MCL Literature Feed

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.

Pre-clinical CD20 CAR-T cells armed with H. pylori protein (NAP) kill rituximab-relapsed MCL cells and induce a bystander immune effect, potentially overcoming antigen-loss resistance.

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.

This review outlines emerging treatment strategies for relapsed/refractory MCL patients who progress after CAR-T therapy, addressing a significant and growing unmet clinical need in this setting.

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.

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 MZL case identifies BTK C481S and PLCG2 D334H co-mutations driving zanubrutinib resistance, a mechanism highly relevant to BTKi failure and subsequent treatment strategies in relapsed MCL.

M2-like macrophages secrete IL-1 receptor antagonist (IL-1ra), impairing CAR-T19 function in MCL, suggesting targeting the IL-1 pathway could overcome this novel resistance mechanism.

The novel metabolism-targeting agent KAT/3BP demonstrates preclinical activity in aggressive B-cell lymphomas, introducing a new therapeutic class with potential future applications for treating MCL.

In Chinese patients with relapsed/refractory MCL previously treated with a covalent BTKi, the non-covalent BTKi pirtobrutinib achieved a 62.9% overall response rate, confirming its global efficacy.

This paper likely characterizes the clinical features, treatment patterns, and poor outcomes of isolated central nervous system relapse in MCL, highlighting a major unmet clinical need.

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.

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.

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.

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.

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.

This review synthesizes mechanisms of BTKi resistance and highlights next-generation strategies like noncovalent BTKi and PROTACs to overcome this critical challenge in relapsed/refractory MCL.

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.

Optical genome mapping reveals diverse cryptic CCND1/2 rearrangements in ~10% of MCLs lacking the classic t(11;14), improving diagnosis and identifying high genomic complexity associated with poor outcomes.

The novel TBL1X inhibitor tegavivint induces DNA damage and synergizes with PARP inhibitors in preclinical MCL models, establishing TBL1X as a new therapeutic target for genomic instability.

This case report describes a rare paraneoplastic syndrome in MCL causing severe thrombocytopenia via both bone marrow failure and immune destruction, which responded to lymphoma-directed chemoimmunotherapy but not standard ITP treatment.

Genomic analysis of a single MCL patient identified specific mechanisms of resistance to PD-L1 blockade, providing crucial insights into why checkpoint inhibitors are often ineffective in this lymphoma.

This review details the evolution of BTK inhibitors from discovery to clinical use in MCL, covering first-generation agents like ibrutinib and newer agents designed to overcome resistance.

This review summarizes the evolution of BTK inhibitors, highlighting how next-generation agents like pirtobrutinib offer improved selectivity, reduced toxicity, and options to overcome resistance in MCL.

The protein TRIM24 regulates autophagy-mediated resistance to the proteasome inhibitor bortezomib, offering a potential new therapeutic target to overcome drug resistance in relapsed/refractory MCL.

This review outlines emerging therapeutic strategies, including non-covalent BTKis, CAR-T, and bispecifics, for managing the clinically challenging population of MCL patients relapsing after covalent BTK inhibitors.

This preclinical CLL study validates 5-lipoxygenase inhibitors for disrupting tumor-microenvironment adhesion, reinforcing this novel mechanism, previously identified by the authors, as a potential therapeutic strategy for MCL.

This review details intrinsic (NF-κB, apoptosis, DNA repair) and extrinsic (tumor microenvironment) resistance mechanisms, identifying new therapeutic vulnerabilities to guide personalized strategies for high-risk MCL patients.

This review synthesizes clinical, molecular, and genomic markers to define high-risk MCL, guiding risk-stratified treatment and highlighting future therapies like bispecifics for this poor-prognosis population.

Real-world data show BTKi refractoriness and poor in-vivo brexu-cel expansion predict worse survival, identifying high-risk patients for early relapse and highlighting CAR-T kinetics as a key biomarker.