MCL Literature Feed

The chemotherapy-free triplet of acalabrutinib (BTKi), umbralisib (PI3Ki), and ublituximab (anti-CD20) achieved high response and MRD-negativity rates in untreated MCL, presenting a novel frontline option.

Ibrutinib monotherapy rapidly resolved bilateral intraocular MCL recurrence presenting as pseudo-uveitis and glaucoma, demonstrating its efficacy in this rare CNS sanctuary site relapse.

This review details the evolution of BTK inhibitors from discovery to clinical use in MCL, covering first-generation agents like ibrutinib and newer agents designed to overcome resistance.

This review summarizes the evolution of BTK inhibitors, highlighting how next-generation agents like pirtobrutinib offer improved selectivity, reduced toxicity, and options to overcome resistance in MCL.

A rare case of co-existing CNS DLBCL and systemic MCL was successfully treated with a multi-modal approach including chemotherapy, ibrutinib bridging, and autologous transplant, achieving 3-year remission.

In high-risk, relapsed/refractory MCL, real-world data shows BTKi plus venetoclax is highly effective, with no added survival benefit from an anti-CD20 monoclonal antibody.

In a small real-world study of 38 relapsed/refractory MCL patients, zanubrutinib was associated with fewer select adverse events like hypertension and hemorrhage compared to acalabrutinib.

Combining acalabrutinib with bendamustine-rituximab is safe and highly active, achieving a 78% complete response rate and unreached median progression-free survival at 47.6 months in treatment-naive mantle cell lymphoma.

This review outlines emerging therapeutic strategies, including non-covalent BTKis, CAR-T, and bispecifics, for managing the clinically challenging population of MCL patients relapsing after covalent BTK inhibitors.

This review summarizes how BTKi integration into frontline therapy (TRIANGLE trial) challenges the role of transplant, while CAR-T cells are established as the best option after BTKi failure.

Brexu-cel CAR-T therapy induced a durable 15-month complete remission in a rapidly progressing, relapsed/refractory MCL patient post-BTKi, highlighting its efficacy despite manageable rare cardiovascular toxicities.

This case report illustrates the efficacy of CAR-T therapy in a relapsed/refractory MCL patient who progressed after both autologous transplant and BTK inhibitor treatment, reinforcing its clinical value.

Long-term follow-up of the Philemon trial confirms durable responses for the chemotherapy-free triplet of ibrutinib, lenalidomide, and rituximab in relapsed/refractory MCL.

This modeling study in CLL suggests lower ibrutinib doses (140-280mg) maintain full BTK occupancy, implying potential for dose reduction to manage toxicity in MCL patients without compromising efficacy.

This preclinical CLL study validates 5-lipoxygenase inhibitors for disrupting tumor-microenvironment adhesion, reinforcing this novel mechanism, previously identified by the authors, as a potential therapeutic strategy for MCL.

A new laboratory method was developed to measure pirtobrutinib in rat plasma, providing a foundational tool for preclinical pharmacokinetic studies essential for this BTKi's clinical development.

This review summarizes current and emerging therapies for relapsed/refractory MCL, highlighting key strategies like BTKi/BCL2i combinations, CAR-T, and bispecific antibodies for this poor-prognosis population.

An MCL patient on ibrutinib had persistent COVID-19 missed by nasopharyngeal swabs but diagnosed via bronchoalveolar lavage, underscoring the need for deeper sampling in immunosuppressed patients.

Real-world data show BTKi refractoriness and poor in-vivo brexu-cel expansion predict worse survival, identifying high-risk patients for early relapse and highlighting CAR-T kinetics as a key biomarker.

This review summarizes how second-generation BTK inhibitors like zanubrutinib offer improved target selectivity and tolerability over first-generation agents, providing a potentially safer therapeutic option for MCL patients.

In relapsed/refractory MCL, the phase 3 SYMPATICO trial established ibrutinib plus venetoclax as superior to ibrutinib alone, significantly improving median progression-free survival by nearly 10 months.

The chemotherapy-free BOVen regimen (zanubrutinib, obinutuzumab, venetoclax) shows high efficacy (88% CR) and deep MRD negativity in previously untreated, high-risk TP53-mutated MCL, a historically chemo-refractory population.

A real-world Japanese study identified BTK inhibitor-based therapy and length of hospitalization as the main drivers of increased healthcare costs, providing crucial data for health economic planning.

Pirtobrutinib achieves an 81% overall response rate in MCL patients intolerant to prior covalent BTKis, offering a well-tolerated sequential option to maintain effective BTK pathway inhibition.

This meta-analysis of tirabrutinib monotherapy in relapsed/refractory B-cell lymphomas, including MCL, shows a pooled 72.5% overall response rate with manageable neutropenia and skin-related toxicities.

This case report describes an MCL diagnosis in a patient with mucous membrane pemphigoid, where frontline acalabrutinib and rituximab resolved both conditions, suggesting a paraneoplastic link.

This preclinical rat study shows the antifungal posaconazole increases zanubrutinib plasma exposure, highlighting a significant drug-drug interaction that may necessitate dose adjustments in MCL patients to avoid toxicity.

A case of ganciclovir-resistant CMV encephalitis in a pirtobrutinib-treated MCL patient highlights a rare but severe infectious complication, urging vigilance for CNS symptoms with this non-covalent BTKi.

Ibrutinib oral suspension has comparable bioavailability to tablets/capsules and is compatible with enteral tubes, providing a crucial administration option for MCL patients with dysphagia or requiring tube feeding.

The novel, chemotherapy-free triplet of alisertib, ibrutinib, and rituximab demonstrates clinical activity in MCL, providing a new therapeutic strategy for likely relapsed/refractory patients.