ALTERATIONS OF MULTIPLE TUMOR-SUPPRESSOR GENES (P53 (17P13), P16(INK4) (9P21), AND DBM (13Q14)) IN B-CELL CHRONIC LYMPHOCYTIC-LEUKEMIA

Citation
Ew. Newcomb et al., ALTERATIONS OF MULTIPLE TUMOR-SUPPRESSOR GENES (P53 (17P13), P16(INK4) (9P21), AND DBM (13Q14)) IN B-CELL CHRONIC LYMPHOCYTIC-LEUKEMIA, Molecular carcinogenesis, 14(3), 1995, pp. 141-146
Citations number
25
Categorie Soggetti
Oncology,Biology
Journal title
ISSN journal
08991987
Volume
14
Issue
3
Year of publication
1995
Pages
141 - 146
Database
ISI
SICI code
0899-1987(1995)14:3<141:AOMTG(>2.0.ZU;2-F
Abstract
B-cell chronic lymphocytic leukemia (B-CLL) samples were screened for alterations in multiple tumor suppressor genes (p53 (17p13), p16(INK4) (9p21), and disrupted in B-cell malignancy (DBM) (13q14)) by using po lymerase chain reaction-based assays. Eleven percent (11 of 96) of the B-CLL cases analyzed in this study and a previous study had mutations in the p53 gene. In contrast, analysis of the p16 gene showed none of 80 B-CLL cases had mutations and five cases (6%) had homozygous delet ions. Deletions of 13q14 (DBM) occurred in 18% (17 of 96) of patients surveyed. Thus, 28 of 96 cases showed an alteration in one or more of the three tumor suppressor loci examined. However, cases with p53 muta tions rarely showed simultaneous loss of DBM. Our results suggest that inactivation of the tumor suppressor genes p53 and DBM may be mutuall y exclusive, thus providing alternate pathways for tumor development i n B-CLL patients. (C) 1995 Wiley-Liss, Inc.