MCL Literature Feed

Reviewing the TRIANGLE trial, this paper argues that adding ibrutinib to frontline induction makes omitting autologous stem cell transplant consolidation a non-inferior, less toxic option for young patients.

This review synthesizes the evolution of BTK-targeted therapies, from covalent inhibitors to non-covalent agents and degraders, outlining current treatment paradigms and future combination strategies for frontline and relapsed MCL.

Reviewing AIM and SYMPATICO trials, the ibrutinib-venetoclax combination shows high efficacy in relapsed/refractory MCL, supporting a potential fixed-duration, MRD-guided treatment strategy.

This review summarizes the clinical development and efficacy of BTK inhibitors in MCL, detailing common resistance mutations and outlining future directions for this crucial targeted therapy class.

This retrospective case series strengthens the link between ibrutinib and delayed-onset uveitis, a potentially vision-threatening toxicity that resolves upon drug cessation, highlighting a key clinical management consideration.

This phase 1 trial establishes the safety and preliminary efficacy of combining the HDAC inhibitor abexinostat with ibrutinib in relapsed/refractory MCL, suggesting a potential new BTKi-based combination strategy.

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.

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.

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.

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.

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.

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.

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.

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

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.

Preclinically, dual inhibition of Hedgehog/GLI1 and Wnt/β-catenin pathways synergistically suppresses MCL cells and enhances sensitivity to chemotherapy and ibrutinib, suggesting a new approach to overcome resistance.

This review synthesizes current and emerging therapies for relapsed/refractory MCL, including BTKi, BCL2i, CAR-T, and bispecifics, emphasizing the evolving challenge of post-BTKi treatment sequencing.

In younger, BTKi-naïve MCL patients with late relapse (>24 months), second-line BTKi significantly improved PFS and OS versus chemoimmunotherapy, establishing it as the preferred approach in this setting.

Seven-year follow-up of venetoclax-ibrutinib in relapsed/refractory MCL shows durable responses (30% PFS) and demonstrates feasibility of MRD-guided treatment-free remission, supporting a long-term chemotherapy-free strategy.

This large, real-world French database study on ibrutinib focuses exclusively on patients with CLL, providing no specific data or insights relevant to mantle cell lymphoma.

This review summarizes the evolving treatment landscape for relapsed/refractory MCL, highlighting survival gains from BTKi and CAR-T and outlining emerging therapies like bispecifics for multiply-refractory patients.

A rare case of MCL presenting as diffuse polyposis throughout the entire GI tract achieved complete response after R-CHOP followed by salvage chemotherapy plus ibrutinib, highlighting this unusual presentation.

This case report identifies life-threatening aplastic anemia as a rare but fatal toxicity of acalabrutinib in MCL, urging clinicians to consider it in patients developing pancytopenia.

This study analyzes molecular responses in exceptional responders to the BTKi tirabrutinib, aiming to identify biomarkers for deep, durable remissions in relapsed/refractory mantle cell lymphoma.

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.