MCL Literature Feed
164 papers on mantle cell lymphoma from PubMed. Updated daily.
Pirtobrutinib, a non-covalent BTKi, gained FDA accelerated approval for MCL after prior BTKi failure, offering a 50% overall response rate for this high-unmet-need population.
Pirtobrutinib, the first approved non-covalent BTKi, offers a crucial new therapy for relapsed/refractory MCL by overcoming resistance mechanisms, including C481 mutations, from prior covalent BTK inhibitors.
This indirect comparison of ZUMA-2 (brexucabtagene autoleucel) and SCHOLAR-2 (standard of care) demonstrates a substantial overall survival benefit for CAR-T therapy in relapsed/refractory MCL after BTKi failure.
This review synthesizes MCL's genomic heterogeneity with the evolving therapeutic landscape, focusing on novel agents like BTKi and CAR-T and strategies for overcoming resistance in relapsed/refractory disease.
Pirtobrutinib, a non-covalent BTKi, shows a 52% overall response rate in relapsed/refractory MCL, including in patients previously treated with covalent BTKi, offering a new therapeutic option.
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Italian real-world data highlights the poor prognosis and significant unmet clinical needs for relapsed/refractory MCL patients following covalent BTKi failure, emphasizing the urgency for novel treatment strategies.
A preclinical prostate cancer model shows Bortezomib resistance is driven by autophagy induction and reduced oxidative stress, suggesting potential combination strategies with autophagy inhibitors for MCL.
This review explores targeting tumor-associated macrophages within the MCL microenvironment as a novel immunotherapeutic strategy to enhance anti-tumor activity and potentially overcome drug resistance.
This review identifies the lncRNA LINK-A as an upregulated oncogene in MCL, presenting it as a potential biomarker and therapeutic target involved in oncogenic pathways and therapy resistance.
A novel SRC-3 inhibitor, SI-10, demonstrates preclinical efficacy in ibrutinib-resistant MCL models, identifying SRC-3 as a potential therapeutic target to overcome BTKi resistance.
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This preclinical study identifies a novel STAT5B-DCAF13-p53/xCT pathway that suppresses ferroptosis to promote MCL progression, revealing ferroptosis induction as a potential new therapeutic strategy.
Magnetic Resonance Spectroscopy (MRS) can non-invasively detect metabolic changes, like lactate and alanine, offering an early biomarker to predict response or resistance to BTK inhibitors in MCL.
This review summarizes the evolving Japanese MCL treatment landscape, highlighting novel therapies like BTKi, BCL2i, and CAR-T to address resistance in high-risk subsets like TP53-mutated and blastoid.
This case of classical MCL rapidly transforming to a blastoid variant with CNS involvement highlights the poor prognosis and failure of BTKi and chemotherapy in this aggressive setting.