sizes ( > 25) to implement. Because the majority of microarray studies are conducted using much smaller sample sizes, existing methods are not sufficient. We propose parametric and non-parametric empirical Bayes frameworks for adjusting data for batch effects that is robust to outliers in small sample sizes and performs comparable to existing methods for large samples. We illustrate our methods using two example data sets and show that our methods are justifiable, easy to apply, and useful in practice. Software for our method is freely available at: http://biosun1.harvard.edu/complab/batch/.},
  keywords = {*Bayes Theorem *Data Interpretation, Statistical Gene Expression Profiling/methods Humans Oligonucleotide Array Sequence Analysis/*methods},
  year = {2007},
}


@article{Kaelin2005,
  author = {Kaelin, Jr, WG},
  title = {The concept of synthetic lethality in the context of anticancer therapy},
  journal = {Nat Rev Cancer},
  volume = {5},
  number = {9},
  pages = {689-98},
  abstract = {Two genes are synthetic lethal if mutation of either alone is compatible with viability but mutation of both leads to death. So, targeting a gene that is synthetic lethal to a cancer-relevant mutation should kill only cancer cells and spare normal cells. Synthetic lethality therefore provides a conceptual framework for the development of cancer-specific cytotoxic agents. This paradigm has not been exploited in the past because there were no robust methods for systematically identifying synthetic lethal genes. This is changing as a result of the increased availability of chemical and genetic tools for perturbing gene function in somatic cells.},
  year = {2005},
}


@article{Kaelin2009,
  author = {Kaelin, Jr, WG},
  title = {Synthetic Lethality: a framework for the development of wiser cancer therapeutics},
  journal = {Genome Med},
  volume = {1},
  pages = {99},
  year = {2009},
}


@article{Lehner2006,
  author = {Lehner, B. and Crombie, C. and Tischler, J. and Fortunato, A. and Fraser, A. G.},
  title = {Systematic mapping of genetic interactions in Caenorhabditis elegans identifies common modifiers of diverse signaling pathways},
  journal = {Nat Genet},
  volume = {38},
  number = {8},
  pages = {896-903},
  abstract = {Most heritable traits, including disease susceptibility, are affected by interactions between multiple genes. However, we understand little about how genes interact because very few possible genetic interactions have been explored experimentally. We have used RNA interference in Caenorhabditis elegans to systematically test approximately 65,000 pairs of genes for their ability to interact genetically. We identify approximately 350 genetic interactions between genes functioning in signaling pathways that are mutated in human diseases, including components of the EGF/Ras, Notch and Wnt pathways. Most notably, we identify a class of highly connected 'hub' genes: inactivation of these genes can enhance the phenotypic consequences of mutation of many different genes. These hub genes all encode chromatin regulators, and their activity as genetic hubs seems to be conserved across animals. We propose that these genes function as general buffers of genetic variation and that these hub genes may act as modifier genes in multiple, mechanistically unrelated genetic diseases in humans.},
  keywords = {Animals Caenorhabditis elegans/*genetics/metabolism Chromosome Mapping Enhancer Elements, Genetic Epidermal Growth Factor/genetics Female Genes, Helminth Humans Mutation Phenotype RNA Interference Signal Transduction Vulva/growth & development},
  year = {2006},
}


@article{Lord2014,
  author = {Lord, C. J. and Tutt, A. N. and Ashworth, A.},
  title = {Synthetic Lethality and Cancer Therapy: Lessons Learned from the Development of PARP Inhibitors},
  journal = {Annu Rev Med},
  abstract = {The genetic concept of synthetic lethality, in which the combination or synthesis of mutations in multiple genes results in cell death, provides a framework to design novel therapeutic approaches to cancer. Already there are promising indications, from clinical trials exploiting this concept by using poly(ADP-ribose) polymerase (PARP) inhibitors in patients with germline BRCA1 or BRCA2 gene mutations, that this approach could be beneficial. Wediscuss the biological rationale for BRCA-PARP synthetic lethality, how the synthetic lethal approach is being assessed in the clinic, and how mechanisms of resistance are starting to be dissected. Applying the synthetic lethal concept to target non-BRCA-mutant cancers also has clear potential, and we discuss how some of the principles learned in developing PARP inhibitors might also drive the development of additional genetic approaches. Expected final online publication date for the Annual Review of Medicine Volume 66 is January 14, 2015. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.},
  year = {2014},
}


@article{Lu2015,
  author = {Lu, X. and Megchelenbrink, W. and Notebaart, R. A. and Huynen, M. A.},
  title = {Predicting human genetic interactions from cancer genome evolution},
  journal = {PLoS One},
  volume = {10},
  number = {5},
  pages = {e0125795},
  abstract = {Synthetic Lethal (SL) genetic interactions play a key role in various types of biological research, ranging from understanding genotype-phenotype relationships to identifying drug-targets against cancer. Despite recent advances in empirical measuring SL interactions in human cells, the human genetic interaction map is far from complete. Here, we present a novel approach to predict this map by exploiting patterns in cancer genome evolution. First, we show that empirically determined SL interactions are reflected in various gene presence, absence, and duplication patterns in hundreds of cancer genomes. The most evident pattern that we discovered is that when one member of an SL interaction gene pair is lost, the other gene tends not to be lost, i.e. the absence of co-loss. This observation is in line with expectation, because the loss of an SL interacting pair will be lethal to the cancer cell. SL interactions are also reflected in gene expression profiles, such as an under representation of cases where the genes in an SL pair are both under expressed, and an over representation of cases where one gene of an SL pair is under expressed, while the other one is over expressed. We integrated the various previously unknown cancer genome patterns and the gene expression patterns into a computational model to identify SL pairs. This simple, genome-wide model achieves a high prediction power (AUC = 0.75) for known genetic interactions. It allows us to present for the first time a comprehensive genome-wide list of SL interactions with a high estimated prediction precision, covering up to 591,000 gene pairs. This unique list can potentially be used in various application areas ranging from biotechnology to medical genetics.},
  year = {2015},
}


@article{Ravnan2012,
  author = {Ravnan, M. C. and Matalka, M. S.},
  title = {Vemurafenib in patients with BRAF V600E mutation-positive advanced melanoma},
  journal = {Clin Ther},
  volume = {34},
  number = {7},
  pages = {1474-86},
  abstract = {BACKGROUND: Vemurafenib is an oral, small-molecule kinase inhibitor that selectively targets activated BRAF V600E and has been approved for the treatment of advanced BRAF mutation-positive melanoma. OBJECTIVE: This article reviews the clinical pharmacology, efficacy, tolerability, and pharmacokinetics of vemurafenib and in addition outlines proposed mechanisms of vemurafenib resistance. METHODS: A literature search of MEDLINE and ScienceVerse Scopus was performed using the key words malignant melanoma, BRAF, vemurafenib, and PLX4032. Scientific abstracts, US Food and Drug Administration Web site data (www.accessdata.fda.gov), the manufacturer-submitted approval data from ClinicalTrials.gov (www.clinicaltrials.gov), and the references from applicable publications were also consulted. RESULTS: Clinical studies have reported that vemurafenib is efficacious and acceptably well-tolerated. In a Phase I study (BRIM-1), a 960-mg BID dose achieved an objective response rate of 81% among 32 patients with melanoma who carried a BRAF V600E mutation. Of the 26 responders, 2 achieved a complete response and 24 a partial response. In BRIM-2, 132 BRAF V600E-positive patients achieved an overall response rate of 53% (95% CI, 44%-62%); 6% achieved a complete response and 47%, a partial response. Response was noted at 6 weeks and lasted a median of 6.7 months (95% CI, 5.6-8.6). Median survival was 15.9 months (95% CI, 11.6-18.3); 77% of patients survived to 6 months (95% CI, 70-85) and 58% to 12 months (95% CI, 11.6-18.3), and an estimated 43% were expected to survive to 18 months (95% CI, 33-53). The Phase III study (BRIM-3) compared vemurafenib to dacarbazine. The hazard ratio (HR) for death with vemurafenib was 0.37 (95% CI, 0.26-0.55; P < 0.001). At 6 months, overall survival was 84% (95% CI, 78-89) versus 64% (95% CI, 56-73) in the vemurafenib and dacarbazine treatment arms, respectively. The HR for tumor progression in the vemurafenib cohort was 0.26 (95% CI, 0.20-0.33; P < 0.001), and the estimated median progression-free survival was 5.3 months with vemurafenib versus 1.6 months with dacarbazine. Finally, the difference in response rates was significant (48% vs 5%, respectively; P < 0.001). The most common adverse events reported have been arthralgia, rash, photosensitivity, fatigue, pruritus, alopecia, cutaneous squamous cell carcinoma, diarrhea, and mild to moderate nausea. CONCLUSIONS: Vemurafenib is effective for advanced melanomas expressing the BRAF V600E mutations. Resistance to BRAF inhibition can be problematic, but new evidence suggests that combination therapy may attenuate the issue. Targeting the cellular activity of melanoma cells is reported to be efficacious and is expected to delay progression and prolong survival.},
  keywords = {Antineoplastic Agents/adverse effects/pharmacology/*therapeutic use Disease-Free Survival Drug Resistance, Neoplasm Humans Indoles/adverse effects/pharmacology/*therapeutic use Melanoma/*drug therapy/genetics/pathology Mutation Proto-Oncogene Proteins B-raf/genetics Skin Neoplasms/*drug therapy/genetics/pathology Sulfonamides/adverse effects/pharmacology/*therapeutic use Survival Rate Treatment Outcome},
  year = {2012},
}


