A 50-year-old patient with a history of H. pylori gastritis develops a gastric low-grade B-cell lymphoma. Histology shows centrocyte-like cells infiltrating the mucosa. The pathogenesis involves antigen-driven proliferation where H. pylori-specific T-cells stimulate neoplastic B-cells. Which molecular event, when acquired, makes this lymphoma H. pylori-eradication therapy RESISTANT?

• A t(14;18)(q32;q21) involving BCL2
• B MYC rearrangement with IGH
• C Deletion of TP53 on chromosome 17
• D t(11;18)(q21;q21) producing API2-MALT1 fusion gene ✓

Explanation

MALT lymphoma of the stomach is H. pylori-driven and responds to antibiotic eradication in ~75% of early cases — the antigen-driven proliferation regresses when H. pylori is eliminated. However, the t(11;18)(q21;q21) API2-MALT1 fusion activates NF-κB constitutively, rendering the lymphoma antigen-independent and refractory to H. pylori eradication. This translocation is the most common in MALT lymphomas (~25% of gastric MALT). These cases require rituximab ± radiation therapy.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.