Punctuated Evolution of Prostate Cancer Genomes
By S. Baca, D. Prandi, M. Lawrence, J. Mosquera, A. Romanel, Y. Drier, K. Park, Naoki Kitabayashi, T. Macdonald, Mahmoud Ghandi and 33 more. Cell, 2013
1,269 citations recorded by the source corpus.
SUMMARY The analysis of exonic DNA from prostate cancers has identified recurrently mutated genes, but the spectrum of genome-wide alterations has not been profiled extensively in this disease. We sequenced the genomes of 57 prostate tumors and matched normal tissues to characterize somatic alterations and to study how they accumulate during oncogenesis and progression. By modeling the genesis of genomic rearrangements, we identified abundant DNA translocations and deletions that arise in a highly interdependent manner. This phenomenon, which we term “chromoplexy”, frequently accounts for the dysregulation of prostate cancer genes and appears to disrupt multiple cancer genes coordinately. Our modeling suggests that chromoplexy may induce considerable genomic derangement over relatively few events in prostate cancer and other neoplasms, supporting a model of punctuated cancer evolution. By characterizing the clonal hierarchy of genomic lesions in prostate tumors, we charted a path of oncogenic events along which chromoplexy may drive prostate carcinogenesis.
Subfields: Cancer Research, Molecular Biology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/265d774de9721a5f9a9f37d36af7eafdf1916b3a
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Citations in the corpus
- The long tail of oncogenic drivers in prostate cancer (2018, neutral): “Unfiltered MuTect mutation call are located in Supplementary Table 9.”
- Organoid cultures derived from patients with advanced prostate cancer (2014, neutral): “In the accompany manuscript (Karthaus et al., 2014, this issue), we developed conditions optimized for continuous propagation of both normal human basal and luminal prostate epithelial cells.”
- Genetics and biology of prostate cancer (2018, background): “1, a PSA-regulated homeobox gene, is frequently deleted in prostate cancer (He et al. 1997; Barbieri et al. 2012; Baca et al. 2013), and NKX3.”