Expression profiling reveals coordinated dysregulation of autophagy-associated proteins in marginal zone lymphoma and therapeutic implications.
1/5 보강
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
16 patients with MZL compared with 16 reactive lymphoid hyperplasia (RLH) controls.
I · Intervention 중재 / 시술
추출되지 않음
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
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.
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 r
- p-value P<0.05
APA
Ruan J, Zhou X, et al. (2026). Expression profiling reveals coordinated dysregulation of autophagy-associated proteins in marginal zone lymphoma and therapeutic implications.. Oncology letters, 31(2), 68. https://doi.org/10.3892/ol.2025.15421
MLA
Ruan J, et al.. "Expression profiling reveals coordinated dysregulation of autophagy-associated proteins in marginal zone lymphoma and therapeutic implications.." Oncology letters, vol. 31, no. 2, 2026, pp. 68.
PMID
41415477
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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