MCL Literature Feed

A case of TP53-mutated, indolent non-nodal MCL suggests this high-risk marker may not mandate immediate therapy in this specific subtype, supporting a watch-and-wait approach.

This review synthesizes clinical, molecular, and genomic markers to define high-risk MCL, guiding risk-stratified treatment and highlighting future therapies like bispecifics for this poor-prognosis population.

This review advocates for using prognostic tools like MIPI and TP53 status to guide risk-adapted therapy in MCL, intensifying for high-risk and de-escalating for low-risk patients.

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.

The Australasian Lymphoma Alliance provides consensus guidelines for MCL diagnosis and management, integrating novel therapies and risk-stratification using biomarkers like TP53, blastoid morphology, and high Ki67.

This review highlights that TP53-mutated MCL represents a distinct high-risk entity with poor outcomes to chemoimmunotherapy, underscoring the urgent need for novel, non-chemotherapy frontline approaches in these patients.

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.

Analysis of European MCL Network trial data shows specific gene mutations predict patient outcomes, providing a genetic basis for risk stratification to guide therapy selection beyond clinical scores.

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.

Preclinical data shows the novel CTPS1 inhibitor STP-B has single-agent activity in high-risk MCL (blastoid, TP53-mutated) and synergizes with venetoclax by downregulating MCL1, offering a new combination strategy.

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.

This review explains MCL's clinical heterogeneity through distinct molecular subtypes and genomic alterations like TP53, which serve as key prognostic biomarkers and guide development of novel therapies.

This large Chinese retrospective study of blastoid/pleomorphic MCL links progression of disease within 12 months (POD12) to a distinct mutation profile (TP53, SMARCA4) and poor prognosis.

This review synthesizes current knowledge on MCL genetic markers, advocating for a personalized medicine approach that integrates molecular profiles like TP53 to improve risk stratification and guide therapy.

This review positions allogeneic transplant as a key curative option for high-risk (e.g., TP53-mutated) and relapsed/refractory MCL, despite its changing role with the advent of novel therapies.

A rare, non-nodal MCL case with hairy cell-like features and a TP53 mutation showed an indolent course, challenging prognostic assumptions and emphasizing comprehensive genomic and pathologic evaluation.

A transplant-sparing frontline regimen of lenalidomide-R-CHOP/R-HiDAC showed favorable outcomes in TP53 wild-type high-risk MCL, but not TP53-mutated MCL, reinforcing the prognostic power of sequential MRD monitoring.

MCL with concurrent EZH2 expression and TP53 mutation is frequent and identifies a patient subgroup with a dismal outcome, establishing a powerful negative prognostic biomarker combination.

This review summarizes fundamental MCL characteristics, including the t(11;14) translocation and key high-risk features (high Ki67, blastoid variant, TP53 mutation) essential for patient risk stratification.

Real-world UK data show first-line ibrutinib is effective and tolerable for older MCL patients, but high-risk subgroups (TP53-mutated, blastoid) have significantly inferior survival, highlighting an unmet need.

Combining time-limited ibrutinib with CTL019 CAR-T in relapsed/refractory MCL achieved an 80% CR rate with manageable toxicity, showing efficacy even in BTKi-pretreated and TP53-mutated patients.

This review summarizes the evolution of MCL treatment, focusing on BTK inhibitor efficacy, toxicity, and their role in enabling personalized therapeutic strategies based on patient and disease factors.

This review summarizes the evolving Japanese MCL treatment landscape, highlighting novel therapies like BTKi, BCL2i, and CAR-T to address resistance in high-risk subsets like TP53-mutated and blastoid.