Answers are grounded in this paper and cite their sources.
Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is an antigen-driven malignancy in which Helicobacter pylori ( H. pylori ) eradication achieves remission in most localized cases, yet the genomic underpinnings of biological heterogeneity across H. pylori subgroups remain poorly defined. We performed targeted next-generation sequencing on formalin-fixed paraffin-embedded tumor tissue from 28 patients with stage IE gastric MALT lymphoma, classified as H. pylori -negative (HPN; n = 8) or H. pylori -positive (HPP; n = 20). Recurrently altered genes were grouped into three functional categories: epigenetic and transcriptional regulatory genes, NF-κB signaling-related genes, and immune-related genes. Overall mutational burden was low (median: 1 altered gene per case; range, 0–9), with PTEN , KMT2D , and TET2 as the most frequently mutated genes, distributed across both subgroups. Across the predefined functional categories, epigenetic/transcriptional regulatory alterations were more frequent in HPN cases (62.5% vs. 30.0%), with NCOR1 and ZFHX3 detected only in this group. NF-κB-related alterations were comparable between groups (12.5% vs. 15.0%). Immune-related alterations ( B2M , CD274 ) were observed only in HPP cases (0.0% vs. 20.0%). No differences reached statistical significance. Gastric MALT lymphoma harbors a shared low mutational burden across H. pylori subgroups, with modest differences in recurrent mutation profiles that did not reach statistical significance.
No takes yet. Share an insight, caveat, or question.
Lee et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: