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NOTES
Beroukhim, RameenMermel, Craig HPorter, DaleWei, GuoRaychaudhuri, SoumyaDonovan, JerryBarretina, JordiBoehm, Jesse SDobson, JenniferUrashima, MitsuyoshiMc Henry, Kevin TPinchback, Reid MLigon, Azra HCho, Yoon-JaeHaery, LeilaGreulich, HeidiReich, MichaelWinckler, WendyLawrence, Michael SWeir, Barbara ATanaka, Kumiko EChiang, Derek YBass, Adam JLoo, AliceHoffman, CarterPrensner, JohnLiefeld, TedGao, QingYecies, DerekSignoretti, SabinaMaher, ElizabethKaye, Frederic JSasaki, HidefumiTepper, Joel EFletcher, Jonathan ATabernero, JosepBaselga, JoseTsao, Ming-SoundDemichelis, FrancescaRubin, Mark AJanne, Pasi ADaly, Mark JNucera, CarmeloLevine, Ross LEbert, Benjamin LGabriel, StaceyRustgi, Anil KAntonescu, Cristina RLadanyi, MarcLetai, AnthonyGarraway, Levi ALoda, MassimoBeer, David GTrue, Lawrence DOkamoto, AikouPomeroy, Scott LSinger, SamuelGolub, Todd RLander, Eric SGetz, GadSellers, William RMeyerson, MatthewengK08CA122833/CA/NCI NIH HHS/K08 AR055688-03/AR/NIAMS NIH HHS/U54 HG003067/HG/NHGRI NIH HHS/P01CA 098101/CA/NCI NIH HHS/K08 CA122833-02/CA/NCI NIH HHS/K08 CA134931/CA/NCI NIH HHS/T32 GM007753/GM/NIGMS NIH HHS/R01CA109038/CA/NCI NIH HHS/K08 CA122833-01A1/CA/NCI NIH HHS/R01 CA109038/CA/NCI NIH HHS/P01 CA085859/CA/NCI NIH HHS/K08 CA122833/CA/NCI NIH HHS/P01CA085859/CA/NCI NIH HHS/P01 CA098101/CA/NCI NIH HHS/P50CA90578/CA/NCI NIH HHS/P50 CA090578/CA/NCI NIH HHS/R01 CA109467/CA/NCI NIH HHS/Howard Hughes Medical Institute/K08 CA122833-03/CA/NCI NIH HHS/R01CA109467/CA/NCI NIH HHS/K08 AR055688-04/AR/NIAMS NIH HHS/K08 AR055688/AR/NIAMS NIH HHS/U24 CA126546/CA/NCI NIH HHS/Research Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov'tEnglandNature. 2010 Feb 18;463(7283):899-905. doi: 10.1038/nature08822.
Abstract
A powerful way to discover key genes with causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here we present high-resolution analyses of somatic copy-number alterations (SCNAs) from 3,131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across several cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-kappaBeta pathway. We show that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types.
Last updated on 02/17/2021