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Cancer Research 68, 8657, November 1, 2008. doi: 10.1158/0008-5472.CAN-08-2084
© 2008 American Association for Cancer Research
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Conspirators in a Capital Crime: Co-deletion of p18INK4c and p16INK4a/p14ARF/p15INK4b in Glioblastoma Multiforme

David A. Solomon1,2, Jung-Sik Kim2, Walter Jean3 and Todd Waldman2

1 Tumor Biology Training Program, 2 Department of Oncology, Lombardi Comprehensive Cancer Center, and 3 Department of Neurosurgery, Georgetown University School of Medicine, Washington, District of Columbia

Requests for reprints: Todd Waldman, Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, New Research Building E304, 3970 Reservoir Road Northwest, Washington, DC 20057. Phone: 202-687-1340; Fax: 202-687-7505; E-mail: waldmant{at}georgetown.edu.

Glioblastoma multiforme (GBM) is one of the most dreaded cancer diagnoses due to its poor prognosis and the limited treatment options. Homozygous deletion of the p16INK4a/p14ARF/p15INK4b locus is among the most common genetic alterations in GBM. Two recent studies have shown that deletion and mutation of another INK4 family member, p18INK4c, also drives the pathogenesis of GBM. This minireview will discuss the known roles for p18INK4c in the initiation and progression of cancer and suggest opportunities for future studies. [Cancer Res 2008;68(21):8657–60]




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D. A. Solomon, J.-S. Kim, H. W. Ressom, Z. Sibenaller, T. Ryken, W. Jean, D. Bigner, H. Yan, and T. Waldman
Sample Type Bias in the Analysis of Cancer Genomes
Cancer Res., July 15, 2009; 69(14): 5630 - 5633.
[Abstract] [Full Text] [PDF]


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 © 2008 by the American Association for Cancer Research.