Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (120)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Ueki, K.
Right arrow Articles by Louis, D. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ueki, K.
Right arrow Articles by Louis, D. N.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1994 Oxford University Press

OTHER

MTS1/CDKN2 gene mutations are rare in primary human astrocytomas with allelic loss of chromosome 9p

Keisuke Ueki1, Mari-Paz Rubio1, Vijaya Ramesh2, Katia M. Correa1, Joni L. Rutter2, Andreas von Deimling4, Alan J. Buckler2, James F. Gusella2 and David N. Louis1,3,*

1Molecular Neuro-Oncology Laboratory, Neurosurgical Service, Massachusetts General Hospital and Harvard Medical School Boston, MA 02129, USA 2Molecular Neurogenetics Unit Massachusetts General Hospital and Harvard Medical School Boston, MA 02129, USA 3Department of Pathology (Neuropathology), Massachusetts General Hospital and Harvard Medical School Boston, MA 02129, USA 4Institute for Neuropathology, University Hospital Bonn, Germany

*To whom correspondence should be addressed at: Molecular Neuro-Oncology Laboratory, CNY6, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129, USA

Received June 14, 1994; Revised July 19, 1994; Accepted July 19, 1994

Human astrocytomas frequently have allelic losses of chromosome 9p, suggesting the presence of a 9p astrocytoma tumor suppressor gene. The MTS1 (or CDKN2) gene on chromosome 9p encodes a cell-cycle regulator and is deleted in approximately 80% of astrocytoma cell lines. To determine whether MTS1 is the tumor suppressor gene involved in human astrocytoma formation in vivo, we have analyzed chromosome 9p allelic loss and the MTS1 gene in 30 primary astrocytomas. Deletion mapping demonstrated 15 cases with allelic loss of chromosome 9p, with all losses either flanking or involving the MTS1 gene. Direct analysis of the MTS1 gene, however, revealed only a single missense mutation in a high-grade tumor that had lost the second allele. The low frequency of MTS1 mutations in primary astrocytomas with allelic 9p loss suggests that MTS1 may be more important for in vitro than in vivo astrocytoma growth, and that another 9p tumor suppressor gene may be involved in astrocytoma formation in vivo. Analysis of the MTS1 gene also demonstrated two intragenic polymorphisms, one in exon 2 and one in the 3' untranslated region, that can be used to assay allelic loss directly at MTS1.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cancer Res.Home page
D. A. Solomon, J.-S. Kim, J. C. Cronin, Z. Sibenaller, T. Ryken, S. A. Rosenberg, H. Ressom, W. Jean, D. Bigner, H. Yan, et al.
Mutational Inactivation of PTPRD in Glioblastoma Multiforme and Malignant Melanoma
Cancer Res., December 15, 2008; 68(24): 10300 - 10306.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Epidemiol. Biomarkers Prev.Home page
Y. Zheng, H. Shen, E. M. Sturgis, L.-E Wang, S. Shete, M. R. Spitz, and Q. Wei
Reply
Cancer Epidemiol. Biomarkers Prev., January 1, 2003; 12(1): 72 - 72.
[Full Text] [PDF]

Home page
 Clin. Cancer Res.Home page
K. Ueki, R. Nishikawa, Y. Nakazato, T. Hirose, J. Hirato, N. Funada, T. Fujimaki, S. Hojo, O. Kubo, T. Ide, et al.
Correlation of Histology and Molecular Genetic Analysis of 1p, 19q, 10q, TP53, EGFR, CDK4, and CDKN2A in 91 Astrocytic and Oligodendroglial Tumors
Clin. Cancer Res., January 1, 2002; 8(1): 196 - 201.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
H. Sasaki, M. C. Zlatescu, R. A. Betensky, Y. Ino, J. G. Cairncross, and D. N. Louis
PTEN Is a Target of Chromosome 10q Loss in Anaplastic Oligodendrogliomas and PTEN Alterations Are Associated with Poor Prognosis
Am. J. Pathol., July 1, 2001; 159(1): 359 - 367.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
P. Schraml, K. Struckmann, R. Bednar, W. Fu, T. Gasser, K. Wilber, J. Kononen, G. Sauter, M. J. Mihatsch, and H. Moch
CDKN2A Mutation Analysis, Protein Expression, and Deletion Mapping of Chromosome 9p in Conventional Clear-Cell Renal Carcinomas : Evidence for a Second Tumor Suppressor Gene Proximal to CDKN2A
Am. J. Pathol., February 1, 2001; 158(2): 593 - 601.
[Abstract] [Full Text] [PDF]

Home page
 Neuro Oncol DukeHome page
R. N. Wiltshire, B.K. A. Rasheed, H. S. Friedman, A. H. Friedman, and S. H. Bigner
Comparative genetic patterns of glioblastoma multiforme: Potential diagnostic tool for tumor classification
Neuro-oncol, July 1, 2000; 2(3): 164 - 173.
[Abstract] [PDF]

Home page
 Mol. Cell. Biol.Home page
M. A. Dickson, W. C. Hahn, Y. Ino, V. Ronfard, J. Y. Wu, R. A. Weinberg, D. N. Louis, F. P. Li, and J. G. Rheinwald
Human Keratinocytes That Express hTERT and Also Bypass a p16INK4a-Enforced Mechanism That Limits Life Span Become Immortal yet Retain Normal Growth and Differentiation Characteristics
Mol. Cell. Biol., February 15, 2000; 20(4): 1436 - 1447.
[Abstract] [Full Text]

Home page
 Am. J. Pathol.Home page
G. P. Nielsen, A. O. Stemmer-Rachamimov, Y. Ino, M. B. Moller, A. E. Rosenberg, and D. N. Louis
Malignant Transformation of Neurofibromas in Neurofibromatosis 1 Is Associated with CDKN2A/p16 Inactivation
Am. J. Pathol., December 1, 1999; 155(6): 1879 - 1884.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
N. Kawahara, H. Kume, K. Ueki, K. Mishima, T. Sasaki, and T. Kirino
VHL gene inactivation in an endolymphatic sac tumor associated with von Hippel- Lindau disease
Neurology, July 1, 1999; 53(1): 208 - 208.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.