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July 2002, Volume 16, Number 7, Pages 1229-1232
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Spotlight on Chronic Lymphocytic Leukemia
Chromosomal imbalances in familial chronic lymphocytic leukaemia: a comparative genomic hybridisation analysis
B Summersgill1, P Thornton2, S Atkinson2, E Matutes2, J Shipley1, D Catovsky2, R S Houlston3 and M R Yuille2

1UK Co-ordinating Centre for the Study of Familial Chronic Lymphocytic Leukaemia, Section of Molecular Carcinogenesis, Institute of Cancer Research, Sutton, UK

2Section of Academic Haematology, Institute of Cancer Research, Sutton, UK

3Section of Cancer Genetics, Institute of Cancer Research, Sutton, UK

Correspondence to: R S Houlston, UK Co-ordinating Centre for the Study of Familial Chronic Lymphocytic Leukaemia, Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey, SM2 5NG, UK

Abstract

A subset of B cell chronic lymphocytic leukaemia (CLL) is familial. Lack of large families makes it attractive to exploit methods in addition to genetic linkage analysis for the identification of a susceptibility locus. One strategy that can localise regions of the genome that may harbour tumour suppressor genes is to identify regions of chromosomal imbalance using comparative genomic hybridisation (CGH) analysis. We examined 24 familial CLL cases by CGH analysis. Losses that are documented as arising frequently in sporadic CLL were observed at a comparable frequency in familial CLL. However, gains and losses in two regions of the X chromosome - Xp11.2-p21 and Xq21-qter - appear more common in familial CLL than in sporadic CLL. This suggests these regions may harbour a susceptibility locus for CLL. There is also some evidence that chromosome regions 2p12-p14 and 4q11-q21 may harbour predisposition genes.

Leukemia (2002) 16, 1229-1232. doi:10.1038/sj.leu.2402321

Keywords

familial chronic lymphocytic leukaemia; comparative genomic hybridisation

Received 4 April 2001; accepted 14 August 2001
July 2002, Volume 16, Number 7, Pages 1229-1232
Table of contents    Previous  Abstract  Next   Full text  PDF
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