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.

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.

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 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.

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.

Optical Genome Mapping identified a rare IGL::CCND1 translocation in a CD23-positive case, revising a CLL diagnosis to MCL and demonstrating OGM's utility for detecting atypical presentations.

This report identifies KMT2A rearrangement as a rare genetic driver in MCL, defining a distinct subtype often associated with aggressive features like blastoid morphology and poor prognosis.

Integrating genomics and spatial proteomics defines three prognostic MCL subtypes, revealing high-risk TP53-mutated tumors are immune-infiltrated yet exhausted, highlighting potential therapeutic vulnerabilities.

A new immunocompetent mouse model co-expressing SOX11 and CCND1 faithfully recapitulates human MCL, providing a crucial platform for studying disease biology and testing novel immunotherapies.

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.

This review highlights the diagnostic challenge of distinguishing mantle cell lymphoma with plasmacytic differentiation from multiple myeloma, particularly the CCND1-translocated subtype, emphasizing the need for careful molecular workup.

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 the oncogenic role of the FoxO1 transcription factor in MCL, highlighting its potential as a novel therapeutic target with specific preclinical inhibitors under investigation.

In newly diagnosed MCL, ATM deletion predicts shorter progression-free survival in TP53 wild-type patients, whereas ATM mutation may indicate a better prognosis, highlighting their distinct prognostic roles.

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.

High-throughput sequencing accurately identifies IGHV somatic hypermutation status, a key prognostic biomarker in MCL, even in complex, multi-clonal samples, improving risk stratification and MRD tracking.

This transcriptomic study uses mantle cell lymphoma as a comparator to define effusion-based lymphoma as a distinct, post-germinal center entity driven by chronic inflammatory signaling pathways.

ctDNA sequencing in relapsed/refractory MCL identifies SMARCA4 and TP53 mutations as response predictors and offers more sensitive MRD monitoring than qPCR, improving non-invasive risk stratification.

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.

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.

Nodal MCL with leukemic presentation is a high-risk subtype characterized by SOX11-negativity, increased TP53 alterations, and inferior overall survival, requiring distinct clinical consideration.

Digital analysis of p53 immunohistochemistry establishes specific cut-offs (e.g., >50% for 2+/3+ nuclei) that reliably identify TP53 mutations and predict worse survival, improving rapid risk stratification.

A rare case of composite CLL/MCL highlights diagnostic challenges from overlapping immunophenotypes, reinforcing the critical need for molecular and cytogenetic studies like FISH for t(11;14) for definitive diagnosis.

The t(11;14) translocation in MCL upregulates entire gene regulons across the chromosome arm via long-range chromatin interactions, revealing a novel mechanism of widespread oncogenic dysregulation beyond just CCND1.

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.