MCL Literature Feed

In a retrospective analysis of 95 MCL cases, specific histopathological patterns of bone marrow involvement were identified as key prognostic indicators, aiding in initial patient risk stratification.

This case series characterizes the immunohistochemical and molecular genetic profile of rare lacrimal gland MCL, providing crucial diagnostic insights for this uncommon extranodal presentation.

PRMT5 promotes MCL growth via MYC-driven lipid metabolism reprogramming, identifying it as a poor prognostic marker and a novel therapeutic target with preclinical inhibitor activity.

This retrospective study confirms that progression of disease within 24 months (POD24) after initial therapy is a strong negative prognostic marker for overall survival in MCL patients.

This systematic analysis of MAIT cells across hematological malignancies provides foundational insights into the MCL immune microenvironment, potentially identifying novel biomarkers or immunotherapy targets.

This report describes two contrasting presentations of MCL with plasmacytic differentiation, highlighting the diagnostic challenge of this rare variant which can mimic plasma cell neoplasms, impacting management.

Gene expression profiling identifies two distinct molecular MCL subtypes, C1 and C2, with C2 showing high proliferation and poor prognosis, providing a powerful new biomarker for risk stratification.

This preclinical study identifies SOX11 as an endogenous inhibitor of SAMHD1, which sensitizes mantle cell lymphoma to cytarabine, suggesting SOX11 status as a predictive biomarker for chemotherapy efficacy.

This B-ALL study reveals MALT1 inhibitors downregulate MYC, providing a novel mechanism and strong rationale for testing this strategy in aggressive, MYC-driven mantle cell lymphoma.

A rare, non-nodal MCL case with hairy cell-like features and a TP53 mutation showed an indolent course, challenging prognostic assumptions and emphasizing comprehensive genomic and pathologic evaluation.

The EHA/EBMT ICAHT grading system better predicts severe infections and mortality post-CAR-T than CTCAE, which is highly relevant as MCL patients showed the highest rates of severe hematotoxicity.

MNDA is highly expressed in nearly 80% of mantle cell lymphoma cases, but its utility in distinguishing MCL from marginal zone lymphoma is limited due to overlapping expression.

This preclinical study identifies DNMT3A-mediated metabolic reprogramming to oxidative phosphorylation as a novel ibrutinib resistance mechanism, which can be overcome by low-dose decitabine.

This preclinical study identifies that SOX11 upregulates the antioxidant PRDX2, promoting chemoresistance in aggressive MCL, and suggests PRDX2 as a novel therapeutic target to overcome drug resistance.

MYC overexpression is a critical biomarker defining high-risk mantle cell lymphoma, helping to stratify patients with poor prognosis and potentially guiding novel therapeutic approaches for this aggressive disease.

This retrospective analysis shows peripheral blood Ig-HTS MRD testing (clonoSEQ) effectively predicts relapse earlier than imaging in MCL patients, supporting its use as a surveillance tool post-frontline therapy.

Using computational screening and machine learning, this study identifies novel PIM2 inhibitors, presenting a potential new therapeutic target for future drug development in hematologic malignancies, including MCL.

MCL with concurrent EZH2 expression and TP53 mutation is frequent and identifies a patient subgroup with a dismal outcome, establishing a powerful negative prognostic biomarker combination.

This review summarizes fundamental MCL characteristics, including the t(11;14) translocation and key high-risk features (high Ki67, blastoid variant, TP53 mutation) essential for patient risk stratification.

This paper does not study MCL but finds high Notch1 protein expression in methotrexate-associated DLBCL, suggesting a pathogenic role for this pathway, which is also altered in MCL.

Palbociclib plus venetoclax shows preclinical synergy in ibrutinib-refractory MCL by downregulating MCL1, offering a chemo-free option for patients without RB1 deletion.

Phospho-flow cytometry reveals that high constitutive AKT and inducible STAT5/SYK B-cell receptor signaling activity predicts shorter survival and ibrutinib resistance, offering a functional biomarker for high-risk MCL.

This review details BTK inhibitor resistance mechanisms, particularly C481S mutations, and highlights non-covalent BTKi (pirtobrutinib) and PROTACs as key strategies to overcome relapse in MCL.

Mendelian randomization analysis reveals that genetically longer telomeres are a causal risk factor for developing hematological malignancies, including MCL, suggesting a potential inherited predisposition for the disease.

Large B-cell lymphoma with IRF4 rearrangement can mimic blastoid MCL by presenting in older adults and expressing CD5, but negativity for Cyclin D1 and SOX11 is crucial for differential diagnosis.

A Mendelian randomization study provides causal evidence that genetically predicted longer telomere length increases the risk of developing MCL, suggesting a role for enhanced cellular proliferation in pathogenesis.

This multi-modal single-cell atlas of the human tonsil provides a high-resolution map of normal B-cell development, enabling a deeper understanding of MCL's cellular origins and heterogeneity.

Targeting the epigenetic modifier KDM5 shows preclinical activity in mantle cell lymphoma, identifying a novel therapeutic vulnerability for potential future treatments.

This workshop report summarizes recent advances in MCL biology and treatment, including BTKi and CAR-T, and outlines key research priorities to overcome resistance and clinical heterogeneity for future progress.

This case report identifies a rare, leukemic, cyclin D1/SOX11-negative MCL driven by a CCND3::IGH rearrangement, highlighting a diagnostic pitfall and the importance of molecular testing in atypical cases.