@article{Soon2011,
  author = {Soon, W. W. and Miller, L. D. and Black, M. A. and Dalmasso, C. and Chan, X. B. and Pang, B. and Ong, C. W. and Salto-Tellez, M. and Desai, K. V. and Liu, E. T.},
  title = {Combined genomic and phenotype screening reveals secretory factor SPINK1 as an invasion and survival factor associated with patient prognosis in breast cancer},
  journal = {EMBO Mol Med},
  volume = {3},
  number = {8},
  pages = {451-64},
  abstract = {Secretory factors that drive cancer progression are attractive immunotherapeutic targets. We used a whole-genome data-mining approach on multiple cohorts of breast tumours annotated for clinical outcomes to discover such factors. We identified Serine protease inhibitor Kazal-type 1 (SPINK1) to be associated with poor survival in estrogen receptor-positive (ER+) cases. Immunohistochemistry showed that SPINK1 was absent in normal breast, present in early and advanced tumours, and its expression correlated with poor survival in ER+ tumours. In ER- cases, the prognostic effect did not reach statistical significance. Forced expression and/or exposure to recombinant SPINK1 induced invasiveness without affecting cell proliferation. However, down-regulation of SPINK1 resulted in cell death. Further, SPINK1 overexpressing cells were resistant to drug-induced apoptosis due to reduced caspase-3 levels and high expression of Bcl2 and phospho-Bcl2 proteins. Intriguingly, these anti-apoptotic effects of SPINK1 were abrogated by mutations of its protease inhibition domain. Thus, SPINK1 affects multiple aggressive properties in breast cancer: survival, invasiveness and chemoresistance. Because SPINK1 effects are abrogated by neutralizing antibodies, we suggest that SPINK1 is a viable potential therapeutic target in breast cancer.},
  keywords = {Apoptosis Breast Neoplasms/*genetics/mortality/*pathology Carrier Proteins/analysis/antagonists & inhibitors/*genetics Female *Genetic Testing Humans Immunohistochemistry Neoplasm Invasiveness/*genetics/*pathology Prognosis Receptors, Estrogen/analysis Survival Analysis},
  year = {2011},
}


@article{Telford2015,
  author = {Telford, B. J. and Chen, A. and Beetham, H. and Frick, J. and Brew, T. P. and Gould, C. M. and Single, A. and Godwin, T. and Simpson, K. J. and Guilford, P.},
  title = {Synthetic lethal screens identify vulnerabilities in GPCR signalling and cytoskeletal organization in E-cadherin-deficient cells},
  journal = {Mol Cancer Ther},
  abstract = {The CDH1 gene, which encodes the cell-to-cell adhesion protein E-cadherin, is frequently mutated in lobular breast cancer (LBC) and diffuse gastric cancer (DGC). However, because E-cadherin is a tumor suppressor protein and lost from the cancer cell, it is not a conventional drug target. To overcome this, we have taken a synthetic lethal approach to determine whether the loss of E-cadherin creates druggable vulnerabilities. We first conducted a genome wide siRNA screen of isogenic MCF10A cells with and without CDH1 expression. Gene ontology analysis demonstrated that G-protein coupled receptor (GPCR) signalling proteins were highly enriched amongst the synthetic lethal candidates. Diverse families of cytoskeletal proteins were also frequently represented. These broad classes of E-cadherin synthetic lethal hits were validated using both lentiviral-mediated shRNA knockdown and specific antagonists including the JAK inhibitor LY2784544, Pertussis toxin and the aurora kinase inhibitors Alisertib and Danusertib. Next, we conducted a 4,057 known drug screen and time course studies on the CDH1 isogenic MCF10A cell lines and identified additional drug classes with linkages to GPCR signalling and cytoskeletal function that showed evidence of E-cadherin synthetic lethality. These included multiple histone deacetylase inhibitors including Vorinostat and Entinostat, phosphoinositide 3-kinase inhibitors, and the tyrosine kinase inhibitors Crizotinib and Saracatinib. Together, these results demonstrate that E-cadherin loss creates druggable vulnerabilities that have the potential to improve the management of both sporadic and familial LBC and DGC.},
  volume = {14},
  number = {5},
  pages = {1213-1223},
  year = {2015},
}

@article{Chen2014,
  doi = {10.1186/1471-2407-14-552},
  year = {2014},
  month = {jul},
  publisher = {Springer Nature},
  volume = {14},
  number = {1},
  pages = {552},
  author = {Augustine Chen and Henry Beetham and Michael A Black and Rashmi Priya and Bryony J Telford and Joanne Guest and George A R Wiggins and Tanis D Godwin and Alpha S Yap and Parry J Guilford},
  title = {E-cadherin loss alters cytoskeletal organization and adhesion in non-malignant breast cells but is insufficient to induce an epithelial-mesenchymal transition},
  journal = {{BMC} Cancer}},
}


@article{Tiong2014,
  author = {Tiong, K. L. and Chang, K. C. and Yeh, K. T. and Liu, T. Y. and Wu, J. H. and Hsieh, P. H. and Lin, S. H. and Lai, W. Y. and Hsu, Y. C. and Chen, J. Y. and Chang, J. G. and Shieh, G. S.},
  title = {CSNK1E/CTNNB1 are synthetic lethal to TP53 in colorectal cancer and are markers for prognosis},
  journal = {Neoplasia},
  volume = {16},
  number = {5},
  pages = {441-50},
  abstract = {Two genes are called synthetic lethal (SL) if their simultaneous mutations lead to cell death, but each individual mutation does not. Targeting SL partners of mutated cancer genes can kill cancer cells specifically, but leave normal cells intact. We present an integrated approach to uncovering SL pairs in colorectal cancer (CRC). Screening verified SL pairs using microarray gene expression data of cancerous and normal tissues, we first identified potential functionally relevant (simultaneously differentially expressed) gene pairs. From the top-ranked pairs, ~20 genes were chosen for immunohistochemistry (IHC) staining in 171 CRC patients. To find novel SL pairs, all 169 combined pairs from the individual IHC were synergistically correlated to five clinicopathological features, e.g. overall survival. Of the 11 predicted SL pairs, MSH2-POLB and CSNK1E-MYC were consistent with literature, and we validated the top two pairs, CSNK1E-TP53 and CTNNB1-TP53 using RNAi knockdown and small molecule inhibitors of CSNK1E in isogenic HCT-116 and RKO cells. Furthermore, synthetic lethality of CSNK1E and TP53 was verified in mouse model. Importantly, multivariate analysis revealed that CSNK1E-P53, CTNNB1-P53, MSH2-RB1, and BRCA1-WNT5A were independent prognosis markers from stage, with CSNK1E-P53 applicable to early-stage and the remaining three throughout all stages. Our findings suggest that CSNK1E is a promising target for TP53-mutant CRC patients which constitute ~40% to 50% of patients, while to date safety regarding inhibition of TP53 is controversial. Thus the integrated approach is useful in finding novel SL pairs for cancer therapeutics, and it is readily accessible and applicable to other cancers.},
  year = {2014},
}


