Catch my drift? Making sense of genomic intra-tumour heterogeneity.
MetadataShow full item record
The cancer genome is shaped by three components of the evolutionary process: mutation, selection and drift. While many studies have focused on the first two components, the role of drift in cancer evolution has received little attention. Drift occurs when all individuals in the population have the same likelihood of producing surviving offspring, and so by definition a drifting population is one that is evolving neutrally. Here we focus on how neutral evolution is manifested in the cancer genome. We discuss how neutral passenger mutations provide a magnifying glass that reveals the evolutionary dynamics underpinning cancer development, and outline how statistical inference can be used to quantify these dynamics from sequencing data. We argue that only after we understand the impact of neutral drift on the genome can we begin to make full sense of clonal selection. This article is part of a Special Issue entitled: Evolutionary principles - heterogeneity in cancer? Edited by Dr. Robert A. Gatenby.
Version of record
Clonal evolution of cancer
Next generation sequencing
Cell Transformation, Neoplastic
Gene Expression Regulation, Neoplastic
Genetic Predisposition to Disease
Evolutionary Genomics & Modelling
License start date
Biochim Biophys Acta, 1867 (2), pp. 95 - 100
Showing items related by title, author, creator and subject.
Association of breast cancer risk in BRCA1 and BRCA2 mutation carriers with genetic variants showing differential allelic expression: identification of a modifier of breast cancer risk at locus 11q22.3. Hamdi, Y; Soucy, P; Kuchenbaeker, KB; Pastinen, T; Droit, A; Lemaçon, A; Adlard, J; Aittomäki, K; Andrulis, IL; Arason, A; Arnold, N; Arun, BK; Azzollini, J; Bane, A; Barjhoux, L; Barrowdale, D; Benitez, J; Berthet, P; Blok, MJ; Bobolis, K; Bonadona, V; Bonanni, B; Bradbury, AR; Brewer, C; Buecher, B; Buys, SS; Caligo, MA; Chiquette, J; Chung, WK; Claes, KBM; Daly, MB; Damiola, F; Davidson, R; De la Hoya, M; De Leeneer, K; Diez, O; Ding, YC; Dolcetti, R; Domchek, SM; Dorfling, CM; Eccles, D; Eeles, R; Einbeigi, Z; Ejlertsen, B; EMBRACE; Engel, C; Gareth Evans, D; Feliubadalo, L; Foretova, L; Fostira, F; Foulkes, WD; Fountzilas, G; Friedman, E; Frost, D; Ganschow, P; Ganz, PA; Garber, J; Gayther, SA; GEMO Study Collaborators; Gerdes, A-M; Glendon, G; Godwin, AK; Goldgar, DE; Greene, MH; Gronwald, J; Hahnen, E; Hamann, U; Hansen, TVO; Hart, S; Hays, JL; HEBON; Hogervorst, FBL; Hulick, PJ; Imyanitov, EN; Isaacs, C; Izatt, L; Jakubowska, A; James, P; Janavicius, R; Jensen, UB; John, EM; Joseph, V; Just, W; Kaczmarek, K; Karlan, BY; KConFab Investigators; Kets, CM; Kirk, J; Kriege, M; Laitman, Y; Laurent, M; Lazaro, C; Leslie, G; Lester, J; Lesueur, F; Liljegren, A; Loman, N; Loud, JT; Manoukian, S; Mariani, M; Mazoyer, S; McGuffog, L; Meijers-Heijboer, HEJ; Meindl, A; Miller, A; Montagna, M; Mulligan, AM; Nathanson, KL; Neuhausen, SL; Nevanlinna, H; Nussbaum, RL; Olah, E; Olopade, OI; Ong, K-R; Oosterwijk, JC; Osorio, A; Papi, L; Park, SK; Pedersen, IS; Peissel, B; Segura, PP; Peterlongo, P; Phelan, CM; Radice, P; Rantala, J; Rappaport-Fuerhauser, C; Rennert, G; Richardson, A; Robson, M; Rodriguez, GC; Rookus, MA; Schmutzler, RK; Sevenet, N; Shah, PD; Singer, CF; Slavin, TP; Snape, K; Sokolowska, J; Sønderstrup, IMH; Southey, M; Spurdle, AB; Stadler, Z; Stoppa-Lyonnet, D; Sukiennicki, G; Sutter, C; Tan, Y; Tea, M-K; Teixeira, MR; Teulé, A; Teo, S-H; Terry, MB; Thomassen, M; Tihomirova, L; Tischkowitz, M; Tognazzo, S; Toland, AE; Tung, N; van den Ouweland, AMW; van der Luijt, RB; van Engelen, K; van Rensburg, EJ; Varon-Mateeva, R; Wappenschmidt, B; Wijnen, JT; Rebbeck, T; Chenevix-Trench, G; Offit, K; Couch, FJ; Nord, S; Easton, DF; Antoniou, AC; Simard, JPURPOSE: Cis-acting regulatory SNPs resulting in differential allelic expression (DAE) may, in part, explain the underlying phenotypic variation associated with many complex diseases. To investigate whether common variants ...
