MCL Literature Feed

A novel nanostructured lipid carrier (NLC) formulation increased ibrutinib's oral bioavailability by 1.82-fold in a rat model, suggesting a potential strategy to enhance drug delivery and efficacy.

A novel αCD20-EndoP125A antibody fusion protein inhibits MCL growth and dissemination in preclinical models by disrupting tumor-vessel interactions, including angiogenesis, lymphangiogenesis, and vessel co-option.

Real-world, intention-to-treat data from the French DESCAR-T registry confirms brexucabtagene autoleucel efficacy in relapsed/refractory MCL, providing practical outcomes for all patients intended for treatment.

This first case report of concurrent zanubrutinib and radiotherapy demonstrates a manageable safety profile, suggesting BTKi therapy may not require interruption for necessary radiation in MCL patients.

Long-term follow-up after autologous stem cell transplant in MCL is critical for detecting late relapses and managing treatment-related toxicities, guiding post-transplant surveillance strategies.

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

This large, single-center retrospective study characterizes the aggressive nature and poor outcomes of MCL with cutaneous involvement, providing crucial real-world data for managing this rare presentation.

This meta-analysis quantifies the poor prognosis (median OS ~9 months) for r/r MCL patients post-covalent BTKi treated with standard therapies, highlighting the superior efficacy of brexucabtagene autoleucel.

Preclinically, bortezomib-induced apoptosis depends exclusively on the protein NOXA, which inactivates both MCL-1 and BCL-XL, providing a refined understanding of its mechanism and potential resistance.

Bendamustine-induced lymphopenia in frontline MCL resolves by 12 months, suggesting a minimum 9-month wait before leukapheresis for CAR-T therapy to ensure sufficient lymphocyte collection.

MCL can relapse late as isolated soft tissue tumors in the extremities, a rare clinical presentation clinicians must recognize for timely diagnosis, even without concurrent nodal disease.

This review highlights that excellent outcomes with modern frontline chemo-immunotherapy plus BTK inhibitors are challenging the traditional role of autologous transplant consolidation in mantle cell lymphoma.

In a small retrospective study of nine untreated aggressive MCL patients, adding a BTKi to chemoimmunotherapy achieved a 100% objective response rate with manageable toxicity, suggesting a promising frontline strategy.

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.

The VALERIA trial demonstrates that an MRD-guided, fixed-duration venetoclax-lenalidomide-rituximab regimen is a highly effective, personalized, chemotherapy-free strategy for patients with relapsed/refractory MCL.

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.

This retrospective study confirms poor outcomes for blastoid MCL with chemo-immunotherapy, advocating for upfront 2nd/3rd generation BTKi-based therapies to improve survival in this high-risk population.

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.

A rare case of primary bone MCL presenting as a psoas abscess with multiple vertebral lesions highlights a diagnostic pitfall where extranodal lymphoma can mimic musculoskeletal infection.

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.

This review positions pirtobrutinib, a non-covalent BTKi, as a highly effective and safe treatment for relapsed/refractory MCL, especially for patients who have progressed on prior covalent BTK inhibitors.

This case report describes a rare presentation of MCL in the oral cavity, highlighting the key microscopic features necessary for differential diagnosis from other lymphoid neoplasms at this extranodal site.

The KRD regimen (carfilzomib, lenalidomide, dexamethasone) is highly toxic and ineffective for BTKi-relapsed/refractory MCL, with only 13% 12-month OS, establishing this is not a viable salvage therapy.

Real-world US Medicare data shows elderly MCL patients post-cBTKi have a dismal median OS of 9.4 months and high costs, highlighting the urgent need for effective therapies.

The non-covalent BTK inhibitor pirtobrutinib shows a 58% overall response rate in relapsed/refractory MCL, providing a crucial new option for patients previously treated with covalent BTK inhibitors.

A validated LC-MS/MS assay simultaneously measures plasma ibrutinib, its active metabolite, and zanubrutinib, enabling therapeutic drug monitoring to potentially optimize dosing and manage toxicity in MCL.

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.

This case of cardiac MCL with a mobile tumor highlights the risk of fatal pulmonary embolism post-chemotherapy, suggesting a potential role for pre-treatment surgical intervention in this rare presentation.

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.