MCL Literature Feed

Overexpression of IL-16 drives BTKi resistance via the CD9/NF-κB/AKT axis in MCL models, presenting a novel therapeutic target to overcome treatment failure and restore drug sensitivity.

High p62 expression predicts poor survival in MCL by upregulating CCND1 transcription via Nrf2, identifying p62 as a novel prognostic biomarker and potential non-BTK/BCL2 therapeutic target.

A novel single-cell genomic research model tracks MCL clonal evolution, providing a high-resolution tool to dissect mechanisms of therapeutic resistance and identify potential new targets.

This review synthesizes mechanisms of BTKi resistance and highlights next-generation strategies like noncovalent BTKi and PROTACs to overcome this critical challenge in relapsed/refractory MCL.

The novel TBL1X inhibitor tegavivint induces DNA damage and synergizes with PARP inhibitors in preclinical MCL models, establishing TBL1X as a new therapeutic target for genomic instability.

This preclinical study reveals bortezomib, unlike carfilzomib, induces unique multi-organelle stress in endothelial cells, providing a specific mechanism for its cardiovascular toxicity relevant to MCL patients.

The protein TRIM24 regulates autophagy-mediated resistance to the proteasome inhibitor bortezomib, offering a potential new therapeutic target to overcome drug resistance 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.

A novel Mcl1-degrading AUTAC compound synergizes with proteasome inhibitors by hijacking the adaptive autophagy response, offering a preclinical strategy to overcome proteasome inhibitor resistance in MCL.

In MCL cells, the RNA processing factor NUDT21 undergoes alternative polyadenylation to evade miRNA-mediated suppression, revealing a novel mechanism of gene regulation that could be a future therapeutic target.

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.

A novel electrochemical sensor was developed for highly sensitive bortezomib detection, potentially enabling therapeutic drug monitoring to personalize dosing and manage toxicity in MCL patients.

This review of PROTAC design outlines a novel protein degradation technology with potential to overcome resistance to targeted therapies like BTK inhibitors in mantle cell lymphoma.

Bioinformatic analysis reveals a positive correlation between STING expression and cytolytic score in MCL, suggesting STING may be a biomarker for immune activity and a potential immunotherapy target.

The novel agent Ironomycin induces MCL cell death by targeting iron metabolism addiction, identifying a potential new therapeutic strategy based on a metabolic vulnerability.

Preclinical Galectin-9 induces cell death in MCL cell lines by disrupting autophagy, a novel, apoptosis-independent mechanism to potentially overcome chemoresistance.

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.

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.

This CLL study reveals venetoclax rapidly activates a BAFF-driven survival axis in residual tumor cells, a key resistance mechanism potentially targetable in MCL to deepen BCL2i responses.

This preclinical study explains bortezomib-induced pulmonary toxicity, showing it increases endothelial RhoA/RhoC proteins, which synergize with inflammation to cause vascular hyperpermeability and capillary leak syndrome.

This preclinical, biophysical study characterizes bortezomib's binding to serum albumin, providing fundamental pharmacokinetic data with no direct clinical implications for treating MCL patients.

A novel nanostructured lipid carrier (NLC) formulation increased ibrutinib's oral bioavailability by 1.82-fold in a rat model, suggesting a potential strategy to enhance drug delivery and efficacy.

A novel αCD20-EndoP125A antibody fusion protein inhibits MCL growth and dissemination in preclinical models by disrupting tumor-vessel interactions, including angiogenesis, lymphangiogenesis, and vessel co-option.

Preclinically, bortezomib-induced apoptosis depends exclusively on the protein NOXA, which inactivates both MCL-1 and BCL-XL, providing a refined understanding of its mechanism and potential resistance.

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.

Longitudinal single-cell analysis of refractory MCL reveals co-evolving tumor heterogeneity and immune evasion, providing a roadmap for overcoming treatment resistance and identifying new therapeutic targets.

This preclinical study identifies a novel CERS6-AS1/FGFR1 axis driving stromal-supported MCL proliferation and stemness, suggesting that co-targeting nucleolin and FGFR1 could overcome microenvironment-mediated resistance.

This CML review details targeting the ubiquitin-proteasome system to overcome TKI resistance, offering a potential mechanistic strategy for addressing BTKi resistance in MCL.