|
|
||||||||
From INSERM U495 (Drs. He, Hoang-Xuan, Delattre, and Sanson, Y. Marie and P. Leuraud), the Fédération de Neurologie Mazarin (Drs. Hoang-Xuan, Delattre, and Sanson), and the Laboratory of Neuropathology "R. Escourolle" (Dr. Mokhtari), Hôpital de la Salpêtrière; and the Laboratoire dHistologie-Embryologie-Cytogénétique (Dr. Kujas), Hôpital de la Pitié, Paris, France.
Address correspondence and reprint requests to Dr. Marc Sanson, Clinique Neurologique, Hôpital de la Salpêtrière, 47, Bd de lHôpital, 75013 Paris, France; e-mail: sanson{at}ccr.jussieu.fr
Article abstractP18INK4C is a good candidate to be the tumor suppressor gene involved in oligodendrogliomas on 1p32. Loss of heterozygosity on 1p, mutation(s), homozygous deletion(s), and expression of p18 in 30 oligodendroglial tumors were investigated. Loss of heterozygosity on 1p was found in 15 tumors. A p18 mutation was found at an recurrence of an anaplastic oligodendroglioma, but not in the primary, low-grade tumor. No homozygous deletions were found and p18 was expressed in all cases. These results show that p18 alteration is involved in tumor progression in a subset of oligodendrogliomas.
This article has been cited by other articles:
![]() |
D. A. Solomon, J.-S. Kim, W. Jean, and T. Waldman Conspirators in a Capital Crime: Co-deletion of p18INK4c and p16INK4a/p14ARF/p15INK4b in Glioblastoma Multiforme Cancer Res., November 1, 2008; 68(21): 8657 - 8660. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |