MCL Literature Feed

A case report demonstrates that MCL can relapse in rare sites like skeletal muscle after rituximab maintenance, underscoring the value of PET/CT for detecting atypical disease progression.

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.

A deep learning model fusing PET/CT and EHR data creates a new signature that better predicts survival in frontline MCL, potentially improving risk-adapted therapy selection.

This case report identifies a rare, aggressive MCL variant with blastoid morphology, TdT expression, and MYC rearrangement, broadening the known clinicopathological spectrum and posing significant diagnostic challenges.

A real-world, retrospective study demonstrates that clinical next-generation sequencing panels provide significant prognostic and predictive data in mantle cell lymphoma, aiding in the optimization of patient management.

Genomic analysis reveals MCL relapse is driven by the expansion of pre-existing resistant subclones, not new mutations, highlighting the need for deep sequencing at diagnosis to prevent recurrence.

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.

This retrospective analysis evaluates transplant outcomes in relapsed/refractory MCL after ibrutinib failure, identifying risk factors to guide patient selection for this intensive consolidation therapy.

This large, real-world study demonstrates that any disease progression, even occurring more than 6 years after initial therapy, significantly worsens overall survival in mantle cell lymphoma.

This comprehensive review synthesizes emerging biomarkers beyond standard prognosticators, including MRD, ctDNA, and advanced imaging, to better guide personalized treatment in the targeted therapy era.

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.

An AI-based platform provides more objective and reproducible immunohistochemistry quantification than manual interpretation, improving the diagnostic accuracy in differentiating MCL from CLL/SLL.

High serum sTNFR2 at diagnosis is a strong prognostic biomarker for inferior overall survival in MCL, implicating the tumor microenvironment and suggesting a new therapeutic target.

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.

Absence of CD38 expression in conventional nodal MCL strongly correlates with TP53 inactivation and a distinct genetic profile, identifying a high-risk subgroup via routine flow cytometry.

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.

A family history of hematological malignancy is associated with inferior event-free survival in mantle cell lymphoma, suggesting it may be a novel adverse prognostic factor.

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.

This Chinese real-world study characterizes the clinical features and poor prognosis of blastoid/pleomorphic MCL, providing data to help risk-stratify and manage this aggressive subtype.

This first comprehensive proteogenomic analysis of MCL demonstrates that integrating protein data with genomics improves survival prediction and identifies molecular subtypes linked to IGHV/CCND1 mutations, offering new prognostic tools.

A case of CD5+ cutaneous DLBCL highlights a diagnostic pitfall, as it can mimic MCL but is distinguished by cyclin D1 negativity, reinforcing the need for complete immunohistochemical workup.

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.

The oral AKT inhibitor capivasertib showed modest single-agent activity (30% ORR) in relapsed/refractory MCL, with PTEN deficiency emerging as a potential predictive biomarker for patient selection.

Bridging radiotherapy before CAR-T effectively controls disease in MCL patients, with most showing rapid tumor reduction and no local progression, supporting its use as a pre-CAR-T strategy.

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.