CAST (Calpastatin)

It repressed the release of mitochondrial cytochrome c and apoptosis-inducing factor (AIF) to hinder caspase-dependent and caspase-independent apoptotic neuronal death. Oxytocin could be a promising candidate for HD management by hampering both mitochondrial and non-mitochondrial apoptosis through inhibition of calpain-2/p25 Cdk5/MEF-2 pathway.

Finally, cells with high levels of TXNIP expression displayed increased susceptibility to IL-24 and WP1066, a specific STAT3 inhibitor, suggesting possible predictive value for TXNIP. Collectively, these findings unveil novel TXNIP-dependent pathways that may contribute to breast cancer pathogenesis, enriching our understanding of this molecule's intricate role in cancer and potentially paving the way for clinical translation.

Gene and protein expression proved a downregulation of MAPK, VEGF/VEGFRs, and Bcl-2, and an upregulation of caspases and Bax-family mediators. Overall, the differential expression of calpains and their correlation with patient survival suggest a novel promising target pathway, whose blockade showed encouraging results toward precision medicine strategies.

Transfection of hcast 3-25-V5 into two selected GSCs indicated that hcast 3-25 effectively associates with calpains, supporting the digestion of selected calpain targets. Hcast 3-25 possibly affects the stem state promoting a differentiated, less aggressive phenotype.

Our results highlight transcriptomic similarities and differences in ET patients according to the degree of maturation of the malignant clone and the type of mutation. The genes and processes altered in both CD34 + cells and mature neutrophils may reveal altered sustained processes that could be studied as future therapeutic targets for ET patients.

We present the case of a patient with germline CHEK2-mutated metastatic castration-resistant prostate cancer (mCRPC) who responded to bipolar androgen therapy (BAT) combined with pembrolizumab after progressing through multiple lines of therapy...Single case report outcomes should not be used as evidence of efficacy for treatment regimes. Our case supports further investigation into BAT plus immunotherapy for patients with DNA repair-deficient mCRPC.

P3, N=1207, Active, not recruiting, Aragon Pharmaceuticals, Inc. | Trial completion date: Nov 2022 --> Oct 2023

P1, N=6, Active, not recruiting, Aragon Pharmaceuticals, Inc. | Trial completion date: Sep 2022 --> Jun 2023

P1, N=10, Recruiting, University of Kansas Medical Center | Not yet recruiting --> Recruiting

P1, N=3, Terminated, Pharmicell Co., Ltd. | N=10 --> 3 | Trial completion date: Dec 2022 --> Feb 2022 | Recruiting --> Terminated | Trial primary completion date: Dec 2022 --> Feb 2022; Difficult recruitment