ArticleOncology letters2026
Expression profiling reveals coordinated dysregulation of autophagy-associated proteins in marginal zone lymphoma and therapeutic implications.
Article in Oncology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The role of endoplasmic reticulum stress-mediated autophagy in cadmium-induced liver injury in rats.Frontiers in veterinary science · 2026Article
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4 authors.
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Abstract
Dysregulated autophagy and its therapeutic targeting have emerged as focal points in oncology research; however, specific studies investigating autophagy in marginal zone lymphoma (MZL) pathogenesis remain limited. The present study comprehensively characterized the expression profiles of key autophagy-related proteins in MZL, providing novel mechanistic insights and an experimental rationale for therapeutic intervention. Immunohistochemical analysis assessed the expression of Beclin-1, light chain (LC)3, sequestosome (SQSTM)1/p62 and Bcl-2 in formalin-fixed paraffin-embedded tissues from 16 patients with MZL compared with 16 reactive lymphoid hyperplasia (RLH) controls. MZL specimens exhibited significant autophagy pathway dysregulation, characterized by ~35-40% decreased expression of Beclin-1 and LC3 and 30-45% increased expression of SQSTM1/p62 and Bcl-2 compared with RLH tissues (P<0.05 for all proteins analyzed). The present findings delineate a distinct profile of autophagy dysfunction in MZL, highlighting aberrant Beclin-1, LC3, SQSTM1/p62 and Bcl-2 expression as potential disease biomarkers and therapeutic targets. This study provides a critical basis for elucidating the molecular mechanisms underlying MZL pathogenesis and underscores the therapeutic potential of modulating autophagy-related pathways.
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