[Some genomic aberrations in B-cell chronic lymphocytic leukemia and their clinical relevance. Part II. Trisomy 12 in B-cell chronic lymphocytic leukemia detected by fluorescence in situ hybridization].

Among 75 untreated patients with typical (CD19+, CD5/CD19+, CD23/CD19+) B-cell chronic lymphocytic leukemia (B-CLL) cytogenetic aberrations of peripheral blood cells were evaluated, using fluorescence in situ hybridization techniques. Two cytogenetic aberrations were evaluated: trisomy 12 and TP53 deletion. The clonality was determined when > or = 10% of the cells had of trisomy 12 or deletion TP53 gene. Trisomy 12 in 7 patients was detected, while trisomy 12 and TP53 deletion simultaneously in 6 patients were present. If the first group will be linked to the second one then 13 patients among 75 (17%) will have trisomy 12. In group of patients with trisomy 12 and TP53 deletion percentage of cells with trisomy 12 was almost two time more compare to patients with trisomy 12 as a single aberration. It is possible, that TP53 deletion ("the guardian of the genome") facilitates proliferation clones with others genomic aberrations. In two patients with trisomy 12 control cytogenetic study was performed. Increase of percentage cells with trisomy 12 for 8% and 30% respectively was detected. However, proliferation of cells with TP53 deletion was observed too. Clinical course of B-CLL in group of patient with trisomy 12, trisomy 12 and TP53 deletion simultaneously is more aggressive compared to the course of disease of patients with no cytogenetic aberrations (patients of Group I from Part I of paper). Frequency of IGHV gain mutation occurrence was not analyzed in both groups of patients. But trisomy 12 together with unmutated IGHV gene is found by some authors. The absence IGHV gene mutation is independent unfavourable prognostic factor.