@article{Tutt2010,
  author = {Tutt, A. and Robson, M. and Garber, J. E. and Domchek, S. M. and Audeh, M. W. and Weitzel, J. N. and Friedlander, M. and Arun, B. and Loman, N. and Schmutzler, R. K. and Wardley, A. and Mitchell, G. and Earl, H. and Wickens, M. and Carmichael, J.},
  title = {Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and advanced breast cancer: a proof-of-concept trial},
  journal = {Lancet},
  volume = {376},
  number = {9737},
  pages = {235-44},
  abstract = {BACKGROUND: Olaparib, a novel, orally active poly(ADP-ribose) polymerase (PARP) inhibitor, induced synthetic lethality in BRCA-deficient cells. A maximum tolerated dose and initial signal of efficacy in BRCA-deficient ovarian cancers have been reported. We therefore assessed the efficacy, safety, and tolerability of olaparib alone in women with BRCA1 or BRCA2 mutations and advanced breast cancer. METHODS: Women (aged >or=18 years) with confirmed BRCA1 or BRCA2 mutations and recurrent, advanced breast cancer were assigned to two sequential cohorts in a phase 2 study undertaken in 16 centres in Australia, Germany, Spain, Sweden, the UK, and the USA. The first cohort (n=27) was given continuous oral olaparib at the maximum tolerated dose (400 mg twice daily), and the second (n=27) was given a lower dose (100 mg twice daily). The primary efficacy endpoint was objective response rate (ORR). This study is registered with ClinicalTrials.gov, number NCT00494234. FINDINGS: Patients had been given a median of three previous chemotherapy regimens (range 1-5 in cohort 1, and 2-4 in cohort 2). ORR was 11 (41%) of 27 patients (95% CI 25-59) in the cohort assigned to 400 mg twice daily, and six (22%) of 27 (11-41) in the cohort assigned to 100 mg twice daily. Toxicities were mainly at low grades. The most frequent causally related adverse events in the cohort given 400 mg twice daily were fatigue (grade 1 or 2, 11 [41%]; grade 3 or 4, four [15%]), nausea (grade 1 or 2, 11 [41%]; grade 3 or 4, four [15%]), vomiting (grade 1 or 2, three [11%]; grade 3 or 4, three [11%]), and anaemia (grade 1 or 2, one [4%]; grade 3 or 4, three [11%]). The most frequent causally related adverse events in the cohort given 100 mg twice daily were nausea (grade 1 or 2, 11 [41%]; none grade 3 or 4) and fatigue (grade 1 or 2, seven [26%]; grade 3 or 4, one [4%]). INTERPRETATION: The results of this study provide positive proof of concept for PARP inhibition in BRCA-deficient breast cancers and shows a favourable therapeutic index for a novel targeted treatment strategy in patients with tumours that have genetic loss of function of BRCA1-associated or BRCA2-associated DNA repair. Toxicity in women with BRCA1 and BRCA2 mutations was similar to that reported previously in those without such mutations. FUNDING: AstraZeneca.},
  keywords = {Adult Aged Antineoplastic Agents/*therapeutic use Breast Neoplasms/*drug therapy/*genetics/pathology Female Genes, BRCA1 Genes, BRCA2 Germ-Line Mutation Humans Maximum Tolerated Dose Middle Aged Phthalazines/*therapeutic use Piperazines/*therapeutic use Poly(ADP-ribose) Polymerases/*antagonists & inhibitors Prospective Studies},
  year = {2010},
}


@article{Wang2013,
  author = {Wang, Xiaosheng and Simon, Richard},
  title = {Identification of potential synthetic lethal genes to p53 using a computational biology approach},
  journal = {BMC Medical Genomics},
  volume = {6},
  number = {1},
  pages = {30},
  abstract = {BACKGROUND:Identification of genes that are synthetic lethal to p53 is an important strategy for anticancer therapy as p53 mutations have been reported to occur in more than half of all human cancer cases. Although genome-wide RNAi screening is an effective approach to finding synthetic lethal genes, it is costly and labor-intensive.METHODS:To illustrate this approach, we identified potentially druggable genes synthetically lethal for p53 using three microarray datasets for gene expression profiles of the NCI-60 cancer cell lines, one next-generation sequencing (RNA-Seq) dataset from the Cancer Genome Atlas (TCGA) project, and one gene expression data from the Cancer Cell Line Encyclopedia (CCLE) project. We selected the genes which encoded kinases and had significantly higher expression in the tumors with functional p53 mutations (somatic mutations) than in the tumors without functional p53 mutations as the candidates of druggable synthetic lethal genes for p53. We identified important regulatory networks and functional categories pertinent to these genes, and performed an extensive survey of literature to find experimental evidence that support the synthetic lethality relationships between the genes identified and p53. We also examined the drug sensitivity difference between NCI-60 cell lines with functional p53 mutations and NCI-60 cell lines without functional p53 mutations for the compounds that target the kinases encoded by the genes identified.RESULTS:Our results indicated that some of the candidate genes we identified had been experimentally verified to be synthetic lethal for p53 and promising targets for anticancer therapy while some other genes were putative targets for development of cancer therapeutic agents.CONCLUSIONS:Our study indicated that pre-screening of potential synthetic lethal genes using gene expression profiles is a promising approach for improving the efficiency of synthetic lethal RNAi screening.},
  year = {2013},
}

@Manual{safe,
    title = {safe: Significance Analysis of Function and Expression},
    author = {William T. Barry},
    year = {2016},
    note = {R package version 3.14.0},
}




@article{limma,
  author = {Matthew E Ritchie and Belinda Phipson and Di Wu and Yifang Hu and Charity W Law and Wei Shi and Gordon K Smyth},
  title = {{limma} powers differential expression analyses for {RNA}-sequencing and microarray studies},
  journal = {Nucleic Acids Research},
  year = {2015},
  volume = {43},
  number = {7},
  pages = {e47},
}


@article{genesetdb,
  author = {Araki, H. and Knapp, C. and Tsai, P. and Print, C.},
  title = {GeneSetDB: A comprehensive meta-database, statistical and visualisation framework for gene set analysis},
  journal = {FEBS Open Bio},
  volume = {2},
  pages = {76-82},
  abstract = {Most omics experiments require comprehensive interpretation of the biological meaning of gene lists. To address this requirement, a number of gene set analysis (GSA) tools have been developed. Although the biological value of GSA is strictly limited by the breadth of the gene sets used, very few methods exist for simultaneously analysing multiple publically available gene set databases. Therefore, we constructed GeneSetDB (http://genesetdb.auckland.ac.nz/haeremai.html), a comprehensive meta-database, which integrates 26 public databases containing diverse biological information with a particular focus on human disease and pharmacology. GeneSetDB enables users to search for gene sets containing a gene identifier or keyword, generate their own gene sets, or statistically test for enrichment of an uploaded gene list across all gene sets, and visualise gene set enrichment and overlap using a clustered heat map.},
  issn = {2211-5463 (Electronic) 2211-5463 (Linking)},
  doi = {10.1016/j.fob.2012.04.003},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/23650583},
  year = {2012},
  type = {Journal Article},
}


@Manual{gplots,
  title = {gplots: Various R Programming Tools for Plotting Data},
  author = {Gregory R. Warnes and Ben Bolker and Lodewijk Bonebakker and Robert Gentleman and Wolfgang Huber Andy Liaw and Thomas Lumley and Martin Maechler and Arni Magnusson and Steffen Moeller and Marc Schwartz and Bill Venables},
  year = {2015},
  note = {R package version 2.17.0},
  url = {https://CRAN.R-project.org/package=gplots},
}


