Open AccessMicrosatellite Instability and Other Molecular Abnormalities in Human Prostate Cancer
Author(s) -
Suzuki Hiroyoshi,
Komiya Akira,
Aida Sara,
Akimoto Susumu,
Shiraishi Taizo,
Yatani Ryuichi,
Igarashi Tatsuo,
Shimazaki Jun
Publication year - 1995
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1995.tb03007.x
Subject(s) - microsatellite instability , microsatellite , loss of heterozygosity , biology , prostate cancer , cancer , prostate , colorectal cancer , genetics , dna mismatch repair , cancer research , genome instability , chromosome instability , gene , allele , chromosome , dna damage , dna
Microsatellites are highly polymorphic, short‐tandem repeat sequences dispersed throughout the genome. Instability of these repeat sequences at multiple genetic loci may result from mismatch repair errors, and occurs in hereditary nonpolyposis colorectal carcinoma and certain sporadic cancers. To examine microsatellite instability during the pathogenesis of human prostate cancer, we screened 48 prostate cancer cases (20 stage B, 10 stage C and 18 endocrine therapy‐resistant cancer‐death cases) for replication error at 17 microsatellite marker loci on 9 chromosomes. Microsatellite instabilities were found in 7 of 48 cases (14.6%), and all 7 cases showing the instability were poorly differentiated adenocarcinomas. Moreover, microsatellite instabilities were more frequently observed in cancer‐death cases (6/18, 33%) than in stage B+C cases (1/30, 3.3%). These data suggest that micro‐satellite instability is an important genetic change related to the progression of a subset of human prostate cancer cases. It is suggested to be associated with extensive, concurrent molecular changes including androgen receptor gene mutations, as well as frequent loss of heterozygosity at chromosomal regions 8p, 10q, and 16q.