MCL Literature Feed

This longitudinal study reveals MCL acquires new high-risk genetic features after chemoimmunotherapy, explaining relapse and emphasizing the need for genomic profiling to guide subsequent therapies.

This paper details a new UPLC-MS/MS method for rapid venetoclax plasma quantification, which could facilitate therapeutic drug monitoring to optimize dosing and toxicity management in MCL.

Undetectable MRD after induction chemotherapy identifies mantle cell lymphoma patients who may safely omit consolidative autologous stem cell transplant, enabling a personalized, de-escalation treatment strategy.

In a retrospective ZUMA-2 analysis, prior ibrutinib exposure, versus acalabrutinib, improved brexu-cel CAR-T efficacy and PFS by inducing a more favorable cytotoxic T-cell phenotype.

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.

High expression of the lncRNA MALAT1 is a novel, independent biomarker for favorable prognosis in MCL, inversely correlating with proliferation signatures and EZH2 activity.

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 case report describes the rare co-occurrence of MCL and CLL/SLL, highlighting the diagnostic and therapeutic challenges that require careful pathologic evaluation to guide appropriate treatment.

Flow cytometry is crucial for accurately diagnosing leukemic-phase blastoid MCL, resolving morphological ambiguity with other acute leukemias and ensuring correct treatment for this aggressive variant.

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.

Co-expression of PD-L1/PD-1 with CXCR3 and systemic inflammation indices (SIRI, SII) identified advanced stage and poor survival in a mixed lymphoma cohort, offering potential prognostic biomarkers for MCL.

This study demonstrates that TP53 mutation heterogeneity, not just presence, defines distinct prognostic subgroups in MCL, enabling more precise risk stratification beyond a simple binary classification.

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.

In the phase 3 TRIANGLE trial for young, fit MCL, adding ibrutinib to induction immunochemotherapy improves failure-free survival, with noninvasive genotyping confirming its efficacy and treatment dynamics.

A new genomic model integrating mutations (e.g., TP53) and copy number variations improves risk stratification for elderly, newly diagnosed MCL patients treated with chemoimmunotherapy.

In the MCL0208 trial for young patients, IGHV mutation status and stereotyped receptors predicted outcomes after intensive chemoimmunotherapy and transplant, offering a new biomarker for frontline risk stratification.

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.

A new prognostic model integrating peripheral blood immune cells and cytokines with clinical data improves risk stratification in MCL, offering a more accessible biomarker approach than tissue-based assays.

This real-world Colombian cohort confirms MIPI score as a key prognostic factor in MCL, where age-stratified frontline chemotherapy resulted in comparable responses despite different treatment intensities.

In a large low-grade lymphoma cohort, MCL histology was a key risk factor for lymphoma-related death, while secondary malignancies drove non-lymphoma mortality, underscoring diverse survival threats.

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 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.

In newly diagnosed MCL, higher total lymphocyte and B-cell counts in the bone marrow correlated with a lower percentage of disease progression, suggesting a potential prognostic flow cytometry biomarker.

A systematic review finds MCL has particularly high uptake on CXCR4-targeted [68Ga]Ga-Pentixafor PET, suggesting its utility for staging and response assessment, potentially superior to FDG-PET.

This study confirms a rare DLBCL subtype with CCND1 rearrangement, molecularly distinct from MCL by its SOX11-negativity and DLBCL-like mutations, posing a critical diagnostic and therapeutic challenge.

In the frontline MANTLE-FIRST study, fitness status and time to first progression (PFS1) were identified as key prognostic factors for elderly MCL patients, impacting subsequent outcomes.

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.