The molecular heterogeneity and clinical impact of genomic driver alterations in prostate cancer - Nature
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IntroductionProstate cancer is the most common malignancy in men that accounts for 10% of male cancer-related deaths and is expected to increase in incidence in the coming decades1. Its clinical trajectory is highly variable, with disease courses ranging from localised disease with long indolent phases that often require no therapy, to early-onset cancer that typically necessitates definitive treatment with curative intent2 and life-threatening metastatic prostate cancer3. The management of newly diagnosed prostate cancer is primarily based on established clinical and pathological information along with small gene or mRNA panels. The most pressing unmet clinical needs include reliable prognostic approaches to minimize overtreatment and the identification of therapeutic targets4. This is especially challenging due to the considerable molecular heterogeneity of the disease. Its genomic landscape is dominated by structural variation (SV) and copy-number alteration (CNA) drivers, while in contrast, drivers involving small mutations including single-nucleotide variants (SNVs) and insertions-deletions (indels) are relatively infrequent5,6.
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