MCL Literature Feed
267 papers on mantle cell lymphoma from PubMed. Updated daily.
This preclinical study identifies that the miR-17-92 cluster suppresses the tumor suppressor BTG2, leading to B-cell receptor signaling overactivation and suggesting BTG2 as a prognostic biomarker.
PLSCR1 induction by retinoic acid/interferon-α enhances immunogenic cell death in MCL, improving the efficacy of dendritic cell-based vaccines by boosting anti-tumor T-cell responses in vitro.
SOX11 expression in cyclin D1-negative large B-cell neoplasms defines them as a variant of blastoid MCL, not DLBCL, solidifying SOX11 as a crucial diagnostic marker for aggressive MCL.
This preclinical study identifies the protease SENP3 as a novel driver of MCL proliferation via the Wnt10a signaling pathway, presenting SENP3 as a potential new therapeutic target.
Optical genomic mapping (OGM) identifies rare CCND1 rearrangements, securing an MCL diagnosis in atypical CD5-negative, non-nodal cases that mimic other indolent B-cell lymphomas.
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This retrospective study of 134 patients demonstrates that adding a BTK inhibitor to chemotherapy improves efficacy and prolongs progression-free survival in relapsed/refractory MCL.
Preclinically, chlorambucil and ibrutinib show synergistic apoptosis in an MCL cell line, suggesting a novel chemo-BTKi combination strategy potentially mediated by inhibiting the AKT signaling pathway.
A novel BRAF N581S mutation was identified in mantle cell lymphoma, expanding the known genomic landscape and suggesting a potential new therapeutic target for this rare patient subset.
An MRD-driven, finite-duration venetoclax-lenalidomide-rituximab regimen is effective in relapsed/refractory MCL, even post-BTKi, allowing nearly half of patients to stop therapy and maintain durable molecular remissions.
The deubiquitinase USP35 stabilizes CXCR3 protein expression in MCL cells, promoting oncogenic signaling via JAK/STAT and c-Myc, identifying the USP35-CXCR3 axis as a novel therapeutic target.
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Upregulation of the mTOR pathway drives acquired resistance to PRMT5 inhibitors in preclinical MCL models; combining with an mTOR inhibitor like temsirolimus overcomes this resistance and improves survival.
Final overall survival data from a phase 2 trial confirm durable responses to acalabrutinib monotherapy in relapsed/refractory MCL, including in patients with poor prognostic features.
Combining the MCL35 gene signature with s-MIPI and blastoid cytology powerfully risk-stratifies older, frontline MCL patients receiving bendamustine-rituximab, identifying a dismal prognosis subgroup.
A machine learning algorithm accurately classifies MCL versus other B-cell lymphomas using standard peripheral blood flow cytometry data, offering a tool to standardize and accelerate initial diagnosis.
This dual-center retrospective analysis of 20 patients with blastoid MCL characterizes its clinical features and prognosis, adding to the limited evidence base for this aggressive subtype.
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A preclinical prostate cancer model shows Bortezomib resistance is driven by autophagy induction and reduced oxidative stress, suggesting potential combination strategies with autophagy inhibitors for MCL.
This case of blastoid MCL with aberrant CD10 expression highlights a rare immunophenotype, creating a diagnostic pitfall that can mimic other aggressive B-cell lymphomas.
This review identifies the lncRNA LINK-A as an upregulated oncogene in MCL, presenting it as a potential biomarker and therapeutic target involved in oncogenic pathways and therapy resistance.
A novel SRC-3 inhibitor, SI-10, demonstrates preclinical efficacy in ibrutinib-resistant MCL models, identifying SRC-3 as a potential therapeutic target to overcome BTKi resistance.
This review identifies the lncRNA ROR1-AS1 as a pro-oncogenic factor in mantle cell lymphoma, suggesting it may serve as a novel biomarker or therapeutic target.
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This case report describes a rare transformation of CD5-negative MCL into an EBV-positive pleomorphic variant, highlighting a potential role for EBV in aggressive disease progression and diagnosis.
This preclinical study identifies a novel STAT5B-DCAF13-p53/xCT pathway that suppresses ferroptosis to promote MCL progression, revealing ferroptosis induction as a potential new therapeutic strategy.
This single-center retrospective study characterizes the aggressive clinical and pathological features of blastoid MCL, underscoring its diagnostic challenges and the need for novel therapeutic approaches for this high-risk subtype.
Magnetic Resonance Spectroscopy (MRS) can non-invasively detect metabolic changes, like lactate and alanine, offering an early biomarker to predict response or resistance to BTK inhibitors in MCL.
This study shows ROR1 is heterogeneously expressed in 44% of MCL tumors, indicating that patient selection will be critical for developing ROR1-targeted therapies like ADCs or CAR-T.
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A novel 7-gene signature linked to ferroptosis predicts overall survival in MCL, identifying high-risk patients and suggesting potential new therapeutic targets like the MEK inhibitor Trametinib.
In a real-world cohort including MCL, the Hematotox-Score predicted early cytopenias post-CAR-T but not survival, underscoring the need for improved prognostic tools for toxicity management.