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Targeting of the G9a, DNMT1 and UHRF1 epigenetic complex as an effective strategy against pancreatic ductal adenocarcinoma.
J Exp Clin Cancer Res
January 2025
Hepatology Laboratory, Solid Tumors Program, CIMA, CCUN, University of Navarra, Pamplona, Spain.
Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with limited treatment options and a poor prognosis. The critical role of epigenetic alterations such as changes in DNA methylation, histones modifications, and chromatin remodeling, in pancreatic tumors progression is becoming increasingly recognized. Moreover, in PDAC these aberrant epigenetic mechanisms can also limit therapy efficacy.
View Article and Find Full Text PDFPhosphorylation of Bok at Ser-8 blocks its ability to suppress IPR-mediated calcium mobilization.
Cell Commun Signal
January 2025
Department of Pharmacology, SUNY Upstate Medical University, Syracuse, NY, 13210, USA.
Background: Bok is a poorly characterized Bcl-2 protein family member with roles yet to be clearly defined. It is clear, however, that Bok binds strongly to inositol 1,4,5-trisphosphate (IP) receptors (IPRs), which govern the mobilization of Ca from the endoplasmic reticulum, a signaling pathway required for many cellular processes. Also known is that Bok has a highly conserved phosphorylation site for cAMP-dependent protein kinase at serine-8 (Ser-8).
View Article and Find Full Text PDFElectronic structure modulation of ultrathin PtRuMoCoNi high-entropy alloy nanowires for boosting peroxidase-like activity and sensitive colorimetric determination of isoniazid and hydrazine.
Mikrochim Acta
January 2025
Department of General Surgery, Hui Ya Hospital of The First Affiliated Hospital, Sun Yat-Sen University, Huizhou, 516081, Guangdong, China.
Self-supported ultrathin PtRuMoCoNi high-entropy alloy nanowires (HEANWs) were synthesized by a one-pot co-reduction method, whose peroxidase (POD)-like activity and catalytic mechanism were elaborated in detail. As expected, the PtRuMoCoNi HEANWs showed excellent POD-like activity. It can quickly catalyze the oxidization of colorless 3,3',5,5'-tetramethylbenzidine (TMB) to blue TMB through decomposition of HO to superoxide radicals.
View Article and Find Full Text PDFOrphan nuclear receptor NR2E3 is a new molecular vulnerability in solid tumors by activating p53.
Cell Death Dis
January 2025
Center for Precision Medicine Research, Marshfield Clinic Research Institute, Marshfield Clinic Health System, Marshfield, WI, USA.
The orphan nuclear receptor NR2E3 has emerged as a potential tumor suppressor, yet its precise mechanisms in tumorigenesis require further investigation. Here, we demonstrate that the full-length protein isoform of NR2E3 instead of its short isoform activates wild-type p53 and is capable of rescuing certain p53 mutations in various cancer cell lines. Importantly, we observe a higher frequency of NR2E3 mutations in three solid tumors compared to the reference population, highlighting its potential significance in tumorigenesis.
View Article and Find Full Text PDFApplication of thrombopoietic agents in cancer therapy-induced thrombocytopenia: A comprehensive review.
Blood Rev
January 2025
State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, RenJi Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200032, China; Department of Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China. Electronic address:
Cancer therapy-induced thrombocytopenia (CT-IT) is one of the most common hematological toxicities of anti-cancer therapy, often leading to treatment dose reduced, postponed, or treatment plans altered or even discontinued. Thrombopoietin (TPO) is the only key regulatory factor in platelet production, and TPO receptor is considered an ideal target for the treatment of thrombocytopenia. Thrombopoietic agents, including recombinant human thrombopoietin (rhTPO) and thrombopoietin receptor agonists (TPO-RAs), bind to different regions of the TPO receptor, activating downstream signaling pathways to increase platelet levels.
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