Abstract
During the last ten years our knowledge of genetic alterations in prostate cancer has significantly increased. For example, several chromosomal loci possibly harboring predisposing or somatically mutated genes have been suggested. Still, we lack the comprehensive molecular model for the development and progression of prostate cancer. Only a few genes have been found to be aberrant in a significant proportion of prostate cancer. These include GSTP1, PTEN, TP53, and AR. Thus, they are natural targets for new treatment strategies.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Acyltransferases / genetics
-
Chromosome Mapping
-
Forecasting
-
Genetic Predisposition to Disease
-
Homeodomain Proteins / genetics
-
Humans
-
Male
-
Molecular Biology / trends
-
PTEN Phosphohydrolase
-
Phosphoric Monoester Hydrolases / genetics
-
Prostatic Neoplasms / genetics*
-
Receptors, Androgen / genetics
-
Transcription Factors / genetics
-
Tumor Suppressor Protein p53 / genetics
-
Tumor Suppressor Proteins / genetics
Substances
-
Homeodomain Proteins
-
NKX3-1 protein, human
-
Receptors, Androgen
-
Transcription Factors
-
Tumor Suppressor Protein p53
-
Tumor Suppressor Proteins
-
Acyltransferases
-
fatty acyl ethyl ester synthase
-
Phosphoric Monoester Hydrolases
-
PTEN Phosphohydrolase
-
PTEN protein, human