Evidence map›Paper›PMID 42293725›Full record

ReviewSaudi medical journal2026

Molecular Mechanisms of Diffuse Large B-Cell Lymphoma and the Complexities of Tumor Development.

Wael I Alzahrani

Abstract readReview
In one paragraph

Review in Saudi medical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Wael I AlzahraniDepartment of Clinical Laboratory Science, College of Applied Medical Sciences-Qurayyat, Jouf University, Al Jouf, Saudi Arabia.ORCID 0009-0008-5999-4990

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diffuse large B-cell lymphoma (DLBCL), the most prevalent aggressive non-Hodgkin lymphoma, exhibits substantial molecular heterogeneity and arises from germinal center or post-germinal center B cells through recurrent genetic and epigenetic dysregulation of critical signaling pathways. Aberrations involving BCL6, MYC, MYD88, and components of B cell receptor and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling play central roles in lymphomagenesis, treatment resistance, and clinical outcomes. Gene expression profiling has defined major molecular subgroups in DLBCL, including germinal center B cell-like and activated B cell-like tumors, that show distinct pathogenesis and prognosis. High-risk entities, such as double- and triple-hit lymphomas, remain therapeutically challenging despite advances in immunochemotherapy. Recent progress in molecular diagnostics and targeted therapies, including immune checkpoint inhibition, Bruton tyrosine kinase inhibitors, B-cell lymphoma 2 (BCL2) antagonists, and Chimeric antigen receptor-T cells, has expanded precision-based treatment strategies. This review summarizes advances in understanding the molecular mechanisms of DLBCL and emphasizes emerging therapeutic approaches informed by genomic and microenvironmental discoveries.

Indexed as

Lymphoma, Large B-Cell, DiffuseEpigenesis, GeneticHumansMyeloid Differentiation Factor 88Proto-Oncogene Proteins c-bcl-6Signal TransductionBCL6 protein, humanMyeloid Differentiation Factor 88Proto-Oncogene Proteins c-bcl-6Diffuse large B-cell lymphomaEpigenetic regulationGenetic alterationsMolecular pathogenesisTargeted therapy

Identifiers

PMID42293725
PMCPMC13264149

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.