MCL Literature Feed

Identifies splicing factors SRSF1, hnRNP F, and PTBP1 as drivers of MCL aggressiveness and potential therapeutic targets, whose high expression with MYC predicts poor survival.

This case report details MCL transformation into CD19-negative classic Hodgkin lymphoma after CAR-T, a novel resistance mechanism driven by immunotherapeutic pressure and lineage plasticity in a high-risk patient.

A novel single-cell method combining biophysical and transcriptomic data identifies distinct MCL subpopulations, offering new insights into tumor heterogeneity and potential therapeutic resistance.

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.

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.

This review summarizes preclinical nanocarrier strategies designed to improve ibrutinib's bioavailability and targeted delivery, potentially enhancing efficacy and reducing off-target toxicity for MCL patients in the future.

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.

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.

This review explains how tumor microenvironment crosstalk with B-cell receptor signaling promotes MCL survival and BTKi resistance, underscoring the need to target these interactions for improved therapies.

An albumin nanocomplex of the BCL-2/xL inhibitor APG-1252 reduces thrombocytopenia and enhances anti-MCL efficacy in mouse models, offering a potential strategy to improve the therapeutic window.

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.

This preclinical study engineers novel nanocarriers for cytarabine, aiming to improve drug delivery and anti-lymphoma efficacy, which could enhance existing high-dose MCL chemotherapy regimens.

The novel oral CDK9 inhibitor YX0798 demonstrates high selectivity and potent preclinical activity in MCL by downregulating MYC/MCL-1, offering a potential strategy to overcome therapeutic resistance.

This review details how MCL cell adhesion within the microenvironment promotes survival, explaining the mechanism of action for TME-disrupting therapies and its role in drug resistance.

This review summarizes advanced 3D culture models that better mimic the MCL microenvironment, offering improved platforms for preclinical drug screening and developing personalized medicine.

Single-cell analysis reveals pre-existing minor clones with unique mutations drive relapse, explaining patient-specific progression and the need to target intratumoral heterogeneity at diagnosis.

A novel 3D bioprinted hydrogel model improves primary MCL cell survival ex vivo, offering a more physiologically relevant platform for preclinical drug screening and studying the tumor microenvironment.

Comprehensive cfDNA analysis non-invasively tracks MCL disease burden and detects high-risk mutations, offering a powerful liquid biopsy tool for monitoring and risk stratification.

BRG1-driven suppression of ferroptosis is a key mechanism of BTKi resistance in MCL, and pharmacologic BRG1 inhibition restores BTKi sensitivity, suggesting a new combination therapy.

Cyclin D1 overexpression induces replication stress and a dependency on POLQ-mediated DNA repair, identifying POLQ inhibition as a novel, targeted therapeutic strategy for mantle cell lymphoma.

Real-world data on commercially insured B-cell NHL patients, including MCL, reveals a 48% relapse rate at 12 months post-CAR-T, with subsequent therapies incurring significant patient out-of-pocket costs.

A novel dual PI3K/HDAC inhibitor demonstrates enhanced pro-apoptotic activity in lymphoma cells, presenting a potential new preclinical strategy for MCL by simultaneously targeting two key pathways.

This review characterizes the rare transformation of MCL into aggressive Burkitt lymphoma, a distinct form of Richter's syndrome, highlighting its unique pathogenesis, clinical features, and poor prognosis.

High NSD2 expression and specific mutations correlate with aggressive MCL variants, poorer treatment response, and inferior survival, establishing NSD2 as a key prognostic biomarker and potential therapeutic target.

Genomic analysis of MCL treated sequentially with BTKi and venetoclax identifies specific copy number alterations (e.g., 9p21.3 deletion) as novel biomarkers for primary and acquired resistance.

The SOX11:SMARCA4 complex is a key oncogenic driver in MCL, and targeting SMARCA4 with a PROTAC degrader shows preclinical activity, offering a novel therapeutic strategy for relapsed patients.