MCL Literature Feed

This review details diverse BTKi resistance mechanisms beyond BTK mutations, providing a framework for developing next-generation inhibitors and combination strategies to overcome treatment failure in MCL.

In real-world relapsed/refractory MCL, ibrutinib dose reduction to manage toxicity is common and does not compromise response rates, PFS, or OS, validating this as a practical clinical strategy.

Single-cell multi-omics reveals genetic and non-genetic pirtobrutinib resistance mechanisms in MCL, identifying the cohesin complex as a potential target to restore drug sensitivity.

Consensus guidelines recommend the BOVen triplet (zanubrutinib, obinutuzumab, venetoclax) for TP53-mutated MCL and CAR-T for BTKi-refractory disease, providing expert guidance for managing high-risk patients.

This review outlines the evolving MCL treatment paradigm, detailing the integration of BTKi, CAR-T, and bispecific antibodies in both frontline and relapsed/refractory settings to improve patient outcomes.

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 review contextualizes MCL-approved BTK inhibitors by summarizing their distinct covalent and non-covalent binding mechanisms, which underlie differences in efficacy, toxicity, and overcoming resistance.

This review outlines evidence for sequencing BTKis, CAR-T, and bispecifics in relapsed/refractory MCL, a growing challenge as targeted therapies are increasingly used in the frontline setting.

Frontline zanubrutinib-rituximab induction achieved an 88% complete response rate, enabling a shortened R-DHAOx consolidation, offering a highly effective, chemotherapy-de-escalation strategy for newly diagnosed MCL.

An expert panel opinion advocates for personalized MCL therapy, positioning BTKi as a frontline standard for transplant-ineligible patients and a potential alternative to consolidation transplant for others.

This German real-world study (2015-2020) reveals rising MCL incidence and poor outcomes, highlighting a dismal median OS of 3.0 months after cBTKi discontinuation, underscoring a critical unmet need.

In a real-world R/R MCL cohort, zanubrutinib demonstrated significantly longer overall survival versus ibrutinib and favorable trends versus acalabrutinib, guiding clinical selection of covalent BTKis.

Adding ibrutinib to intensive frontline immunochemotherapy for newly diagnosed, fit MCL patients aims to deepen responses and improve outcomes, often as induction before transplant consolidation.

Zanubrutinib plus age-adapted bendamustine-rituximab induction followed by zanubrutinib maintenance demonstrates high efficacy (75% 2-year PFS) and deep responses (94% uMRD) in elderly, frontline MCL patients.

This meta-analysis suggests zanubrutinib monotherapy yields superior complete and overall response rates over ibrutinib and acalabrutinib in relapsed/refractory MCL, informing optimal BTKi selection.

This review provides a treatment and sequencing algorithm for relapsed/refractory MCL, navigating the complex landscape of BTKi, BCL2i, CAR-T, bispecifics, and transplant for individualized patient care.

This phase 2 study of frontline acalabrutinib, lenalidomide, and anti-CD20 demonstrates high molecular response rates (67-90%) and 76% 4-year PFS, supporting a time-limited, MRD-driven, chemotherapy-free treatment strategy.

In a retrospective ZUMA-2 analysis, prior ibrutinib exposure, versus acalabrutinib, improved brexu-cel CAR-T efficacy and PFS by inducing a more favorable cytotoxic T-cell phenotype.

This US real-world study describes treatment patterns and outcomes for covalent BTK inhibitors in relapsed/refractory MCL, providing crucial benchmarks for routine clinical practice outside of trial settings.

This case report identifies fingertip fissures as a rare dermatologic toxicity of ibrutinib in an elderly MCL patient, expanding the known adverse event profile for this common therapy.

This report summarizes the 2025 LRF MCL Workshop, highlighting key research developments in pathogenesis, resistance, and novel therapies, thereby setting the agenda for future clinical and translational research.

This real-world study shows bendamustine-rituximab is the most common frontline therapy and BTK inhibitors for second-line, but median overall survival plummets in later lines, highlighting significant unmet need.

The combination of acalabrutinib with bendamustine-rituximab is evaluated as a frontline therapy for elderly MCL patients, aiming to improve outcomes over standard chemoimmunotherapy.

A novel fluorescence-based assay quantifies pirtobrutinib in biological fluids, potentially enabling therapeutic drug monitoring to optimize dosing, manage toxicity, and study resistance in MCL patients.

Real-world data from an Italian compassionate use program confirms pirtobrutinib's efficacy in heavily pre-treated, relapsed/refractory MCL, including patients who have failed prior covalent BTK inhibitors.

This review summarizes cutaneous toxicities across different BTK inhibitors, highlighting the improved skin safety profile of newer agents, which is critical for managing long-term MCL therapy.

This review outlines the evolution of BTK inhibitors, highlighting how non-covalent agents like pirtobrutinib overcome C481-mediated resistance, extending the therapeutic sequence for relapsed/refractory MCL.

This review highlights the improved cardiovascular safety of next-generation BTK inhibitors over ibrutinib, which is critical for MCL treatment selection and long-term management of associated cardiac toxicities.

This preclinical mouse study shows zanubrutinib mitigates pulmonary fibrosis by inhibiting the Wnt/β-catenin pathway, a novel off-target mechanism potentially relevant to managing toxicities in MCL patients.

In the phase 3 TRIANGLE trial for young, fit MCL, adding ibrutinib to induction immunochemotherapy improves failure-free survival, with noninvasive genotyping confirming its efficacy and treatment dynamics.