MCL Literature Feed

This systematic review finds all AI models for lymphoma histopathology, including MCL, have a high risk of bias, questioning their reported high accuracy and current clinical readiness.

A case of TP53-mutated, indolent non-nodal MCL suggests this high-risk marker may not mandate immediate therapy in this specific subtype, supporting a watch-and-wait approach.

This review details intrinsic (NF-κB, apoptosis, DNA repair) and extrinsic (tumor microenvironment) resistance mechanisms, identifying new therapeutic vulnerabilities to guide personalized strategies for high-risk MCL patients.

This review synthesizes clinical, molecular, and genomic markers to define high-risk MCL, guiding risk-stratified treatment and highlighting future therapies like bispecifics for this poor-prognosis population.

This review clarifies that cyclin D1-negative MCL is driven by CCND2 or CCND3 translocations, proposing new terminology to improve diagnostic accuracy for this rare and often missed subtype.

An MCL patient on ibrutinib had persistent COVID-19 missed by nasopharyngeal swabs but diagnosed via bronchoalveolar lavage, underscoring the need for deeper sampling in immunosuppressed patients.

This review advocates for using prognostic tools like MIPI and TP53 status to guide risk-adapted therapy in MCL, intensifying for high-risk and de-escalating for low-risk patients.

In MCL cells, the RNA processing factor NUDT21 undergoes alternative polyadenylation to evade miRNA-mediated suppression, revealing a novel mechanism of gene regulation that could be a future therapeutic target.

A rare case of MCL transdifferentiating into a clonally-related T-cell lymphoma demonstrates a novel transformation mechanism where B-cell markers are lost, complicating diagnosis at relapse.

This review highlights stereotyped B-cell receptors in MCL, suggesting common antigen-driven pathways that could provide a basis for molecular subclassification to refine patient risk stratification.

This methods paper details using sensitive qPCR and ddPCR to detect MRD in B-cell lymphomas by targeting Ig gene rearrangements and chromosomal translocations, relevant for MCL's t(11;14).

Bioinformatic analysis reveals a positive correlation between STING expression and cytolytic score in MCL, suggesting STING may be a biomarker for immune activity and a potential immunotherapy target.

This case report identifies a novel jumping translocation of 3q in an MCL patient, linking this rare cytogenetic event to clonal evolution and a potential poor prognosis.

Epigenetic profiling reveals a unique DNA methylation signature for B-cell prolymphocytic leukemia, providing a novel biomarker to differentiate it from its mimics, including mantle cell lymphoma.

This review highlights that TP53-mutated MCL represents a distinct high-risk entity with poor outcomes to chemoimmunotherapy, underscoring the urgent need for novel, non-chemotherapy frontline approaches in these patients.

A rare case of composite MCL and lymphoplasmacytic lymphoma in bone marrow highlights the necessity of advanced diagnostics like NGS and FISH to differentiate from MCL with plasmacytic differentiation.

Analysis of European MCL Network trial data shows specific gene mutations predict patient outcomes, providing a genetic basis for risk stratification to guide therapy selection beyond clinical scores.

Malignant effusions, frequently caused by blastoid MCL, are characterized by a T/B cell ratio <1, providing a crucial diagnostic marker from cytological samples.

In preclinical models, PTEN loss activates the PI3K/AKT pathway, reducing BCR signaling dependence and conferring resistance to ibrutinib, venetoclax, and PI3K inhibitors, identifying a key resistance mechanism.

A new LSM gene expression index identifies MCL patients with poor survival by impacting cell division and RNA splicing, proposing LSM proteins as novel prognostic biomarkers and therapeutic targets.

Longitudinal single-cell analysis of refractory MCL reveals co-evolving tumor heterogeneity and immune evasion, providing a roadmap for overcoming treatment resistance and identifying new therapeutic targets.

p53 immunohistochemistry is a practical biomarker for identifying high-risk MCL patients, helping to stratify prognosis and guide selection of more intensive or novel therapies.

This preclinical study identifies a novel CERS6-AS1/FGFR1 axis driving stromal-supported MCL proliferation and stemness, suggesting that co-targeting nucleolin and FGFR1 could overcome microenvironment-mediated resistance.

Bioinformatic analysis of public datasets identified key genes and pathways driving bortezomib resistance in MCL, providing potential biomarkers and therapeutic targets for the relapsed/refractory setting.

SOX11-negative, CCND1-rearranged large B-cell lymphomas can arise via a DLBCL-like mechanism (aberrant CSR/SHM), distinguishing them genetically from classic MCL and highlighting a potential diagnostic challenge.

This preclinical study identifies the CERS6-AS1/FGFR1 axis as a synthetic vulnerability, offering a novel therapeutic strategy to disrupt stromal cell-mediated proliferation and overcome resistance in MCL.

Spatial multiomics reveals CD163+ macrophages activate the MAPK prosurvival pathway in MCL cells, identifying MAPK inhibitors as a potential therapy for patients with high macrophage infiltration.

This study identifies a rare CD5/SOX11 double-negative pleomorphic MCL, showing CCND1 rearrangement is the key feature to differentiate it from cyclin D1-positive DLBCL, ensuring correct diagnosis.

This review summarizes how molecular profiling (e.g., TP53) and MRD are reshaping MCL therapy by integrating novel agents into frontline care, personalizing treatment, and improving high-risk patient outcomes.

This review explains MCL's clinical heterogeneity through distinct molecular subtypes and genomic alterations like TP53, which serve as key prognostic biomarkers and guide development of novel therapies.