MCL Literature Feed

In preclinical models, PTEN loss activates the PI3K/AKT pathway, reducing BCR signaling dependence and conferring resistance to ibrutinib, venetoclax, and PI3K inhibitors, identifying a key resistance mechanism.

The VALERIA trial demonstrates that an MRD-guided, fixed-duration venetoclax-lenalidomide-rituximab regimen is a highly effective, personalized, chemotherapy-free strategy for patients with relapsed/refractory MCL.

A new LSM gene expression index identifies MCL patients with poor survival by impacting cell division and RNA splicing, proposing LSM proteins as novel prognostic biomarkers and therapeutic targets.

Longitudinal single-cell analysis of refractory MCL reveals co-evolving tumor heterogeneity and immune evasion, providing a roadmap for overcoming treatment resistance and identifying new therapeutic targets.

p53 immunohistochemistry is a practical biomarker for identifying high-risk MCL patients, helping to stratify prognosis and guide selection of more intensive or novel therapies.

This preclinical study identifies a novel CERS6-AS1/FGFR1 axis driving stromal-supported MCL proliferation and stemness, suggesting that co-targeting nucleolin and FGFR1 could overcome microenvironment-mediated resistance.

A validated LC-MS/MS assay simultaneously measures plasma ibrutinib, its active metabolite, and zanubrutinib, enabling therapeutic drug monitoring to potentially optimize dosing and manage toxicity in MCL.

Bioinformatic analysis of public datasets identified key genes and pathways driving bortezomib resistance in MCL, providing potential biomarkers and therapeutic targets for the relapsed/refractory setting.

SOX11-negative, CCND1-rearranged large B-cell lymphomas can arise via a DLBCL-like mechanism (aberrant CSR/SHM), distinguishing them genetically from classic MCL and highlighting a potential diagnostic challenge.

This preclinical study identifies the CERS6-AS1/FGFR1 axis as a synthetic vulnerability, offering a novel therapeutic strategy to disrupt stromal cell-mediated proliferation and overcome resistance in MCL.

Hyperleukocytosis from undiagnosed leukemic MCL interfered with an HbA1c test, revealing a novel diagnostic pathway where a common diabetes lab test can signal an underlying hematologic malignancy.

Preclinically, dual inhibition of Hedgehog/GLI1 and Wnt/β-catenin pathways synergistically suppresses MCL cells and enhances sensitivity to chemotherapy and ibrutinib, suggesting a new approach to overcome resistance.

Spatial multiomics reveals CD163+ macrophages activate the MAPK prosurvival pathway in MCL cells, identifying MAPK inhibitors as a potential therapy for patients with high macrophage infiltration.

A survey of US and European hematologists reveals significant knowledge gaps in MCL guidelines, molecular testing, and toxicity management, highlighting a need for improved continuing medical education.

Preclinical models show the PI3K inhibitor idelalisib synergizes with the CDK4/6 inhibitor palbociclib, providing a rationale for a novel combination therapy in relapsed/refractory MCL.

Preclinical data shows the novel CTPS1 inhibitor STP-B has single-agent activity in high-risk MCL (blastoid, TP53-mutated) and synergizes with venetoclax by downregulating MCL1, offering a new combination strategy.

A high monocyte-to-platelet ratio (MPR ≥ 3) at diagnosis is a novel, independent prognostic biomarker for inferior progression-free survival in transplant-ineligible mantle cell lymphoma patients.

This study identifies a rare CD5/SOX11 double-negative pleomorphic MCL, showing CCND1 rearrangement is the key feature to differentiate it from cyclin D1-positive DLBCL, ensuring correct diagnosis.

This study analyzes molecular responses in exceptional responders to the BTKi tirabrutinib, aiming to identify biomarkers for deep, durable remissions in relapsed/refractory mantle cell lymphoma.

This review explains MCL's clinical heterogeneity through distinct molecular subtypes and genomic alterations like TP53, which serve as key prognostic biomarkers and guide development of novel therapies.

This study of Burkitt Lymphoma reveals the key MCL oncogene SOX11 has a context-dependent function, with a transcriptional program and downstream effects differing from its established role in MCL.

This paper identifies a subset of MCL with IRTA1-positive reactive marginal zone expansion, highlighting a potential diagnostic pitfall for pathologists distinguishing it from marginal zone lymphoma.

Preclinical data show combining a BCL-XL inhibitor with venetoclax overcomes resistance in MCL models, even in BIM-deficient cells, suggesting a new strategy for venetoclax-refractory patients.

BTK inhibition suppresses key metabolic pathways, allowing non-invasive imaging of metabolites like lactate and alanine as early, sensitive biomarkers of therapeutic response in MCL patients.

A computational, network-based analysis of MCL transcriptomic data identified novel progression pathways, highlighting VEGFA and SPARC as potential drug targets and providing a framework for drug repurposing.

This large Chinese retrospective study of blastoid/pleomorphic MCL links progression of disease within 12 months (POD12) to a distinct mutation profile (TP53, SMARCA4) and poor prognosis.

This review synthesizes current knowledge on MCL genetic markers, advocating for a personalized medicine approach that integrates molecular profiles like TP53 to improve risk stratification and guide therapy.

In a large real-world cohort, mantle cell lymphoma patients exhibited higher CAR19 expansion than other lymphomas, which directly correlated with increased toxicity and significantly higher steroid requirements.

Profiling T-cell differentiation stages in MCL reveals novel immunotherapeutic targets in specific patient subsets, suggesting a biomarker-driven approach for future immune-based treatments.

The SOX11/PRDX2 axis is identified as a key regulator of chemoresistance in aggressive MCL by controlling redox homeostasis, offering a potential new therapeutic target.