NONRANDOM LOSS OF CHROMOSOME-3 DURING TRANSITION OF HELICOBACTER-PYLORI-ASSOCIATED GASTRIC MALT TO B-CELL MALT LYMPHOMA REVEALED BY FLUORESCENCE IN-SITU HYBRIDIZATION

Acquired gastric mucosa-associated lymphoid tissue (MALT) accumulates as a result of long-standing Helicobacter pylori (H. pylori) infection and from this acquired MALT, low-grade B-cell MALT lymphoma may devel op. Carcinogenesis is a multistep, multifactorial process involving th e progressive accumulation of genetic changes. To determine whether nu merical chromosomal alterations are involved in the transition of H. p ylori-associated human gastric MALT to low-grade B-cell MALT lymphoma, frozen biopsy specimens prospectively obtained from H. pylori positiv e gastric MALT and gastric MALT lymphoma patients, as well as normal c ontrol patients (normal gastroscopy/gastric mucosal histology/H. pylor i negative), were analyzed by fluorescence in situ hybridization (FISH ). Fluorescent, directly labeled alpha-satellite DNA probes, specific for the centromeres of chromosomes 1, 3, 4, 11, 17 and Y were used in this study. The non-random loss of chromosome 3 was detected in two MA LT patients and in all five MALT lymphoma patients. Trisomy 17 was det ected in one MALT patient and one MALT lymphoma patient. Trisomy 1 was detected in a single MALT lymphoma patient as was trisomy 3. None of the MALT patients had trisomy 3 or trisomy 1. Monosomy 17 was noted in one MALT lymphoma patient. Clonal aneusomy was not observed in any pa tient for chromosomes Y, 4 or 11. These results suggest that the consi stent loss of chromosome 3 may be an important genetic alteration in t he transformation of H. pylori-associated gastric MALT into low-grade B-cell gastric MALT lymphoma. 1997 Published by Elsevier Science Irela nd Ltd.