MCL Literature Feed

Single-cell RNA sequencing reveals pre-existing, minor therapy-resistant subclones at diagnosis, which are selected during treatment, explaining early relapse and highlighting cell-cycle dysregulation as a common resistance mechanism.

PRMT5 inhibition sensitizes MCL cells to ferroptosis by disrupting the ATF5-SLC7A11 axis, providing a rationale for combining PRMT5 inhibitors with ferroptosis inducers for relapsed/refractory disease.

Single-cell multi-omics reveals genetic and non-genetic pirtobrutinib resistance mechanisms in MCL, identifying the cohesin complex as a potential target to restore drug sensitivity.

Preclinical data suggests PRMT5 inhibition is a promising combination therapy strategy for high-risk MCL with ATM and TP53 mutations, which are known to confer therapeutic resistance.

Mitochondrial ACSS1 enables nutrient-stressed B-cell lymphomas to produce DNA/RNA building blocks via acetate metabolism, identifying ACSS1 as a novel therapeutic target to overcome metabolic adaptation.

The lymph node microenvironment silences the pro-apoptotic protein BIM via a CD40/PI3K/FOXO1 axis, driving broad drug resistance that can be overcome by bispecific T-cell engager immunotherapy.

This study identifies the SOX11-UHRF1 axis as a new therapeutic target in MCL, demonstrating that the UHRF1 inhibitor CM272 effectively suppresses tumor growth in preclinical models.

A novel single-cell technique, LiP-Seq, identified IFITM2 upregulation in rare persistent MCL cells post-CAR-T, revealing a new mechanism of immune evasion and a potential therapeutic target.

Dual inhibition of anti-apoptotic proteins BIRC5 and MCL-1 is a novel preclinical strategy to overcome drug resistance in mantle cell lymphoma, offering a potential new therapeutic avenue.

The NAMPT inhibitor KPT-9274 sensitizes TP53-mutated MCL to alkylating chemotherapy by disrupting the DNA damage response, offering a novel combination strategy for this high-risk, chemo-resistant population.

Preclinical data shows that inhibiting the cell cycle regulator CDC20 suppresses MCL growth by downregulating the PI3K/AKT pathway, identifying CDC20 as a novel therapeutic target.

A novel preclinical compound dually inhibiting FLT3 and HDAC is developed, introducing a new potential therapeutic mechanism for hematologic malignancies, though its specific relevance to MCL is unknown.

A novel liquid biopsy technique using cell-free chromatin profiling non-invasively tracks disease origin and monitors therapy response, offering a powerful new tool for MRD and biomarker discovery.

Proteomic profiling identified an MCL-specific protein signature, including seven targets missed by RNA analysis, offering novel avenues for CAR-T therapy and personalized treatment.

A distinct DNA demethylation signature in MCL tumors acts as a "fossil record" of early gene activation, offering a novel bioinformatic approach to understand the cancer's developmental origins.

This review summarizes how epigenetic dysregulation drives MCL pathogenesis, highlighting the potential for novel biomarkers and therapeutic targets based on mechanisms like DNA methylation and histone modification.

A new preclinical cell line and patient-derived xenograft model of a non-MCL lymphoma with a CCND1 rearrangement provides a tool to study the specific biological role of this key driver.

The HSP90-MYC-CDK9 molecular network is identified as a key driver of therapeutic resistance in MCL, suggesting HSP90 or CDK9 inhibitors as potential strategies to overcome it.

A novel fluorescence-based assay quantifies pirtobrutinib in biological fluids, potentially enabling therapeutic drug monitoring to optimize dosing, manage toxicity, and study resistance in MCL patients.

This bioinformatic study identified a prognostic network of six circular RNAs in mantle cell lymphoma that regulate key pathways like BCR signaling, suggesting their potential as novel biomarkers.

This preclinical development of an optimized CXCR4-targeting theranostic pair offers a novel strategy to simultaneously image and treat MCL by targeting a key pathway in aggressive disease.

Long-read sequencing systematically identifies novel fusion transcripts in MCL, potentially revealing new prognostic biomarkers and therapeutic targets beyond the canonical t(11;14) translocation.

This preclinical mouse study shows zanubrutinib mitigates pulmonary fibrosis by inhibiting the Wnt/β-catenin pathway, a novel off-target mechanism potentially relevant to managing toxicities in MCL patients.

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.

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.

A novel gene-editing method creates safer allogeneic CAR-T cells, potentially offering a more accessible 'off-the-shelf' cellular therapy option for MCL patients.

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

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.

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.