BCL2 (B-cell CLL/lymphoma 2)

Furthermore, •OH downregulated the antiapoptotic protein Bcl-2, collapsed the mitochondrial membrane potential, and promoted calcium influx into mitochondria, thereby inducing apoptosis. By integrating inorganic cocatalysis with the disruption of calcium signaling, this system overcomes the limitation of conventional CDT and presents an innovative multimodal strategy for tumor therapy.

In the present work, Tocophersolan (TPGS), a water-soluble form of natural Vitamin E, was evaluated as a targeting ligand for delivering the Bruton's Tyrosine Kinase (BTK) inhibitor, Ibrutinib (IBT), for breast cancer (BC) treatment...Results of in-silico study further supported the experimental findings, showing strong correlation with the observed in-vitro and in-vivo effects. Collectively, these results establish TPGS-liposomes as an efficient delivery platform that augments IBT's therapeutic potential in BC through both active and passive targeting.

Emerging therapeutic strategies targeting redox-sensitive nodes, including GPX4 degraders, mitophagy inducers (urolithin A) and chronotherapy, have the potential to overcome resistance. By elucidating the crosstalk between mitochondrial quality control and ferroptotic signaling, the present review provides a mechanistic framework for precision oncology in EC, emphasizing subtype-specific vulnerabilities and spatiotemporal redox profiling.

In conclusion, our findings suggest that c-Myc overexpression and MYC rearrangement are associated with ibrutinib resistance in MCL. Detecting MYC rearrangement in selected MCL cases could be critical for optimizing treatment strategies and improving patient outcomes.

Importantly, antimicrobial screening showed negligible activity against representative Gram-positive and Gram-negative strains, indicating a low risk of microbiota disruption - an important feature for cancer therapy. These findings position furanocoumarin derivatives, particularly compounds 4 and 6, as promising lead structures for the development of selective, microbiota-sparing anticancer agents.

Carfilzomib synergized with BCL2 family protein inhibitors (navitoclax or AZD5991), suggesting that drug combinations could be used to reduce the dose of each drug to minimize toxicity. Notably, thymic carcinomas differed from squamous cell carcinomas in other organs by higher levels of β5i (PSMB8) and constitutive proteasome β5 (PSMB5). We hypothesize that TC (and probably many TH) are uniquely suited for treatment with proteasome inhibitors alone or in combination with selective BH3 mimetics.

An intensification strategy guided by response and MRD deepened remissions in individuals with residual disease and spared early responders further treatment. This approach merits further study as an alternative to fixed-duration triplet therapy.

In summary, the dacarbazine-2-AEH2P combination exhibits synergistic pharmacodynamic activity that enhances cytotoxicity through coordinated modulation of proliferative and apoptotic pathways. These findings highlight its potential as a promising strategy to improve chemotherapeutic efficacy and overcome resistance in melanoma treatment.

P=N/A, N=1000, Active, not recruiting, French Innovative Leukemia Organisation | Recruiting --> Active, not recruiting | Trial primary completion date: Nov 2025 --> Apr 2025

The combination of the B-cell lymphoma 2 inhibitor venetoclax with CIT has emerged as a new first-line benchmark with promising response rates and overall survival...Pirtobrutinib has demonstrated responses even in heavily pretreated patients...For R/R disease, novel BTK inhibitors, bispecific antibodies, and cellular therapies are demonstrating substantial efficacy. Ongoing trials investigating combinations of these agents are poised to further transform RT management.

Docking studies confirmed their interaction with the colchicine-binding site of tubulin. Together, the results support further investigation of these compounds as microtubule-interacting agents with selective antiproliferative activity.

PINK1 acts as a tumor suppressor in colorectal cancer by inhibiting proliferation and migration, promoting apoptosis, and remodeling the epigenetic landscape through altering histone modifications and enhancing chromatin accessibility.