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[Cancer Research 54, 6338-6339, December 15, 1994]
© 1994 American Association for Cancer Research

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Mutation Rate of the CDKN2 Gene in Malignant Gliomas1

Cristiana Giani and Gaetano Finocchiaro2

Istituto Nazionale Neurologico "C. Besta," Divisione di Biochimica e Genetica, via Celoria 11, 20133 Milan, Italy

The CDKN2 gene encodes p16, a protein controlling the cell cycle. CDKN2 is deleted in a relevant number of tumor cell lines, but results of the studies in primary tumors are contradictory. We have investigated by using quantitative polymerase chain reaction and single-strand conformation polymorphism analysis the structure of exon 2 of CDKN2 in 32 malignant gliomas. In 11 tumors the amount of amplified material was 21% of that of controls and in 8 tumors it was 42.3%, suggesting the presence of homozygous and hemizygous deletions of the CDKN2 gene, respectively. However, no abnormality could be detected by single-strand conformation polymorphism analysis. The data confirm in primary gliomas that homozygous deletions are a mechanism of CDKN2 inactivation and suggest that another gene in the vicinity could be targeted by mutations.

1 This work has been partially supported by a grant from the Associazione Italiana per la Ricerca sul Cancro [G. F.].

2 To whom requests for reprints should be addressed.

Received 8/18/94. Accepted 11/ 1/94.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1994 by the American Association for Cancer Research.