MCL Literature Feed
251 papers on mantle cell lymphoma from PubMed. Updated daily.
This review positions CAR-T and bispecific antibodies as complementary tools for relapsed/refractory MCL, advocating for individualized sequencing and combinations to optimize outcomes in heavily pretreated, high-risk patients.
This meta-analysis quantifies the high incidence of neurotoxicity (ICANS) with brexucabtagene autoleucel in MCL, finding 61% of patients experience any grade and 33% experience severe events.
Real-world data from an Italian compassionate use program confirms pirtobrutinib's efficacy in heavily pre-treated, relapsed/refractory MCL, including patients who have failed prior covalent BTK inhibitors.
In a real-world French cohort, MCL patients failing CAR-T therapy have dismal outcomes (median OS 5.8 months), highlighting an urgent need for effective salvage, with bispecific antibodies showing promise.
This review outlines the evolution of BTK inhibitors, highlighting how non-covalent agents like pirtobrutinib overcome C481-mediated resistance, extending the therapeutic sequence for relapsed/refractory MCL.
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This general review of lymphoproliferative disorders reiterates the established role of bortezomib in relapsed/refractory mantle cell lymphoma but provides no new data or specific insights.
A matching-adjusted indirect comparison suggests pirtobrutinib improves survival versus standard of care for relapsed/refractory MCL patients who have progressed on a prior covalent BTKi, supporting its use.
Emapalumab, an interferon-gamma blocker, successfully treated severe immune effector cell-associated HLH-like syndrome (IEC-HS) in a relapsed MCL patient post-CAR-T, offering a targeted approach for this life-threatening toxicity.
This review summarizes mechanisms of resistance and relapse after CAR-T/CAR-NK therapy, such as antigen loss and T-cell exhaustion, offering insights for improving durability in MCL.
This case report demonstrates CD19 downregulation as a key mechanism of resistance and subsequent relapse in a heavily pretreated MCL patient following initially effective CD19-targeted CAR-T therapy.
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Prophylactic siltuximab, guided by rising CRP, effectively managed cytokine release syndrome from bispecifics while minimizing infections by avoiding corticosteroids, a promising toxicity management strategy for MCL patients.
This case report describes an early-onset disseminated adenovirus infection after CAR-T therapy for relapsed/refractory MCL, highlighting a critical and potentially fatal infectious toxicity of this cellular therapy.
Brexucabtagene autoleucel induced a durable 19-month remission in heavily pretreated MCL with intraocular relapse, demonstrating CAR-T efficacy in this rare sanctuary site.
This preclinical study shows a SOX11 inhibitor overcomes BTKi, BCL2i, and CAR-T resistance by targeting the PAX5/CD19 axis, a novel upstream BCR signaling mechanism.
This review summarizes the MCL treatment evolution from chemoimmunotherapy and transplant to targeted agents (BTKi) and immunotherapies (CAR-T, bispecifics), emphasizing a future of personalized, genomics-guided care.
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This review summarizes the rapid clinical integration of T-cell engaging therapies (CAR-T, bispecifics) for B-NHL, including MCL, and outlines future strategies like earlier use and novel constructs.
Acquired MYC rearrangements were found in 43% of ibrutinib-resistant MCL tumors, identifying a key genomic alteration that drives intrinsic resistance and may serve as a critical biomarker.
Pretargeted anti-CD20 radioimmunotherapy safely intensifies BEAM conditioning before autologous transplant in high-risk B-cell lymphomas, including MCL, offering a feasible new consolidation strategy.
This case report describes a rare relapse of mantle cell lymphoma presenting as an isolated laryngeal mass, emphasizing the importance of considering unusual sites of recurrence in MCL patients.
This indirect treatment comparison provides the first comparative evidence between zanubrutinib and acalabrutinib for relapsed/refractory MCL, guiding clinical selection in the absence of a head-to-head trial.
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This review summarizes the evolution of BTK inhibitors, from covalent to reversible agents, to overcome resistance and toxicity, highlighting their central role in current and future MCL therapies.
In the BRUIN study, relapsed/refractory MCL patients previously treated with a BTKi maintained or improved quality of life and symptoms on pirtobrutinib, supporting its favorable long-term tolerability.
Genomic analysis reveals MCL relapse is driven by pre-existing resistant clones from diagnosis, not new mutations, emphasizing the need for deep upfront responses to eradicate these subclones.
A preclinical multi-modal profiling platform integrating genomics, in vitro drug screening, and PDX models identified personalized therapies for BTKi-relapsed/refractory MCL, guiding treatment beyond single gene alterations.
Pirtobrutinib-tolerant MCL persister cells survive via a reversible TCA cycle metabolic switch, presenting a novel metabolic vulnerability to target and prevent drug resistance.
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Blastoid or pleomorphic morphology in mantle cell lymphoma is associated with increased primary and acquired resistance to BTK inhibitors, identifying a high-risk population requiring alternative therapeutic strategies.
This large, real-world analysis confirms a dismal prognosis (median OS 5.4 months) for MCL patients progressing after CAR-T, establishing a benchmark for future trials in this high-risk population.
This review outlines emerging therapeutic strategies, such as bispecific antibodies and novel agents, for managing mantle cell lymphoma patients who have relapsed after CAR-T cell therapy.
A case report of a TP53-deleted splenic marginal zone lymphoma acquiring a secondary CCND1 rearrangement upon high-grade transformation suggests an alternative pathway to cyclin D1-driven lymphomagenesis.
A patient-derived organoid model from prostate-metastatic MCL predicted sensitivity to gemcitabine but resistance to rituximab/oxaliplatin, offering a new platform for personalized therapy selection in heterogeneous disease.