@article{Parker2009,
  title = {Supervised risk predictor of breast cancer based on intrinsic subtypes},
  author = {Bernard, {Philip S.} and Parker, {Joel S.} and Michael Mullins and Cheung, {Maggie C U} and Samuel Leung and David Voduc and Tammi Vickery and Sherri Davies and Christiane Fauron and Xiaping He and Zhiyuan Hu and Quackenhush, {John F.} and Stijleman, {Inge J.} and Juan Palazzo and Matron, {J. S.} and Nobel, {Andrew B.} and Elaine Mardis and Nielsen, {Torsten O.} and Ellis, {Matthew J.} and Perou, {Charles M.}},
  year = {2009},
  month = {3},
  doi = {10.1200/JCO.2008.18.1370},
  volume = {27},
  pages = {1160--1167},
  journal = {Journal of Clinical Oncology},
  issn = {0732-183X},
  number = {8},
}

@article{Brin1998,
title = "The anatomy of a large-scale hypertextual Web search engine",
journal = "Computer Networks and ISDN Systems",
volume = "30",
number = "1",
pages = "107 - 117",
year = "1998",
note = "",
issn = "0169-7552",
doi = "http://dx.doi.org/10.1016/S0169-7552(98)00110-X",
url = "http://www.sciencedirect.com/science/article/pii/S016975529800110X",
author = "Sergey Brin and Lawrence Page",
keywords = "World Wide Web",
keywords = "Search engines",
keywords = "Information retrieval",
keywords = "PageRank",
keywords = "Google",
}

@article{Reactome,
  author = {Croft, D and Mundo, A F and Haw, R and Milacic, M  and Weiser, J and Wu, G and Caudy, M and Garapati, P and Gillespie, M and Kamdar, M R  and Jassal, B and Jupe, S and Matthews, L and May, B and Palatnik, S and Rothfels, K and Shamovsky, V  and Song, H and Williams, M and Birney, E and Hermjakob, H and Stein, L and D'Eustachio, P},
  title = {{The Reactome pathway knowledgebase}},
  year = {2014},
  journal = {Nucleic Acids Res},
  volume = {42},
  number = {database issue},
  pages = {D472–D477},
  abstract = {Reactome (http://www.reactome.org) is a manually curated open-source open-data resource of human pathways and reactions. The current version 46 describes 7088 human proteins (34\% of the predicted human proteome), participating in 6744 reactions based on data extracted from 15 107 research publications with PubMed links. The Reactome Web site and analysis tool set have been completely redesigned to increase speed, flexibility and user friendliness. The data model has been extended to support annotation of disease processes due to infectious agents and to mutation.},
  FAU = {Croft, David},
  doi = {10.1093/nar/gkt1102},
  type = {Journal Article},
}


@article{Gao2015,
  author = {Beichen Gao and Philippe P. Roux},
  title = {Translational control by oncogenic signaling pathways},
  journal = {Biochimica et Biophysica Acta},
  volume = {1849},
  number = {7},
  pages = {753-65},
  year = {2015},
  type = {Journal Article},
}


@Article{Rmpi,
  title = {Rmpi: Parallel Statistical Computing in R},
  author = {Hao Yu},
  journal = {R News},
  year = {2002},
  volume = {2},
  number = {2},
  pages = {10--14},
  url = {http://cran.r-project.org/doc/Rnews/Rnews_2002-2.pdf},
}

@Manual{R_core,
    title = {R: A Language and Environment for Statistical Computing},
    author = {{R Core Team}},
    organization = {R Foundation for Statistical Computing},
    address = {Vienna, Austria},
    year = {2016},
    url = {https://www.R-project.org/},
    note = {R version 3.3.2}
}


@Book{HyperGeo,
  author = {N.L. Johnson, S. Kotz and A.W. Kemp},
  title = {Univariate Discrete Distributions},
  year = {1992},
  publisher = {John Wiley},
  address = {New York},
  edition = {2nd edition},
}


@article{Rivals2007,
  author = {Rivals, Isabelle and Personnaz, Léon and Taing, Lieng and Potier, Marie-Claude},
  title = {Enrichment or depletion of a GO category within a class of genes: which test?},
  volume = {23},
  number = {4},
  pages = {401-407},
  year = {2007},
  doi = {10.1093/bioinformatics/btl633},
  abstract = {Motivation: A number of available program packages determine the significant enrichments and/or depletions of GO categories among a class of genes of interest. Whereas a correct formulation of the problem leads to a single exact null distribution, these GO tools use a large variety of statistical tests whose denominations often do not clarify the underlying P-value computations.Summary: We review the different formulations of the problem and the tests they lead to: the binomial, χ2, equality of two probabilities, Fisher's exact and hypergeometric tests. We clarify the relationships existing between these tests, in particular the equivalence between the hypergeometric test and Fisher's exact test. We recall that the other tests are valid only for large samples, the test of equality of two probabilities and the χ2-test being equivalent. We discuss the appropriateness of one- and two-sided P-values, as well as some discreteness and conservatism issues.Contact:isabelle.rivals@espci.frSupplementary information: Supplementary data are available at Bioinformatics online.},
  url = {http://bioinformatics.oxfordjournals.org/content/23/4/401.abstract},
  eprint = {http://bioinformatics.oxfordjournals.org/content/23/4/401.full.pdf+html},
  journal = {Bioinformatics},
}


@article{Graziano2003,
  author = {Graziano, F. and Humar, B. and Guilford, P.},
  title = {The role of the E-cadherin gene (CDH1) in diffuse gastric cancer susceptibility: from the laboratory to clinical practice},
  volume = {14},
  number = {12},
  pages = {1705-1713},
  year = {2003},
  doi = {10.1093/annonc/mdg486},
  abstract = {Loss of function of the E-cadherin gene (CDH1) has been linked with diffuse gastric cancer susceptibility, and germline inactivating mutations in CDH1 characterise the hereditary diffuse gastric cancer (HDGC) syndrome. Hypermethylation in the CDH1 promoter region is a frequent phenomenon in poorly differentiated, diffuse gastric carcinomas and it was identified as the main mechanism for the inactivation of the remaining wild-type allele in HDGC cases. Specific criteria are used to identify patients with suspected HDGC and who should be investigated for CDH1 germline mutations. Accurate screening is mandatory for unaffected carriers of CDH1 mutations and selected high-risk individuals could be considered for prophylactic gastrectomy. Also, germline CDH1 mutations may predispose to lobular breast carcinoma and prostate cancer.Germline CDH1 mutations are not always detectable in patients who meet the HDGC criteria and the aetiological role of this gene is still under investigation. Families without recognised inactivating CDH1 mutations may have undisclosed CDH1 mutations or mutations in its regulatory sequences or germline mutations in unidentified genes that also contribute to the disease. In recent years, several germline missense CDH1 mutations have been identified, some of which showed a marked negative influence on E-cadherin function in experimental models. CDH1 promoter hypermethylation seems a key event in the carcinogenetic process of poorly differentiated, diffuse gastric cancer and it deserves further investigation as a new target for anticancer therapies with demethylating agents.},
  url = {http://annonc.oxfordjournals.org/content/14/12/1705.abstract},
  eprint = {http://annonc.oxfordjournals.org/content/14/12/1705.full.pdf+html},
  journal = {Annals of Oncology},
}


