Prostate cancer is a common malignancy in men, with a markedly variable clinical course.
Somatic alterations in DNA drive the growth of prostate cancers and may underlie the behavior of aggressive versus indolent tumors. The accelerating application of genomic technologies over the last two decades has identified mutations that drive prostate cancer formation, progression, and therapeutic resistance. Here, we discuss exemplary somatic mutations in prostate cancer, and highlight mutated cellular pathways with biological and possible therapeutic importance. Examples include mutated genes involved in androgen signaling, cell cycle regulation, signal transduction, and development. Some genetic alterations may also predict the clinical course of disease or response to therapy, although the molecular heterogeneity of prostate tumors poses challenges to genomic biomarker identification. The widespread application of massively parallel sequencing technology to the analysis of prostate cancer genomes should continue to advance both discovery-oriented and diagnostic avenues.
Written by:
Baca SC, Garraway LA. Are you the author?
Harvard Medical School, Boston, MA, USA.
Reference: Front Endocrinol (Lausanne). 2012;3:69.
doi: 10.3389/fendo.2012.00069
PubMed Abstract
PMID: 22649426
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