title: [Molecular biological aspect].
abstract: Although adenocarcinoma of the prostate is recently becoming one of most common malignancies in Japanese men, it still poses many questions regarding its etiology, pathology, pathogenesis and clinical management. Many reports have been made on oncogene and tumor suppressor gene, however, frequent genetic alterations have not been identified during prostate cancer development. Loss of heterozygosity (LOH) on 8p might be an important event in the early stage of prostatic carcinogenesis, whereas alteration in 17p is now considered a late event. Numerous reports about the androgen receptor (AR) gene have revealed that mutations in the coding region of AR possibly results in an acquired resistance to androgen blockade therapy and anti-androgen withdrawal syndrome. It has been also shown that shorter CAG repeats of AR gene are associated with a higher risk of prostate cancer. Regarding molecular diagnosis, prostate-specific membrane antigen (PSM) appears to be a new molecule with many potentially valuable applications. PSM-reverse transcriptase-polymerase chain reaction (RT-PCR) is probably more sensitive and specific than PSA-RT-PCR to predict micrometastatic disease. Gene therapy based on the above molecular aspect is currently under investigation but not generally used yet.
authors.affiliation: Dept. of Urology, Institute of Clinical Medicine, University of Tsukuba.
authors.forename: T
authors.initials: T
authors.lastname: Shimazui
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics* / Q000628:therapy; D011905:Genes, ras; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000627:therapeutic use; D006801:Humans; D007376:Interleukin-2 / Q000627:therapeutic use; D019656:Loss of Heterozygosity; D008297:Male; D017354:Point Mutation; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000628:therapy; D011944:Receptors, Androgen / Q000235:genetics
chemical_list: D007376:Interleukin-2; D011944:Receptors, Androgen; D016178:Granulocyte-Macrophage Colony-Stimulating Factor