MCL Literature Feed

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.

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.

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.

Preclinical data show WEE1 inhibition synergizes with bortezomib by inducing mitotic pyroptosis, a novel cell death mechanism, suggesting a potential strategy to overcome proteasome inhibitor resistance in MCL.

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.

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.

This review highlights BTK's non-catalytic scaffolding function as a novel mechanism of BTKi resistance, presenting a new therapeutic target beyond kinase inhibition for treating B-cell lymphomas like MCL.

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.

A computational virtual screen of over 2.4 million compounds identified novel covalent BTK inhibitors, providing a foundation for developing next-generation therapeutics for MCL.

The dual HCK/BTK inhibitor KIN-8194 preclinically overcomes primary and acquired BTKi resistance in MCL by targeting HCK-mediated growth and adhesion, offering a novel therapeutic strategy.

This preclinical study identifies a novel cyclin D1 degradation pathway via SUMOylation, showing its disruption causes an MCL-like phenotype and that arsenic trioxide can therapeutically enhance this process.

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 CDK9 inhibitor enitociclib overcomes resistance to both BTK inhibitors and CAR-T therapy, offering a potential new strategy for double-refractory mantle cell lymphoma.

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.

PRMT5 promotes MCL growth via MYC-driven lipid metabolism reprogramming, identifying it as a poor prognostic marker and a novel therapeutic target with preclinical inhibitor activity.

This systematic analysis of MAIT cells across hematological malignancies provides foundational insights into the MCL immune microenvironment, potentially identifying novel biomarkers or immunotherapy targets.

This preclinical study identifies PLK-1 gene methylation as a key driver of bendamustine resistance, which was reversible with demethylating agents, suggesting a potential new therapeutic strategy.

This preclinical study elucidates acalabrutinib's metabolic pathways, identifying reactive intermediates that may explain potential drug-drug interactions, toxicities, or off-target effects in patients with MCL.

This preclinical study identifies SOX11 as an endogenous inhibitor of SAMHD1, which sensitizes mantle cell lymphoma to cytarabine, suggesting SOX11 status as a predictive biomarker for chemotherapy efficacy.

This B-ALL study reveals MALT1 inhibitors downregulate MYC, providing a novel mechanism and strong rationale for testing this strategy in aggressive, MYC-driven mantle cell lymphoma.

An editor's note highlights a preclinical study where a combined epigenetic therapy shows superior efficacy against MCL cells, suggesting a novel therapeutic strategy for clinical development.

This preclinical study identifies DNMT3A-mediated metabolic reprogramming to oxidative phosphorylation as a novel ibrutinib resistance mechanism, which can be overcome by low-dose decitabine.

This preclinical study identifies that SOX11 upregulates the antioxidant PRDX2, promoting chemoresistance in aggressive MCL, and suggests PRDX2 as a novel therapeutic target to overcome drug resistance.

The CRM1 inhibitor KPT-330 induces protective autophagy in MCL cells; co-treatment with an autophagy inhibitor like chloroquine results in synergistic cell killing, suggesting a novel combination strategy.

Using computational screening and machine learning, this study identifies novel PIM2 inhibitors, presenting a potential new therapeutic target for future drug development in hematologic malignancies, including MCL.

Palbociclib plus venetoclax shows preclinical synergy in ibrutinib-refractory MCL by downregulating MCL1, offering a chemo-free option for patients without RB1 deletion.

This preclinical study of a bortezomib nanoparticle delivery system in glioblastoma cell lines is not relevant to mantle cell lymphoma.