@article{Becker1994,
  author = {Becker, Karl-Friedrich and Atkinson, Michael J. and Reich, Ulrike and Becker, Ingrid and Nekarda, Hjalmar and Siewert, Jörg R. and Höfler, Heinz},
  title = {E-Cadherin Gene Mutations Provide Clues to Diffuse Type Gastric Carcinomas},
  volume = {54},
  number = {14},
  pages = {3845-3852},
  year = {1994},
  abstract = {The calcium-dependent homophilic cell adhesion molecule and candidate suppressor gene, E (epithelial)-cadherin, plays a major role in the organization and integrity of most epithelial tissues. Diffusely growing gastric carcinomas show markedly reduced homophilic cell-to-cell interactions. We speculated that mutations in the E-cadherin gene may be responsible for the scattered phenotype of this type of carcinoma. For that reason we have examined E-cadherin in 26 diffuse type, 20 intestinal type and 7 mixed gastric carcinomas (Laurén's classification) at the DNA, RNA, and protein levels.Reverse transcription polymerase chain reaction and direct sequencing of amplified E-cadherin complementary DNA fragments revealed inframe skipping of either exon 8 or exon 9 in 10 patients with diffuse tumors and an exon 9 deletion in one patient with a mixed carcinoma; both exons encode putative calcium binding domains. These alterations were not seen in nontumorous gastric tissues. Splice site mutations responsible for the exon deletions were identified in six of these patients, eliminating the possibility of alternative splicing mechanisms. Five of these splice site alterations were confirmed as somatic mutations. Non-splice site mutations were observed in three diffuse type tumors, namely a 69-base pair deletion of exon 10 and two point mutations, one of which destroys a putative calcium binding region. Immunohistochemical evaluation showed E-cadherin immunoreactivity in tumors and lymph node metastases of patients expressing abnormal mRNA. The allelic status of the E-cadherin gene was analyzed in one patient, revealing loss of heterozygosity with retention of a mutated E-cadherin allele. Overall, E-cadherin mutations were identified in 50% (13 of 26) of the diffuse type and in 14% (1 of 7) of the mixed carcinomas. In contrast, two silent E-cadherin mutations (not changing the amino acid sequence) were detected in two tumors of the intestinal type.Our study provides strong in vivo evidence that E-cadherin gene mutations may contribute to the development of diffusely growing gastric carcinomas and support a tumor/metastasis suppressor gene hypothesis.},
  url = {http://cancerres.aacrjournals.org/content/54/14/3845.abstract},
  eprint = {http://cancerres.aacrjournals.org/content/54/14/3845.full.pdf+html},
  journal = {Cancer Research},
}


@article{Oliveira2009,
  author = {Oliveira, Carla and Senz, Janine and Kaurah, Pardeep and Pinheiro, Hugo and Sanges, Remo and Haegert, Anne and Corso, Giovanni and Schouten, Jan and Fitzgerald, Rebecca and Vogelsang, Holger and Keller, Gisela and Dwerryhouse, Sarah and Grimmer, Donna and Chin, Suet-Feung and Yang, Han-Kwang and Jackson, Charles E. and Seruca, Raquel and Roviello, Franco and Stupka, Elia and Caldas, Carlos and Huntsman, David},
  title = {Germline CDH1 deletions in hereditary diffuse gastric cancer families},
  volume = {18},
  number = {9},
  pages = {1545-1555},
  year = {2009},
  doi = {10.1093/hmg/ddp046},
  abstract = {Germline CDH1 point or small frameshift mutations can be identified in 30–50% of hereditary diffuse gastric cancer (HDGC) families. We hypothesized that CDH1 genomic rearrangements would be found in HDGC and identified 160 families with either two gastric cancers in first-degree relatives and with at least one diffuse gastric cancer (DGC) diagnosed before age 50, or three or more DGC in close relatives diagnosed at any age. Sixty-seven carried germline CDH1 point or small frameshift mutations. We screened germline DNA from the 93 mutation negative probands for large genomic rearrangements by Multiplex Ligation-Dependent Probe Amplification. Potential deletions were validated by RT–PCR and breakpoints cloned using a combination of oligo-CGH-arrays and long-range-PCR. In-silico analysis of the CDH1 locus was used to determine a potential mechanism for these rearrangements. Six of 93 (6.5%) previously described mutation negative HDGC probands, from low GC incidence populations (UK and North America), carried genomic deletions (UK and North America). Two families carried an identical deletion spanning 193 593 bp, encompassing the full CDH3 sequence and CDH1 exons 1 and 2. Other deletions affecting exons 1, 2, 15 and/or 16 were identified. The statistically significant over-representation of Alus around breakpoints indicates it as a likely mechanism for these deletions. When all mutations and deletions are considered, the overall frequency of CDH1 alterations in HDGC is ∼46% (73/160). CDH1 large deletions occur in 4% of HDGC families by mechanisms involving mainly non-allelic homologous recombination in Alu repeat sequences. As the finding of pathogenic CDH1 mutations is useful for management of HDGC families, screening for deletions should be offered to at-risk families.},
  url = {http://hmg.oxfordjournals.org/content/18/9/1545.abstract},
  eprint = {http://hmg.oxfordjournals.org/content/18/9/1545.full.pdf+html},
  journal = {Human Molecular Genetics},
}


@article{Christofori1999,
  title = {The role of the cell-adhesion molecule E-cadherin as a tumour-suppressor gene},
  journal = {Trends in Biochemical Sciences},
  volume = {24},
  number = {2},
  pages = {73 - 76},
  year = {1999},
  note = {},
  issn = {0968-0004},
  doi = {http://dx.doi.org/10.1016/S0968-0004(98)01343-7},
  url = {http://www.sciencedirect.com/science/article/pii/S0968000498013437},
  author = {Gerhard Christofori and Henrik Semb},
  keywords = {tumour suppressor},
}


@article{Guilford1999,
  title = {E-cadherin downregulation in cancer: fuel on the fire?},
  journal = {Molecular Medicine Today},
  volume = {5},
  number = {4},
  pages = {172 - 177},
  year = {1999},
  note = {},
  issn = {1357-4310},
  doi = {http://dx.doi.org/10.1016/S1357-4310(99)01461-6},
  url = {http://www.sciencedirect.com/science/article/pii/S1357431099014616},
  author = {Parry Guilford},
  keywords = {tumorigenesis},
}


@article{Beavon2000,
  title = {The E-cadherin–catenin complex in tumour metastasis: structure, function and regulation},
  journal = {European Journal of Cancer},
  volume = {36},
  number = {13},
  pages = {1607 - 1620},
  year = {2000},
  note = {},
  issn = {0959-8049},
  doi = {http://dx.doi.org/10.1016/S0959-8049(00)00158-1},
  url = {http://www.sciencedirect.com/science/article/pii/S0959804900001581},
  author = {I.R.G Beavon},
  keywords = {Epidermal growth factor receptor},
}


@article{Pharoah2001,
  title = {Incidence of gastric cancer and breast cancer in \{CDH1\} (E-cadherin) mutation carriers from hereditary diffuse gastric cancer families},
  journal = {Gastroenterology},
  volume = {121},
  number = {6},
  pages = {1348 - 1353},
  year = {2001},
  note = {},
  issn = {0016-5085},
  doi = {http://dx.doi.org/10.1053/gast.2001.29611},
  url = {http://www.sciencedirect.com/science/article/pii/S0016508501595554},
  author = {Paul D.P. Pharoah and Parry Guilford and Carlos Caldas},
}


@article{Kaurah2007,
  author = {Kaurah P and MacMillan A and Boyd N and et al},
  title = {FOunder and recurrent cdh1 mutations in families with hereditary diffuse gastric cancer},
  journal = {JAMA},
  volume = {297},
  number = {21},
  pages = {2360-2372},
  year = {2007},
  doi = {10.1001/jama.297.21.2360},
  url = {+ http://dx.doi.org/10.1001/jama.297.21.2360},
  eprint = {/data/Journals/JAMA/5171/joc70056_2360_2372.pdf},
}


@article{Semb1998,
  author = {Semb, H. and Christofori, G.},
  title = {The tumor-suppressor function of E-cadherin},
  journal = {Am J Hum Genet},
  volume = {63},
  number = {6},
  pages = {1588-93},
  keywords = {Animals Cadherins/genetics/*metabolism Cell Adhesion Cytoskeletal Proteins/physiology Genes, Tumor Suppressor/*genetics Humans Models, Biological Neoplasms/genetics/*metabolism/pathology Signal Transduction *Trans-Activators beta Catenin},
  year = {1998},
}


