학술논문

Molecular Evolution of Early-Onset Prostate Cancer Identifies Molecular Risk Markers and Clinical Trajectories.
Document Type
article
Source
Cancer cell. 34(6)
Subject
Humans
Prostatic Neoplasms
RNA-Binding Proteins
Risk Factors
Evolution
Molecular
DNA Methylation
Gene Expression Regulation
Neoplastic
Mutation
Adult
Middle Aged
Male
Transcriptome
Biomarkers
Tumor
Whole Genome Sequencing
APOBEC
cancer genomics
early-onset cancer
epigenetic risk-score
mutational processes
prostate cancer
structural variants
tumor evolution
tumor evolution prediction
Human Genome
Aging
Prevention
Cancer
Urologic Diseases
Prostate Cancer
Genetics
4.1 Discovery and preclinical testing of markers and technologies
Aetiology
2.1 Biological and endogenous factors
Detection
screening and diagnosis
Neurosciences
Oncology and Carcinogenesis
Oncology & Carcinogenesis
Language
Abstract
Identifying the earliest somatic changes in prostate cancer can give important insights into tumor evolution and aids in stratifying high- from low-risk disease. We integrated whole genome, transcriptome and methylome analysis of early-onset prostate cancers (diagnosis ≤55 years). Characterization across 292 prostate cancer genomes revealed age-related genomic alterations and a clock-like enzymatic-driven mutational process contributing to the earliest mutations in prostate cancer patients. Our integrative analysis identified four molecular subgroups, including a particularly aggressive subgroup with recurrent duplications associated with increased expression of ESRP1, which we validate in 12,000 tissue microarray tumors. Finally, we combined the patterns of molecular co-occurrence and risk-based subgroup information to deconvolve the molecular and clinical trajectories of prostate cancer from single patient samples.