Br J Haematol 2003 Apr;121(1):97-100
Medical Oncology/Haematology, Department of Clinical Research, Inselspital and University of Berne, CH-3010 Berne, Switzerland.
One fifth of B-cell chronic lymphocytic leukaemia (B-CLL) patients exhibit loss of heterozygosity (LOH) at 10q23.3, the site of the tumour suppressor PTEN. Microsatellite markers mapped complete LOH to 10q23.3 in 2/41 B-CLL (5%) and allelic imbalances in 6/41 (15%). No PTEN gene mutations were found. PTEN protein expression was not detected in 11 B-CLL (28%), and was reduced in eight patients (20%). LOH or allelic imbalances at 10q23.3 were fairly frequent in B-CLL, but did not encompass the PTEN gene. Nevertheless, PTEN protein may be absent in B-CLL with a normal PTEN genotype, suggesting a role of this phosphatase in the molecular pathology of B-CLL.