@article{Wong2003,
  author = {Wong, A. S. and Gumbiner, B. M.},
  title = {Adhesion-independent mechanism for suppression of tumor cell invasion by E-cadherin},
  journal = {J Cell Biol},
  volume = {161},
  number = {6},
  pages = {1191-203},
  abstract = {Loss of E-cadherin expression or function in tumors leads to a more invasive phenotype. In this study, we investigated whether the invasion suppressor activity of E-cadherin is mediated directly by tighter physical cell adhesion, indirectly by sequestering beta-catenin and thus antagonizing beta-catenin/T cell factor (TCF) signaling, or by other signaling pathways. To distinguish mechanisms, we expressed wild-type E-cadherin and various E-cadherin mutants in invasive E-cadherin-negative human breast (MDA-MB-231) and prostate (TSU-Pr1) epithelial carcinoma cell lines using a tetracycline-inducible system. Our data confirm that E-cadherin inhibits human mammary and prostate tumor cell invasion. We find that adhesion is neither necessary nor sufficient for suppressing cancer invasion. Rather, the invasion suppressor signal is mediated through the beta-catenin-binding domain of the E-cadherin cytoplasmic tail but not through the p120ctn-binding domain. beta-catenin depletion also results in invasion suppression. However, alteration in the beta-catenin/TCF transcriptional regulation of target genes is not required for the invasion suppressor activity of E-cadherin, suggesting the involvement of other beta-catenin-binding proteins.},
  keywords = {Breast Neoplasms/genetics/metabolism Cadherins/genetics/*metabolism Carcinoma/genetics/metabolism Cell Adhesion/*physiology Cell Membrane/*metabolism Cytoskeletal Proteins/metabolism DNA-Binding Proteins/metabolism Female Humans Lymphoid Enhancer-Binding Factor 1 Male Neoplasm Invasiveness/*physiopathology Neoplasms/*metabolism/physiopathology Prostatic Neoplasms/genetics/metabolism Protein Binding/physiology Protein Structure, Tertiary/physiology Trans-Activators/metabolism Transcription Factors/metabolism Tumor Cells, Cultured beta Catenin},
  year = {2003},
}


@article{Berx1995,
  author = {Berx, G. and Cleton-Jansen, A. M. and Nollet, F. and de Leeuw, W. J. and van de Vijver, M. and Cornelisse, C. and van Roy, F.},
  title = {E-cadherin is a tumour/invasion suppressor gene mutated in human lobular breast cancers},
  journal = {EMBO J},
  volume = {14},
  number = {24},
  pages = {6107-15},
  abstract = {Compelling experimental evidence exists for a potent invasion suppressor role of the cell-cell adhesion molecule E-cadherin. In addition, a tumour suppressor effect has been suggested for E-cadherin. In human cancers, partial or complete loss of E-cadherin expression correlates with malignancy. To investigate the molecular basis for this altered expression we developed a comprehensive PCR/SSCP mutation screen for the human E-cadherin gene. For 49 breast cancer patients the occurrence of tumour-specific mutations in the E-cadherin gene was examined. No relevant DNA changes were encountered in any of 42 infiltrative ductal or medullary breast carcinoma samples. In contrast, four out of seven infiltrative lobular breast carcinomas harboured protein truncation mutations (three nonsense and one frameshift) in the extracellular part of the E-cadherin protein. Each of the four lobular carcinomas with E-cadherin mutations showed tumour-specific loss of heterozygosity of chromosomal region 16q22.1 containing the E-cadherin locus. In compliance with this, no E-cadherin expression was detectable by immunohistochemistry in these four tumours. These findings offer a molecular explanation for the typical scattered tumour cell growth in infiltrative lobular breast cancer.},
  keywords = {Base Sequence Breast Neoplasms/etiology/*genetics/metabolism Cadherins/*genetics/physiology Carcinoma, Ductal, Breast/genetics/metabolism Carcinoma, Lobular/etiology/*genetics/metabolism Chromosomes, Human, Pair 16/genetics DNA Primers/genetics DNA, Neoplasm/genetics Female *Genes, Tumor Suppressor Heterozygote Humans Immunohistochemistry Molecular Sequence Data *Mutation Polymerase Chain Reaction Polymorphism, Single-Stranded Conformational},
  year = {1995},
}


@article{Berx1996,
  author = {Berx, G. and Cleton-Jansen, A. M. and Strumane, K. and de Leeuw, W. J. and Nollet, F. and van Roy, F. and Cornelisse, C.},
  title = {E-cadherin is inactivated in a majority of invasive human lobular breast cancers by truncation mutations throughout its extracellular domain},
  journal = {Oncogene},
  volume = {13},
  number = {9},
  pages = {1919-25},
  abstract = {We have analysed a series of 49 human breast cancers for mutations in the entire coding region plus flanking intron sequences of the E-cadherin gene. The tumours included 41 infiltrating lobular carcinomas, two infiltrating ducto-lobular carcinomas and six infiltrative ductal carcinomas. In the lobular carcinomas 23 different somatic mutations were detected, of which seven were insertions, 11 deletions, two nonsense mutations and three splice site mutations. The other tumours showed no detectable E-cadherin mutations. All the frameshift and nonsense mutations are expected to generate a secreted E-cadherin fragment instead of a transmembrane protein with cell adhesion activity. The majority of the mutations (21 of 23) were found in combination with loss of heterozygosity of the wild type E-cadherin locus (16q22.1), a hallmark of classical tumour suppressor genes. The mutations were scattered over the whole coding region and no hot spots could be identified. All mutations described here were previously unreported. In conclusion, we have identified up to now E-cadherin mutations in 27 of 48 (56%) infiltrating lobular breast carcinomas and in 0 of 50 breast cancers of other histopathological subtypes. These data provide strong evidence that frequent E-cadherin mutations are involved in the particular etiology of sporadic lobular breast cancers.},
  keywords = {Binding Sites Breast Neoplasms/*genetics/pathology Cadherins/*genetics/metabolism Carcinoma, Lobular/genetics/pathology Chromosomes, Human, Pair 16 DNA Mutational Analysis Heterozygote Humans Immunohistochemistry Molecular Sequence Data *Mutation Neoplasm Invasiveness/genetics Polymerase Chain Reaction Polymorphism, Genetic Polymorphism, Single-Stranded Conformational Sequence Analysis, DNA},
  year = {1996},
}


@article{Guilford2010,
  author = {Guilford, P. and Humar, B. and Blair, V.},
  title = {Hereditary diffuse gastric cancer: translation of CDH1 germline mutations into clinical practice},
  journal = {Gastric Cancer},
  volume = {13},
  number = {1},
  pages = {1-10},
  abstract = {Hereditary diffuse gastric cancer (HDGC) is the only known cancer syndrome that is dominated by gastric adenocarcinoma. HDGC is caused by germline mutation of the CDH1 gene that encodes the cell adhesion protein E-cadherin. Mutation carriers have a more than 70% lifetime risk of developing DGC and an elevated risk of lobular breast cancer. Intestinal-type gastric cancer is not part of the syndrome. Clinical management of HDGC involves predictive genetic testing beginning at or near 16 years of age. It is recommended that mutation carriers undergo prophylactic gastrectomy after about 20 years of age. Anatomical mapping has demonstrated that mutation carriers develop multifocal stage T1a signet ring cell carcinomas, with up to several hundred foci being observed in single stomachs. These foci develop following the somatic inactivation of the second CDH1 allele by mechanisms that include DNA promoter hypermethylation.},
  keywords = {Cadherins/*genetics Carcinoma, Signet Ring Cell/*genetics/pathology/prevention & control Gastrectomy Genetic Predisposition to Disease Genetic Testing *Germ-Line Mutation Humans Penetrance Prognosis Risk Factors Stomach Neoplasms/*genetics/pathology/prevention & control},
  year = {2010},
}


@article{Ryan2014,
  author = {Ryan, Colm J and Lord, Christopher J and Ashworth, Alan},
  title = {DAISY: Picking Synthetic Lethals from Cancer Genomes},
  journal = {Cancer Cell},
  volume = {26},
  number = {3},
  pages = {306-308},
  abstract = {A better understanding of genetic interactions in cancer might help identify new therapeutic approaches that exploit the concept of synthetic lethality. Ruppin and colleagues have developed a new computational method, DAISY, that predicts such interactions and potentially facilitates the delineation and validation of comprehensive genetic interaction networks.},
  year = {2014},
}


@article{Crunkhorn2014,
  author = {Crunkhorn, S.},
  title = {Cancer: Predicting synthetic lethal interactions},
  journal = {Nat Rev Drug Discov},
  volume = {13},
  number = {11},
  pages = {812},
  year = {2014},
}


