Analysis of-the P53, RB/D13S25, and P16 tumor suppressor genes in marginalzone B-cell lymphoma: An interphase fluorescence in situ hybridization study

The genetic mechanisms underlying the genesis, disease progression, and hig h-grade transformation of marginal zone B-cell lymphoma (MZBCL) are poorly understood. We analyzed 33 cases of histologically and immunophenotypically well-characterized MZBCL (12 extranodal, ii nodal, and 10 splenic MZBCL; 2 7 at primary diagnosis and six during the course of disease) by dual-color interphase fluorescence in situ hybridization (FISH) for deletions of tumor suppressor genes. We investigated loci known to play a role in the genesis or disease progression of other subtypes of lymphoid malignancies, namely the P53 gene (17p13), the retinoblastoma gene (RE, 13q14), the D13S25 locus (13q14), and the P16(INK4A) gene (9p21). Heterozygous deletions of P53 wer e detected in three out of the 33 cases, including two splenic and one extr anodal MZBCL. One of these patients was analyzed at primary diagnosis and t wo during the course of disease. Heterozygous deletions of the RE gene (nod al MZBCL) and D13825 (splenic MZBCL) were found in one case each. P16 delet ions were not detected in any of our cases. We conclude that deletions of t he analyzed tumor suppressor genes are relatively rare in MZBCL, which cont rasts with the findings in some other subtypes of NHL. (C) 2000 Elsevier Sc ience Inc. All rights reserved.