Restricted chromosome breakpoint sites on 11q22-q23.1 and 11q25 in varioushematological malignancies without MLL/ALL-1 gene rearrangement

Citation
K. Tanaka et al., Restricted chromosome breakpoint sites on 11q22-q23.1 and 11q25 in varioushematological malignancies without MLL/ALL-1 gene rearrangement, CANC GENET, 124(1), 2001, pp. 27-35
Citations number
35
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
CANCER GENETICS AND CYTOGENETICS
ISSN journal
01654608 → ACNP
Volume
124
Issue
1
Year of publication
2001
Pages
27 - 35
Database
ISI
SICI code
0165-4608(20010101)124:1<27:RCBSO1>2.0.ZU;2-4
Abstract
We analyzed 32 patients with various hematological malignancies including a cute myelocytic leukemia and non-Hodgkin lymphoma with a breakpoint at 11q2 2-q25 of chromosome 11, but who did not have rearrangements of the MLL/ALL- 1 gene. The breakpoint in each patient was identified by fluorescence in si tu hybridization using 21 cosmid probes and 2 YAC probes. Breakpoints for e ach "rearrangement" involving translocations such as t(1;11), t(2;11), inv( 11), t(11;15), and t(10;11) found in 5 of the 11 patients had breakpoints i n a small region from Cc111-430 to Cc111-526 at 11q22-q23.1. Furthermore, b reakpoints for chromosome deletions at 11q21-q23 in 10 patients were locate d in the same region as that of translocations. A commonly deleted region a mong 8 patients was identified from Cc111-526 to Cc111-555 at 11q23.1. Fluo rescence in situ hybridization analysis revealed that breakpoints for addit ive chromosome [add(11)] aberrations, which had additional material of unkn own origin at 11q23 to 11925 in 11 patients, were not located at 11q23 but rather at the more telomeric site of Cc111-503 to VIJ(2)2072 at 11q25. Thes e results indicated that the patients had several restricted breakpoint sit es, which means that these chromosomal regions have recurrent oncogenes and tumor suppressor genes for pathogenesis for leukemia and lymphoma. (C) 200 1 Elsevier Science Inc. All rights reserved.