Tag results:
ABT-199
Hematopoiesis News
Lipase-Triggered Drug Release from BCL2 Inhibitor ABT-199-Loaded Nanoparticles to Elevate Anti-leukemic Activity through Enhanced Drug Targeting on the Mitochondrial Membrane
[Acta Biomaterialia] Researchers compared the anti-leukemic ability of pure ABT-199 and PEG-ABT-199 in vitro and in vivo.
Hematopoiesis News
Hydroquinone Destabilizes BIM mRNA through Upregulation of p62 in Chronic Myeloid Leukemia Cells
[Biochemical Pharmacology] Investigators proposed a mechanism by which hydroquinone induced the malignant progression of chronic myeloid leukemia cells.
Immune Regulation News
Venetoclax Imparts Distinct Cell Death Sensitivity and Adaptivity Patterns in T Cells
[Cell Death & Disease] Scientists focused on the BCL-2 specific inhibitor venetoclax and its effects following short-term and long-term BCL-2 blockade on T cell subsets.
Intestinal Cell News
Effect of ABT-263 on Intestinal Fibrosis in Human Myofibroblasts, Human Intestinal Organoids, and the Mouse Salmonella typhimurium Model
[Inflammatory Bowel Diseases] Scientists evaluated the proapoptotic and antifibrotic efficacy of several classes of BH-3 mimetics in two in vitro fibrogenesis models. The candidate molecule, ABT-263, was advanced to a 3D human intestinal organoid model.
Cancer Stem Cell News
Combining Radiation to EGFR and Bcl-2 Blockade: A New Approach to Target Cancer Stem Cells in Head and Neck Squamous Cell Carcinoma
[Journal of Cancer Research and Clinical Oncology] CSCs had low EGFR expression and, conversely, overexpressed the anti-apoptotic Bcl-2 protein, which is involved in resistance to apoptosis and the invasion/migration capacities of tumor cells.
Dermal Cell News
Dasatinib Stimulates Its Own Mechanism of Resistance by Activating a CRTC3/MITF/Bcl-2 Pathway in Melanoma with Mutant or Amplified C-Kit
[Molecular Cancer Research] Researchers showed that, dasatinib in melanoma stimulated its proper mechanism of resistance, independently of MAPK and PI3K/AKT pathway reactivation commonly associated to secondary c-Kit mutations, but through CRTC3/MITF/Bcl-2 pathway activation at clinically relevant doses.