MCL Literature Feed

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.

This case report describes the specific sonographic features of mantle cell lymphoma presenting as an inguinal mass, which can aid radiologists in the differential diagnosis of regional lymphadenopathy.

The frontline, chemotherapy-free triplet of acalabrutinib, venetoclax, and rituximab achieved 100% ORR and high MRD negativity, establishing a potent, time-limited option despite significant COVID-19 toxicity.

This review synthesizes current data and practical considerations for CAR-T and bispecific antibodies, guiding clinical decision-making and sequencing for these T-cell engaging therapies in relapsed/refractory MCL.

In older, frontline MCL patients, adding bortezomib to BR induction or lenalidomide to rituximab maintenance did not improve PFS, confirming BR-R as a highly effective standard.

This review explores CAR-NK cells as a promising alternative to CAR-T therapy for mantle cell lymphoma, potentially offering comparable efficacy with a significantly improved safety profile and fewer severe toxicities.

This CML review details targeting the ubiquitin-proteasome system to overcome TKI resistance, offering a potential mechanistic strategy for addressing BTKi resistance in MCL.

A meta-analysis of 7,604 patients found mantle cell lymphoma has the highest non-relapse mortality (10.6%) post-CAR-T, with infections being the primary cause, not CAR-T-specific toxicities.

The non-covalent BTK inhibitor pirtobrutinib is now approved in Japan for mantle cell lymphoma, providing a crucial new therapeutic option for patients, including those resistant to covalent BTKis.