Annals of Surgical Oncology Sign the Guestbook
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Calvano, J. E.
Right arrow Articles by Van Zee, K. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Calvano, J. E.
Right arrow Articles by Van Zee, K. J.

Annals of Surgical Oncology, Vol 4, Issue 5 416-420, Copyright © 1997 by Society of Surgical Oncology

ARTICLES

Absence of p16 gene (CDKN2) deletions in microdissected primary breast carcinoma specimens

J. E. Calvano, E. B. Rush, L. K. Tan, P. P. Rosen, P. I. Borgen and K. J. Van Zee
Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.

BACKGROUND: The p16 gene (CDKN2), a tumor suppressor gene located on chromosome 9p21, has been demonstrated to be mutated or deleted with high frequency in a variety of tumor cell lines, including breast. While previous studies have not demonstrated CDKN2 mutations in primary breast carcinomas, it is possible that gene deletion in neoplastic DNA was marked by the presence of contaminating normal stromal DNA in breast carcinoma specimens. METHODS: We investigated the incidence of homozygous deletion of CDKN2 by analyzing 20 microdissected pure populations of primary breast carcinoma cells. Using polymerase chain reaction (PCR) techniques, the entire coding region and intervening introns of CDKN2 were amplified. The PCR products were resolved by agarose gel electrophoresis and single-strand conformation polymorphism (SSCP) analysis. RESULTS: We detected no deletions or mutations of the p16 gene. CONCLUSIONS: CDKN2 is not deleted with high frequency in primary breast carcinomas, and the p16 gene does not play a role in breast carcinogenesis via this mechanism.




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1997 by the Society of Surgical Oncology.