Molecular genetics of prostate cancer.
The molecular mechanisms underlying the development and progression of prostate cancer are poorly understood. Epidemiological studies have suggested that 5-10% of all prostate cancers are familial, and numerous chromosomal loci have been associated with prostate cancer in multicentre linkage studies. However, no putative susceptibility genes harboured in these chromosomal regions have thus far been identified. Several recurrent chromosomal alterations in prostate cancer have been detected in comparative genomic hybridization (CGH) and loss of heterozygosity (LOH) analysis. The target genes for many of these aberrations are still not known. It seems that the androgen receptor (AR) signalling pathway plays a crucial role in both early development as well as in late progression of the disease. Both germ-line and somatic genetic alterations in the AR gene have been demonstrated in prostate cancer patients. The intention of this review is to summarize the current knowledge of molecular mechanisms in the development of prostate cancer.
Elo
J P
JP
Laboratory of Cancer Genetics, Institute of Medical Technology, University of Tampere, Finland.
Visakorpi
T
T
D051792:Basic Helix-Loop-Helix Proteins; D015820:Cadherins / Q000235:genetics; D002471:Cell Transformation, Neoplastic; D003598:Cytoskeletal Proteins / Q000235:genetics; D004268:DNA-Binding Proteins / Q000502:physiology; D016147:Genes, Tumor Suppressor / Q000502:physiology; D018734:Genes, erbB-2 / Q000235:genetics; D008040:Genetic Linkage; D020022:Genetic Predisposition to Disease; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase / Q000502:physiology; D018257:Helix-Loop-Helix Motifs / Q000502:physiology; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D007527:Isoenzymes / Q000502:physiology; D019656:Loss of Heterozygosity; D008297:Male; D009693:Nucleic Acid Hybridization; D051059:PTEN Phosphohydrolase; D010744:Phosphoric Monoester Hydrolases / Q000502:physiology; D011471:Prostatic Neoplasms / Q000235:genetics*; D011944:Receptors, Androgen / Q000235:genetics; D015398:Signal Transduction; D015534:Trans-Activators; D014157:Transcription Factors / Q000502:physiology; D025521:Tumor Suppressor Proteins; D051176:beta Catenin
D051792:Basic Helix-Loop-Helix Proteins; D015820:Cadherins; D003598:Cytoskeletal Proteins; D004268:DNA-Binding Proteins; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; D007527:Isoenzymes; D051059:PTEN Phosphohydrolase; D010744:Phosphoric Monoester Hydrolases; D011944:Receptors, Androgen; D015534:Trans-Activators; D014157:Transcription Factors; D025521:Tumor Suppressor Proteins; D051176:beta Catenin; C495270:CTNNB1 protein, human; C079440:MXI1 protein, human; C496556:GSTP1 protein, human; C494929:PTEN protein, human