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Microsatellite instability and deletion analysis of chromosome 10 in human prostate cancer
Author(s) -
Lacombe Louis,
Orlow Irene,
Reuter Victor E.,
Fair William R.,
Dalbagni Guido,
Zhang ZuoFeng,
CordonCardo Carlos
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19960422)69:2<110::aid-ijc7>3.0.co;2-3
Subject(s) - microsatellite instability , prostate cancer , chromosome instability , biology , genetics , microsatellite , genome instability , chromosome analysis , prostate , chromosome , cancer , medicine , karyotype , gene , dna , dna damage , allele
Despite the clinical relevance of prostate cancer, few aspects regarding the molecular alterations involved in the process of prostate carcinogenesis are clearly understood. Cytogenetic and molecular genetic studies have identified specific abnormalities in prostate tumors, mainly on chromosomes 8, 10 and 16. On the basis of these findings, we designed a study to further characterize the altered regions on chromosome 10, using 15 microsatellite markers on a population composed of 20 paired normal and primary non‐metastatic prostatic‐tumor samples. Overall, 65% (13/20) of the cases analyzed showed molecular alterations, mainly rearrangements and deletions. The locus presenting the highest rate of abnormalities was D10S221, which maps to 10q23‐q24. Another region with frequent alterations was 10q21, at the D10S1091 locus. There was no statistical association between microsatellite abnormalities and Gleason grade or tumor stage in the prostate cancer cases studied. These results suggest that microsatellite alterations on the long arm of chromosome 10 are non‐random events occurring in prostate cancer and that they may play a role in the process of tumorigenesis in these neoplasms. © 1996 Wiley‐Liss, Inc.