Kühnl, A; Cunningham, D; Chau, I (2017-09)After decades of intense research on genetic alterations in cancer and successful implementation of genetically-based targeted therapies, the field of cancer epigenetics is only beginning to be fully recognized. The discovery ...
Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation. Gusev, A; Shi, H; Kichaev, G; Pomerantz, M; Li, F; Long, HW; Ingles, SA; Kittles, RA; Strom, SS; Rybicki, BA; Nemesure, B; Isaacs, WB; Zheng, W; Pettaway, CA; Yeboah, ED; Tettey, Y; Biritwum, RB; Adjei, AA; Tay, E; Truelove, A; Niwa, S; Chokkalingam, AP; John, EM; Murphy, AB; Signorello, LB; Carpten, J; Leske, MC; Wu, SY; Hennis, AJ; Neslund-Dudas, C; Hsing, AW; Chu, L; Goodman, PJ; Klein, EA; Witte, JS; Casey, G; Kaggwa, S; Cook, MB; Stram, DO; Blot, WJ; Eeles, RA; Easton, D; Kote-Jarai, Z; Al Olama, AA; Benlloch, S; Muir, K; Giles, GG; Southey, MC; Fitzgerald, LM; Gronberg, H; Wiklund, F; Aly, M; Henderson, BE; Schleutker, J; Wahlfors, T; Tammela, TL; Nordestgaard, BG; Key, TJ; Travis, RC; Neal, DE; Donovan, JL; Hamdy, FC; Pharoah, P; Pashayan, N; Khaw, KT; Stanford, JL; Thibodeau, SN; McDonnell, SK; Schaid, DJ; Maier, C; Vogel, W; Luedeke, M; Herkommer, K; Kibel, AS; Cybulski, C; Wokolorczyk, D; Kluzniak, W; Cannon-Albright, L; Teerlink, C; Brenner, H; Dieffenbach, AK; Arndt, V; Park, JY; Sellers, TA; Lin, HY; Slavov, C; Kaneva, R; Mitev, V; Batra, J; Spurdle, A; Clements, JA; Teixeira, MR; Pandha, H; Michael, A; Paulo, P; Maia, S; Kierzek, A; Conti, DV; Albanes, D; Berg, C; Berndt, SI; Campa, D; Crawford, ED; Diver, WR; Gapstur, SM; Gaziano, JM; Giovannucci, E; Hoover, R; Hunter, DJ; Johansson, M; Kraft, P; Le Marchand, L; Lindström, S; Navarro, C; Overvad, K; Riboli, E; Siddiq, A; Stevens, VL; Trichopoulos, D; Vineis, P; Yeager, M; Trynka, G; Raychaudhuri, S; Schumacher, FR; Price, AL; Freedman, ML; Haiman, CA; Pasaniuc, B (2016-01)Although genome-wide association studies have identified over 100 risk loci that explain ∼33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data ...