Results of the use of polyplatillen--a preparation consisting of sodium nucleinate (deoxyribonucleic acid) and cisplatin combined in the saline balanced solution by means of the original technique--in cancer of the ovaries (198 patients), liver (62), pancreas (35), lungs (12), stomach (5) are presented. Clearly pronounced specific activity of the preparation developed is noted.
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Mol Oncol
August 2024
Ph.D. Program for Cancer Biology and Drug Discovery, China Medical University and Academia Sinica, Taichung, Taiwan.
Bladder cancer poses a significant challenge to chemotherapy due to its resistance to cisplatin, especially at advanced stages. Understanding the mechanisms behind cisplatin resistance is crucial for improving cancer therapy. The enzyme glutathione S-transferase omega class 1 (GSTO1) is known to be involved in cisplatin resistance in colon cancer.
View Article and Find Full Text PDFBiomolecules
August 2023
Center of Excellence in Environmental Toxicology, Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia, PA 19104, USA.
High mobility group box 1 (HMGB1) is secreted from activated immune cells, necrotic cells, and certain cancers. Previous studies have reported that different patterns of post-translational modification, particularly acetylation and oxidation, mediate HMGB1 release and confer distinct extracellular HMGB1 signaling activity. Here we report that cisplatin but not carboplatin induces secretion of HMGB1 from human A549 non-small cell lung cancer (NSCLC) cells.
View Article and Find Full Text PDFInt J Biochem Cell Biol
September 2023
Department of Biomedical Sciences, Dong-A University, Busan 49315, Republic of Korea. Electronic address:
Cisplatin, a widely prescribed chemotherapeutic agent for treating solid tumors, induces DNA adducts and activates cellular defense mechanisms, including DNA repair, cell cycle checkpoint control, and apoptosis. Considering the circadian rhythmicity displayed by most chemotherapeutic agents and their varying therapeutic efficacy based on treatment timing, our study aimed to investigate whether the circadian clock system influences the DNA damage responses triggered by cisplatin in synchronized cells. We examined the DNA damage responses in circadian-synchronized wild-type mouse embryonic fibroblasts (WT-MEF; clock-proficient cells), cryptochrome1 and 2 double knock-out MEF (CRY; clock-deficient cells), and mouse hepatocarcinoma Hepa1c1c7 cells.
View Article and Find Full Text PDFInt J Mol Sci
February 2022
Chinese Medicine Research and Development Center, China Medical University Hospital, Taichung 404, Taiwan.
Aurora A kinase (Aurora A) is a serine/threonine kinase regulating control of multiple events during cell-cycle progression. Playing roles in promoting proliferation and inhibiting cell death in cancer cells leads Aurora A to become a target for cancer therapy. It is overexpressed and associated with a poor prognosis in ovarian cancer.
View Article and Find Full Text PDFSci Rep
September 2021
Department of Pharmacology and Toxicology, Wright State University Boonshoft School of Medicine, Dayton, OH, 45435, USA.
Nucleotide excision repair (NER) and cell cycle checkpoints impact the ability of the anti-cancer drug cisplatin to inhibit cell proliferation and induce cell death. Genetic studies have shown that both NER and cell cycle progression are impacted by the circadian clock, which has emerged as a novel pharmacological target for the treatment of various disease states. In this study, cultured human cell lines were treated with combinations of cisplatin and the circadian clock modulating compounds KS15 and SR8278, which enhance circadian clock transcriptional output by inhibiting the activities of the cryptochrome and REV-ERB proteins, respectively.
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