MCL Literature Feed
12 papers on mantle cell lymphoma from PubMed. Updated daily.
Preclinical data shows that inhibiting the cell cycle regulator CDC20 suppresses MCL growth by downregulating the PI3K/AKT pathway, identifying CDC20 as a novel therapeutic target.
The oral AKT inhibitor capivasertib showed modest single-agent activity (30% ORR) in relapsed/refractory MCL, with PTEN deficiency emerging as a potential predictive biomarker for patient selection.
This study evaluates the novel, chemotherapy-free combination of PI3Ki copanlisib and BCL2i venetoclax as a new targeted therapy for patients with relapsed/refractory mantle cell lymphoma.
A novel dual PI3K/HDAC inhibitor demonstrates enhanced pro-apoptotic activity in lymphoma cells, presenting a potential new preclinical strategy for MCL by simultaneously targeting two key pathways.
Preclinical data show CBX5 loss drives PI3Kδ inhibitor resistance in MCL, which is reversed by propolis-derived CAPE via induction of CBX5-mediated ferroptosis, a novel therapeutic strategy.
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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.
Preclinical data shows the TKI anlotinib inhibits MCL proliferation by targeting the PI3K/AKT/mTOR pathway and modulates the tumor microenvironment, identifying a potential new oral therapy for MCL.
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.
Preclinical models show the PI3K inhibitor idelalisib synergizes with the CDK4/6 inhibitor palbociclib, providing a rationale for a novel combination therapy in relapsed/refractory MCL.
This commentary discusses the zandelisib (PI3Ki) plus zanubrutinib (BTKi) combination, suggesting a potential role for newer, potentially less toxic PI3K inhibitors in relapsed/refractory MCL.
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The PI3Ki zandelisib plus BTKi zanubrutinib combination shows high efficacy (74% ORR, 47% CR) with manageable toxicity in relapsed/refractory MCL, offering a promising chemotherapy-free regimen.
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.