Frequency of homozygous deletion at p16/CDKN2 in primary human tumours

Paul Cairns, Thomas J. Polascik, Yolanda Eby, Kaori Tokino, Joseph Califano, Adrian Merlo, Li Mao, John Herath, Robert Jenkins, William Westra, Joni L. Rutter, Alan Buckler, Edward Gabrielson, Mel Tockman, Kathleen R. Cho, Lora Hedrick, G. Steven Bova, William Isaacs, Wayne Koch, Donna SchwabDavid Sidransky

Research output: Contribution to journalArticlepeer-review

651 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)210-212
Number of pages3
JournalNature Genetics
Issue number2
StatePublished - Oct 1995

ASJC Scopus subject areas

  • Genetics


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