@article{HDGC,
  author = {Guilford, P. J. and Hopkins, J. B. and Grady, W. M. and Markowitz, S. D. and Willis, J. and Lynch, H. and Rajput, A. and Wiesner, G. L. and Lindor, N. M. and Burgart, L. J. and Toro, T. T. and Lee, D. and Limacher, J. M. and Shaw, D. W. and Findlay, M. P. and Reeve, A. E.},
  title = {E-cadherin germline mutations define an inherited cancer syndrome dominated by diffuse gastric cancer},
  journal = {Hum Mutat},
  volume = {14},
  number = {3},
  pages = {249-55},
  abstract = {To extend earlier observations of germline E-cadherin mutations in kindreds with an inherited susceptibility to diffuse gastric cancer, we searched for germline E-cadherin mutations in five further families affected predominantly by diffuse gastric cancer and one family with a history of diffuse gastric cancer and early-onset breast cancer. Heterozygous inactivating mutations were found in the E-cadherin gene in each of these families. No mutation hotspots were identified. These results demonstrate that germline mutation of the E-cadherin gene is a common cause of hereditary diffuse gastric cancer and suggest a role for these mutations in the incidence of breast cancer.},
  keywords = {Adenocarcinoma/*genetics Adult Aged Aged, 80 and over Breast Neoplasms/*genetics Cadherins/*genetics DNA Mutational Analysis Female *Germ-Line Mutation Humans Leukocytes Loss of Heterozygosity Male Middle Aged Pedigree Polymerase Chain Reaction Polymorphism, Genetic Stomach Neoplasms/*genetics Syndrome},
  year = {1999},
}


@article{Vos1997,
  author = {Vos, C. B. and Cleton-Jansen, A. M. and Berx, G. and de Leeuw, W. J. and ter Haar, N. T. and van Roy, F. and Cornelisse, C. J. and Peterse, J. L. and van de Vijver, M. J.},
  title = {E-cadherin inactivation in lobular carcinoma in situ of the breast: an early event in tumorigenesis},
  journal = {Br J Cancer},
  volume = {76},
  number = {9},
  pages = {1131-3},
  abstract = {In breast cancer, inactivating point mutations in the E-cadherin gene are frequently found in invasive lobular carcinoma (ILC) but never in invasive ductal carcinoma (IDC). Lobular carcinoma in situ (LCIS) adjacent to ILC has previously been shown to lack E-cadherin expression, but whether LCIS without adjacent invasive carcinoma also lacks E-cadherin expression and whether the gene mutations present in ILC are already present in LCIS is not known. We report here that E-cadherin expression is absent in six cases of LCIS and present in 150 cases of ductal carcinoma in situ (DCIS), both without an adjacent invasive component. Furthermore, using mutation analysis, we could demonstrate the presence of the same truncating mutations and loss of heterozygosity (LOH) of the wild-type E-cadherin in the LCIS component and in the adjacent ILC. Our results indicate that E-cadherin is a very early target gene in lobular breast carcinogenesis and plays a tumour-suppressive role, additional to the previously suggested invasion-suppressive role. IMAGES:},
  year = {1997},
}


@article{Masciari2007,
  author = {Masciari, S. and Larsson, N. and Senz, J. and Boyd, N. and Kaurah, P. and Kandel, M. J. and Harris, L. N. and Pinheiro, H. C. and Troussard, A. and Miron, P. and Tung, N. and Oliveira, C. and Collins, L. and Schnitt, S. and Garber, J. E. and Huntsman, D.},
  title = {Germline E-cadherin mutations in familial lobular breast cancer},
  journal = {J Med Genet},
  volume = {44},
  number = {11},
  pages = {726-31},
  abstract = {BACKGROUND: The cell surface glycoprotein E-cadherin (CDH1) is a key regulator of adhesive properties in epithelial cells. Germline mutations in CDH1 are well established as the defects underlying hereditary diffuse gastric cancer (HDGC) syndrome, and an increased risk of lobular breast cancer (LBC) has been described in HDGC kindreds. However, germline CDH1 mutations have not been described in patients with LBC in non-HDGC families. This study aimed to investigate the frequency of germline CDH1 mutations in patients with LBC with early onset disease or family histories of breast cancer without DGC. METHODS: Germline DNA was analysed in 23 women with invasive lobular or mixed ductal and lobular breast cancers who had at least one close relative with breast cancer or had themselves been diagnosed before the age of 45 years, had tested negative for a germline BRCA1 or BRCA2 mutation, and reported no personal or family history of diffuse gastric cancer. The full coding sequence of CDH1 including splice junctions was amplified using PCR and screened for mutations using DHPLC and sequencing. RESULTS: A novel germline CDH1 truncating mutation in the extracellular portion of the protein (517insA) was identified in one woman who had LBC at the age of 42 years and a first degree relative with invasive LBC. CONCLUSIONS: Germline CDH1 mutations can be associated with invasive LBC in the absence of diffuse gastric cancer. The finding, if confirmed, may have implications for management of individuals at risk for this breast cancer subtype. Clarification of the cancer risks in the syndrome is essential.},
  keywords = {Adult Breast Neoplasms/chemistry/*genetics Cadherins/analysis/deficiency/*genetics Carcinoma, Ductal, Breast/genetics Carcinoma, Large Cell/chemistry/*genetics *Codon, Nonsense DNA Methylation Female Genetic Heterogeneity *Germ-Line Mutation Humans Loss of Heterozygosity Neoplasm Invasiveness Neoplasm Proteins/analysis/genetics Neoplastic Syndromes, Hereditary/*genetics Pedigree Stomach Neoplasms/genetics},
  year = {2007},
}


@article{Berx2009,
  author = {Berx, G. and van Roy, F.},
  title = {Involvement of Members of the Cadherin Superfamily in Cancer},
  journal = {Cold Spring Harb Perspect Biol},
  volume = {1},
  pages = {a003129},
  year = {2009},
}


@article{DeLeeuw1997,
  author = {De Leeuw, W. J. and Berx, G. and Vos, C. B. and Peterse, J. L. and Van de Vijver, M. J. and Litvinov, S. and Van Roy, F. and Cornelisse, C. J. and Cleton-Jansen, A. M.},
  title = {Simultaneous loss of E-cadherin and catenins in invasive lobular breast cancer and lobular carcinoma in situ},
  journal = {J Pathol},
  volume = {183},
  number = {4},
  pages = {404-11},
  abstract = {Loss of expression of the intercellular adhesion molecule E-cadherin frequently occurs in invasive lobular breast carcinomas as a result of mutational inactivation. Expression patterns of E-cadherin and the molecules comprising the cytoplasmic complex of adherens junctions, alpha-, beta- and gamma-catenin, were studied in a series of 38 lobular breast carcinomas with known E-cadherin mutation status. The effect of loss of E-cadherin by mutational inactivation (or other mechanisms) on the expression of catenins was investigated. Complete loss of plasma membrane-associated E-cadherin expression was observed in 32 out of 38 invasive lobular carcinomas, for which in 21 cases a mutation was found in the extracellular domain of E-cadherin. In total, 15 frameshift mutations of small deletions or insertions, ranging from 1 to 41 bp, three non-sense mutations, and three splice mutations were identified. Mutations were scattered over the whole coding region and no hot spots could be detected. In all cases, simultaneous loss of E-cadherin and alpha- and beta-catenin expression was found; in 50 per cent of these cases, additional loss of gamma-catenin was observed. In six invasive lobular carcinomas, expression of both E-cadherin and catenins was retained. In none of these carcinomas was an E-cadherin mutation detected. Lobular carcinoma in situ adjacent to invasive lobular carcinoma showed simultaneous loss of E-cadherin and catenins in all the cases studied--remarkably, also, in four cases positive for E-cadherin and catenin expression in the invasive component. These results indicate that simultaneous loss of E-cadherin and alpha-, beta- and gamma-catenin may be an important step in the formation of lobular carcinoma in situ, as a precursor of invasive lobular breast cancer. Events additional to E-cadherin inactivation must be involved in the transition of lobular carcinoma in situ to invasive lobular carcinoma.},
  keywords = {Breast Neoplasms/genetics/*metabolism/pathology Cadherins/genetics/*metabolism Carcinoma in Situ/genetics/metabolism/pathology Carcinoma, Ductal, Breast/genetics/*metabolism/pathology Carcinoma, Lobular/genetics/*metabolism/pathology Cytoskeletal Proteins/*metabolism DNA Mutational Analysis Desmoplakins Female Humans Neoplasm Invasiveness *Trans-Activators alpha Catenin beta Catenin gamma Catenin},
  year = {1997},
}


