Absence of p16/MTS1 gene mutations in human prostate cancer

被引:29
作者
Chen, WW
Weghorst, CM
Sabourin, CLK
Wang, Y
Wang, D
Bostwick, DG
Stoner, GD
机构
[1] OHIO STATE UNIV, ARTHUR JAMES CANC HOSP, DIV ENVIRONM HLTH SCI, SCH PUBL HLTH, COLUMBUS, OH 43210 USA
[2] OHIO STATE UNIV, SCH PUBL HLTH, DEPT PATHOL, COLUMBUS, OH 43210 USA
[3] MED COLL OHIO, DEPT PATHOL, TOLEDO, OH 43699 USA
[4] MAYO CLIN & MAYO FDN, DEPT LAB MED & PATHOL, ROCHESTER, MN 55905 USA
关键词
D O I
10.1093/carcin/17.12.2603
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The tumor suppressor gene p16/MTS1, located on chromosome 9p21, is a cell cycle regulatory gene which is frequently altered in human cancers, The role of this gene in prostate cancer is unknown, To determine the frequency of deletions and point mutations of p16/MTS1 in human prostate cancer, we examined 18 cancer and matched benign and hyperplastic tissue specimens, Deletions of p16/MTS1 were detected by semi-quantitative multiplex polymerase chain reaction in which a portion of exon 2 of the p16/MTS1 gene and a control marker, the glyceraldehyde 3-phosphate dehydrogenase gene, were amplified simultaneously, 'Cold' single-stranded conformational polymorphism (SSCP) analysis was performed to examine exons 1 and 2 of the p16/MTS1 gene for point mutations, Our data indicate no evidence for intragenic homozygous deletion in the prostate tumors, One prostate tumor and matched benign tissue showed mobility shifts, Direct DNA sequencing of the SSCP positive samples showed a G --> A transition in codon 140 which would result in an amino acid change from alanine to threonine, Our results indicate that deletions and point mutations in the p16/MTS1 gene are rare and do not play a major role in human prostate carcinogenesis.
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收藏
页码:2603 / 2607
页数:5
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