Prostate Cancer as a Model System for Genetic Diversity in Tumors

被引：24
作者：
Squire, Jeremy A. [1 ]
Park, Paul C. [1 ]
Yoshimoto, Maisa [1 ]
Alami, Jennifer [1 ]
Williams, Julia L. [1 ]
Evans, Andrew [2 ]
Joshua, Anthony M. [3 ,4 ,5 ]
机构：
[1] Queens Univ, Dept Pathol & Mol Med, Kingston, ON, Canada
[2] Univ Hlth Network, Dept Pathol, Toronto, ON, Canada
[3] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada
[4] Princess Margaret Hosp, Ontario Canc Inst, Div Appl Mol Oncol, Toronto, ON M4X 1K9, Canada
[5] Princess Margaret Hosp, Dept Med Oncol, Toronto, ON M4X 1K9, Canada
来源：
INTRATUMOR DIVERSITY AND CLONAL EVOLUTION IN CANCER | 2011年 / 112卷
关键词：
PROLIFERATIVE INFLAMMATORY ATROPHY; IN-SITU HYBRIDIZATION; ETS TRANSCRIPTION FACTORS; PTEN GENOMIC DELETION; INTRAEPITHELIAL NEOPLASIA HGPIN; CHRONIC OXIDATIVE STRESS; EPITHELIAL STEM-CELLS; STRAND BREAK REPAIR; C-MYC ONCOGENE; ANDROGEN RECEPTOR;
D O I：
10.1016/B978-0-12-387688-1.00007-7
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
This chapter will summarize novel understandings of the early molecular events in prostatic carcinogenesis that may underlie both the genetic and clinical heterogeneity. Areas covered include preneoplasia, stem cell concepts, telomere abnormalities, and the nature of tumor-stromal interactions. The oncogenomics of prostate cancer is reviewed with emphasis on androgen signaling, ETS gene family aberrations, and PTEN deletion. The notion that "field cancerization," coupled with genomic instability may explain both the occurrence of multifocal disease, and the recent observations of genetic diversity of ERG alteration in individual tumors are discussed. Collectively, genomic studies are rapidly moving human prostate cancer closer to the promise of personalized medicine, so that specific genetic profiles of individual tumors will determine the best therapeutic approaches. (C) 2011 Elsevier Inc.
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收藏
页码：183 / 216
页数：34
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