@article{Machado2001,
  author = {Machado, JC and Olivera, C and Carvalh, R and Soares, P and Berx, G and Caldas, C and Sercuca, R and Carneiro, F and Sorbrinho-Simoes, M},
  title = {E-cadherin gene (CDH1) promoter methylation as the second hit in sporadic diffuse gastric carcinoma},
  journal = {Oncogene},
  volume = {20},
  pages = {1525-1528},
  year = {2001},
}


@article{Polyak2009,
  author = {Polyak, K. and Weinberg, R. A.},
  title = {Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits},
  journal = {Nat Rev Cancer},
  volume = {9},
  number = {4},
  pages = {265-73},
  abstract = {Transitions between epithelial and mesenchymal states have crucial roles in embryonic development. Emerging data suggest a role for these processes in regulating cellular plasticity in normal adult tissues and in tumours, where they can generate multiple, distinct cellular subpopulations contributing to intratumoural heterogeneity. Some of these subpopulations may exhibit more differentiated features, whereas others have characteristics of stem cells. Owing to the importance of these tumour-associated phenotypes in metastasis and cancer-related mortality, targeting the products of such cellular plasticity is an attractive but challenging approach that is likely to lead to improved clinical management of cancer patients.},
  keywords = {Animals Epigenesis, Genetic Epithelial Cells/*cytology Humans Mesoderm/*chemistry Mice Neoplasms/genetics/*pathology Neoplastic Stem Cells/*cytology Signal Transduction},
  year = {2009},
}


@article{vanPel2013,
  doi = {10.1371/journal.pgen.1003254},
  url = {http://dx.doi.org/10.1371/journal.pgen.1003254},
  year = {2013},
  month = {jan},
  publisher = {Public Library of Science ({PLoS})},
  volume = {9},
  number = {1},
  pages = {e1003254},
  author = {van Pel, Derek M. and Irene J. Barrett and Yoko Shimizu and Babu V. Sajesh and Brent J. Guppy and Tom Pfeifer and Kirk J. McManus and Philip Hieter},
  editor = {Marshall S. Horwitz},
  title = {An Evolutionarily Conserved Synthetic Lethal Interaction Network Identifies {FEN}1 as a Broad-Spectrum Target for Anticancer Therapeutic Development},
  journal = {{PLoS} Genetics},
}


@article{Azorsa2009,
  doi = {10.1186/1479-5876-7-43},
  url = {http://dx.doi.org/10.1186/1479-5876-7-43},
  year = {2009},
  publisher = {Springer Science $\mathplus$ Business Media},
  volume = {7},
  number = {1},
  pages = {43},
  author = {David O Azorsa and Irma M Gonzales and Gargi D Basu and Ashish Choudhary and Shilpi Arora and Kristen M Bisanz and Jeffrey A Kiefer and Meredith C Henderson and Jeffrey M Trent and Daniel D Von Hoff and Spyro Mousses},
  title = {Synthetic lethal {RNAi} screening identifies sensitizing targets for gemcitabine therapy in pancreatic cancer},
  journal = {Journal of Translational Medicine},
}


@article{Chan2011,
  doi = {10.1038/nrd3374},
  url = {http://dx.doi.org/10.1038/nrd3374},
  year = {2011},
  month = {may},
  publisher = {Nature Publishing Group},
  volume = {10},
  number = {5},
  pages = {351--364},
  author = {Denise A. Chan and Amato J. Giaccia},
  title = {Harnessing synthetic lethal interactions in anticancer drug discovery},
  journal = {Nature Reviews Drug Discovery},
}


@article{vanderMeer2014,
  doi = {10.1158/1078-0432.ccr-13-3116},
  url = {http://dx.doi.org/10.1158/1078-0432.ccr-13-3116},
  year = {2014},
  month = {apr},
  publisher = {American Association for Cancer Research ({AACR})},
  volume = {20},
  number = {12},
  pages = {3211--3221},
  author = {R. van der Meer and H. Yong Song and S.-H. Park and S. A. Abdulkadir and M. Roh},
  title = {{RNAi} Screen Identifies a Synthetic Lethal Interaction between {PIM}1 Overexpression and {PLK}1 Inhibition},
  journal = {Clinical Cancer Research},
}


@article{Diehl2014,
  doi = {10.1016/j.ddtec.2013.12.002},
  url = {http://dx.doi.org/10.1016/j.ddtec.2013.12.002},
  year = {2014},
  month = {mar},
  publisher = {Elsevier {BV}},
  volume = {11},
  pages = {11--18},
  author = {Paul Diehl and Donato Tedesco and Alex Chenchik},
  title = {Use of {RNAi} screens to uncover resistance mechanisms in cancer cells and identify synthetic lethal interactions},
  journal = {Drug Discovery Today: Technologies},
}


@article{Shalem2015,
  doi = {10.1038/nrg3899},
  url = {http://dx.doi.org/10.1038/nrg3899},
  year = {2015},
  month = {apr},
  publisher = {Nature Publishing Group},
  volume = {16},
  number = {5},
  pages = {299--311},
  author = {Ophir Shalem and Neville E. Sanjana and Feng Zhang},
  title = {High-throughput functional genomics using {CRISPR}{\textendash}Cas9},
  journal = {Nat Rev Genet},
}


@article{Hart2015,
  doi = {10.1016/j.cell.2015.11.015},
  url = {http://dx.doi.org/10.1016/j.cell.2015.11.015},
  year = {2015},
  month = {dec},
  publisher = {Elsevier {BV}},
  volume = {163},
  number = {6},
  pages = {1515--1526},
  author = {Traver Hart and Megha Chandrashekhar and Michael Aregger and Zachary Steinhart and Kevin~R. Brown and Graham MacLeod and Monika Mis and Michal Zimmermann and Amelie Fradet-Turcotte and Song Sun and Patricia Mero and Peter Dirks and Sachdev Sidhu and Frederick~P. Roth and Olivia~S. Rissl and Daniel Durocher and Stephane Angers and Jason Moffat},
  title = {High-Resolution {CRISPR} Screens Reveal Fitness Genes and Genotype-Specific Cancer Liabilities},
  journal = {Cell},
}

@article{Thompson2015,
   author = {Thompson, Jordan M. and Nguyen, Quy H. and Singh, Manpreet and Razorenova, Olga V.},
   title = {Approaches to Identifying Synthetic Lethal Interactions in Cancer},
   journal = {The Yale Journal of Biology and Medicine},
   volume = {88},
   number = {2},
   pages = {145-155},
   note = {yjbm882145[PII]
26029013[pmid]
Yale J Biol Med},
   abstract = {Targeting synthetic lethal interactions is a promising new therapeutic approach to exploit specific changes that occur within cancer cells. Multiple approaches to investigate these interactions have been developed and successfully implemented, including chemical, siRNA, shRNA, and CRISPR library screens. Genome-wide computational approaches, such as DAISY, also have been successful in predicting synthetic lethal interactions from both cancer cell lines and patient samples. Each approach has its advantages and disadvantages that need to be considered depending on the cancer type and its molecular alterations. This review discusses these approaches and examines case studies that highlight their use.},
   ISSN = {0044-0086
1551-4056},
   url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445436/},
   year = {2015},
   type = {Journal Article}
}


@article{Gentleman2004,
  doi = {10.1186/gb-2004-5-10-r80},
  year = {2004},
  publisher = {Springer Nature},
  volume = {5},
  number = {10},
  pages = {R80},
  author = {Robert C Gentleman and Vincent J Carey and Douglas M Bates and Ben Bolstad and Marcel Dettling and Sandrine Dudoit and Byron Ellis and Laurent Gautier and Yongchao Ge and Jeff Gentry and Kurt Hornik and Torsten Hothorn and Wolfgang Huber and Stefano Iacus and Rafael Irizarry and Friedrich Leisch and Cheng Li and Martin Maechler and Anthony J Rossini and Gunther Sawitzki and Colin Smith and Gordon Smyth and Luke Tierney and Jean YH Yang and Jianhua Zhang},
  title = {Bioconductor: open software development for computational biology and bioinformatics},
  journal = {Genome Biol},
}