Faculty Collaboration Database

Current status of the molecular genetics of human prostatic adenocarcinomas. Int J Cancer 2003 Jan 20;103(3):285-93

Date

12/10/2002

Pubmed ID

12471610

DOI

10.1002/ijc.10813

Scopus ID

2-s2.0-0037454778 (requires institutional sign-in at Scopus site)   68 Citations

Abstract

Molecular genetic mechanisms involved in the progression of prostate cancer are not well understood due to extensive tumor heterogeneity and lack of suitable models. New methods such as fluorescence in-situ hybridization (FISH), comparative genomic hybridization (CGH) and microsatellite analysis have documented losses or gains on various chromosomes. Altered chromosomal regions have been associated with the activation of oncogenes and the inactivation of tumor suppressor genes or defects in mismatch repair (MMR) genes. It is suggested that increased genomic instability is associated with decreased androgen-responsive and progressive behavior of human prostate tumors, but it remains unclear whether this genomic instability is causing the progression of cancer or is the consequence of cancer. Extended studies on hereditary prostate cancer have identified 7 prostate cancer susceptibility loci on several chromosomes, but no specific gene has been confined for a large proportion of susceptibility. In this review we summarize the ongoing molecular genetic events associated with the sporadic and hereditary prostate cancer development and progression.

Author List

Karan D, Lin MF, Johansson SL, Batra SK

Author

Dev Karan PhD Associate Professor in the Pathology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Adenocarcinoma
Base Pair Mismatch
Cell Transformation, Neoplastic
Disease Progression
Genes, Tumor Suppressor
Genetic Predisposition to Disease
Humans
Loss of Heterozygosity
Male
Molecular Biology
Prostatic Neoplasms
Signal Transduction