FREQUENCY OF HOMOZYGOUS DELETION AT P16/CDKN2 IN PRIMARY HUMAN TUMORS

被引:638
作者
CAIRNS, P
POLASCIK, TJ
EBY, Y
TOKINO, K
CALIFANO, J
MERLO, A
MAO, L
HERATH, J
JENKINS, R
WESTRA, W
RUTTER, JL
BUCKLER, A
GABRIELSON, E
TOCKMAN, M
CHO, KR
HEDRICK, L
BOVA, GS
ISAACS, W
KOCH, W
SCHWAB, D
SIDRANSKY, D
机构
[1] JOHNS HOPKINS UNIV,SCH MED,DEPT OTOLARYNGOL HEAD & NECK SURG,DIV HEAD & NECK CANC RES,BALTIMORE,MD 21205
[2] JOHNS HOPKINS UNIV HOSP,DEPT UROL,BALTIMORE,MD 21287
[3] MAYO CLIN,ROCHESTER,MN 55905
[4] JOHNS HOPKINS UNIV HOSP,DEPT PATHOL,BALTIMORE,MD 21287
[5] HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02129
[6] JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT ENVIRONM HLTH SCI,DIV OCCUPAT HLTH,BALTIMORE,MD 21205
关键词
D O I
10.1038/ng1095-210
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Many tumour types have been reported to have deletion of 9p21 (rets 1-6). A candidate target suppressor gene, p16 (p16INK4a/MTS-1/CDKN2), was recently identified within the commonly deleted region in tumour cell lines7,8. An increasing and sometimes conflicting body of data has accumulated regarding the frequency of homozygous deletion and the importance of p16 in primary tumours. We tested 545 primary tumours by microsatellite analysis with existing and newly cloned markers around the p16 locus. We have now found that small homozygous deletions represent the predominant mechanism of inactivation at 9p21 in bladder tumours and are present in other tumour types, including breast and prostate cancer. Moreover, fine mapping of these deletions implicates a 170 kb minimal region that includes p16 and excludes p15. © 1995 Nature Publishing Group.
引用
收藏
页码:210 / 212
页数:3
相关论文
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