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Fig. 5 | Genome Medicine

Fig. 5

From: Cancer origin tracing and timing in two high-risk prostate cancers using multisample whole genome analysis: prospects for personalized medicine

Fig. 5

Copy number overview and driver phylogenies in GP5 and GP12. a Genome-wide cancer and tissue normal somatic copy number alterations (CNAs), with samples numbered as in Figs. 3a and 4a. Sample “NL” represents a comparison of a noncancerous prostate sample to the blood normal sample. Brackets on the outer rim matching the evolutionary cluster color of panel b show the evolutionary assignment of the CNAs. In GP5, the many red “spokes” in the cancer genome represent the 907 < 5 Mb (tandem) duplicated regions likely due to homozygous loss-of-function of CDK12 in cluster T. Three major chromatid duplications have occurred in chromosomes 3q, 8q, and 12q (red) while large lost regions are detected in chromosomes 13q and 22q (blue). In GP12, major duplications have occurred in chromosomes 1q, 7q, 9, and Xq. Chromosome 4 has lost the ends of both q and p-arms that have subsequently joined together, forming a ring chromosome. b Cancer genomic cladograms with internodal distance scaled to the number of SNVs in each segment. Genetic aberrations targeting reported and candidate [2, 4] prostate cancer driver genes are shown next to the evolutionary clusters matching the point in evolution where the event has occurred. Icons adjacent to gene names are used to mark oncogenic driver events, with up (gain of function) and down (loss of function) icons indicating the type of event. Events depicted for each cluster are in no specific order. Genes without adjacent icons are events in prostate cancer driver genes that lack evidence in the literature of being oncogenic. LN, pelvic lymph node; SV, seminal vesicle

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