MCL Literature Feed
267 papers on mantle cell lymphoma from PubMed. Updated daily.
Genomic analysis of MCL treated sequentially with BTKi and venetoclax identifies specific copy number alterations (e.g., 9p21.3 deletion) as novel biomarkers for primary and acquired resistance.
This Danish population-based study shows real-world ibrutinib outcomes (PFS 5.8 months) are inferior to clinical trials, with high-risk features and toxicity limiting efficacy, underscoring significant unmet needs.
The Endothelial Activation and Stress Index (EASIX) is a novel, independent prognostic biomarker in MCL, with high scores at diagnosis correlating with significantly shorter OS and PFS.
The SOX11:SMARCA4 complex is a key oncogenic driver in MCL, and targeting SMARCA4 with a PROTAC degrader shows preclinical activity, offering a novel therapeutic strategy for relapsed patients.
Preclinical data show CBX5 loss drives PI3Kδ inhibitor resistance in MCL, which is reversed by propolis-derived CAPE via induction of CBX5-mediated ferroptosis, a novel therapeutic strategy.
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A novel para-phenylenediamine-based ROR1 inhibitor demonstrates potent preclinical activity against an MCL cell line (JeKo-1), establishing a new chemical scaffold for targeting this promising therapeutic pathway.
This review outlines key clinical strategies for patient selection, toxicity management, and overcoming resistance to maximize the efficacy and safety of CAR-T therapy in relapsed/refractory MCL.
M2-polarized macrophages drive ibrutinib resistance via the CXCL5/CXCR2 axis; a CXCR2 inhibitor re-sensitizes MCL cells, suggesting a novel combination therapy to overcome BTKi resistance.
A case of benign BCL-6-positive cutaneous mantle zone hyperplasia mimics cutaneous lymphoma, highlighting that cyclin-D1 staining remains essential to differentiate this benign entity from cutaneous mantle cell lymphoma.
IGH/IGK gene rearrangement analysis improves diagnostic accuracy for B-cell lymphomas, with co-occurring IGH and IGK rearrangements being a characteristic feature of mantle cell lymphoma.
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The m6A writer METTL3 promotes MCL progression by degrading Ambra1 mRNA via the reader YTHDF2, identifying a novel, potentially targetable therapeutic axis for mantle cell lymphoma.
This case report of a rectal plasmacytoma misdiagnosed as MCL highlights a critical diagnostic pitfall, emphasizing the need for thorough pathological evaluation to prevent incorrect lymphoma-directed therapy.
New prognostic scores, AMOS and AMES, were developed for Indian MCL patients, showing better predictive accuracy than MIPI using simple clinical factors for improved risk stratification.
This study identifies predictors of outcome for covalent BTKi therapy in relapsed/refractory TP53-mutant MCL, helping to risk-stratify patients and guide subsequent treatment decisions.
The MCL35 gene expression assay identifies high-risk older patients who do not benefit from adding ibrutinib to bendamustine-rituximab, mandating alternative frontline strategies for this molecularly-defined subgroup.
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A targeted NGS panel characterized the mutational landscape of Korean lymphomas, including MCL, demonstrating its utility for identifying clinically relevant mutations like TP53 in diverse subtypes.
A rare composite MCL/LPL case reveals a cryptic IGK::CCND1 fusion driving the MCL, highlighting the diagnostic utility of molecular testing for atypical CCND1 rearrangements.
This review summarizes current MCL risk stratification (MIPI, TP53), highlights emerging genomic biomarkers, and emphasizes MRD monitoring as a key dynamic tool for personalizing therapy, especially for high-risk patients.
This case report describes the rare anaplastic pleomorphic variant of MCL, highlighting its aggressive features and the critical role of pathology in diagnosing high-risk disease subtypes.
This preclinical study identifies CEACAM1 as a novel activator of B-cell receptor signaling by recruiting SYK, revealing a new potential therapeutic target and mechanism of resistance to BCR inhibitors.
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This myeloma review outlines strategies to overcome proteasome inhibitor resistance by targeting other proteostasis pathways, providing a rationale for exploring similar combinations in relapsed/refractory MCL.
The novel circular RNA-based biomarker, circSCORE, demonstrates prognostic value in relapsed/refractory MCL, offering a new tool for risk stratification in this high-risk patient population.
A novel single-cell method integrating biophysical properties with transcriptomics identifies distinct MCL subpopulations, suggesting cell mechanics could be a new biomarker for tumor heterogeneity and therapeutic resistance.
A rare B-ALL subtype with a MEF2D::BCL9 fusion can mimic blastoid MCL by co-expressing CD5 and SOX11, highlighting a critical diagnostic pitfall requiring molecular confirmation.
Overexpression of IL-16 drives BTKi resistance via the CD9/NF-κB/AKT axis in MCL models, presenting a novel therapeutic target to overcome treatment failure and restore drug sensitivity.
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In frontline MCL, pre-treatment ctDNA levels and TP53 mutations predict poor survival, while post-treatment ctDNA clearance identifies patients with favorable outcomes, establishing its clinical utility for prognosis.
This review provides a practical guide for differentiating aggressive B-cell lymphomas, including mantle cell lymphoma, emphasizing the integration of morphology, immunohistochemistry, and molecular testing for accurate diagnosis and classification.
High p62 expression predicts poor survival in MCL by upregulating CCND1 transcription via Nrf2, identifying p62 as a novel prognostic biomarker and potential non-BTK/BCL2 therapeutic target.
A novel single-cell genomic research model tracks MCL clonal evolution, providing a high-resolution tool to dissect mechanisms of therapeutic resistance and identify potential new targets.
NGS-detected TP53 mutations are a major clinical risk factor, enabling precise patient stratification to guide initial therapy selection and identify candidates for novel agents.