Varying the metal to ethacrynic acid ratio in ruthenium(ii)/osmium(ii)-p-cymene conjugates.
Varying the metal to ethacrynic acid ratio in ruthenium(ii)/osmium(ii)-p-cymene conjugates. J Inorg Biochem. 2017 Jul 28;175:198-207 Authors: Păunescu E, Soudani M, Clavel CM, Dyson PJ Abstract Following the identification of a ruthenium(II)-arene complex with an ethacrynic acid-modified imidazole ligand, which inhibits glutathione transferase (GST) and is cytotoxic to chemo-resistant cancer cells, a series of structurally related ruthenium(II)- and osmium(II)-p-cymene compounds have been prepared. In these complexes the ethacrynic acid is linked to the metals via appropriately modified pyridine ligands. The influence of the metal center and the metal:ethacrynic acid ratio on the cytotoxicity of the compounds was evaluated with the derivatives with one metal center and two ethacrynic acid moieties being the most potent against chemo-resistant A2780cisR cells (human ovarian cancer cells with acquired resistance to cisplatin). Moreover, compared to a complex with an ethacrynic acid-modified imidazole ligand (RAIMID-EA, Figure 2), these complexes display a significant degree of cancer cell specificity. PMID: 28779652 [PubMed - as supplied by publisher]
Objective: The incidence of melanoma is increasing. Other than limiting UV exposure, few factors prevent or reduce the risk of melanoma. The aim of this study is to evaluate the relationship between vitamin D intake and melanoma risk in the Prostate, Lung, Colorectal, and Ovarian (PLCO) cancer screening trial. Methods: A secondary data analysis was performed on PLCO data. More than 1,300 participants developed melanoma. Results: Melanoma risk may be increased among men within the highest quartile of vitamin D intake (HR 1.27, 95% CI 0.99, 1.61). Women in the highest quartile of vitamin D intake had a decreased risk...
Contributor : Michael J TopperSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTriple negative breast cancer and ovarian cancer cells were treated with Azacitidine, Talazoparib, or combination for a period of 10 days to assess global transcriptional response. The focus of these transcriptional studies were on the assessment of DNA repair and immune pathway alteration.
AbstractRelevanceIvermectin, as an old anti-parasite drug, can suppress almost completely the growth of various human cancers, including ovarian cancer (OC). However, its anticancer mechanism remained to be further studied at the molecular levels. Ivermectin-related molecule-panel changes will serve a useful tool for its personalized drug therapy and prognostic assessment in OCs.PurposeTo explore the functional significance of ivermectin-mediated lncRNA-EIF4A3-mRNA axes in OCs and ivermectin-related molecule-panel for its personalized drug therapy monitoring.MethodsBased on our previous study, a total of 16 lncRNA expressi...
Publication date: Available online 26 May 2020Source: Life SciencesAuthor(s): Delu Dong, Yuan Dong, Jiaying Fu, Shengyao Lu, Chunli Yuan, Meihui Xia, Liankun Sun
Publication date: Available online 26 May 2020Source: Gynecologic Oncology ReportsAuthor(s): Michelle Marinone, Eliza Shrestha, Anita Thapa, Ruhee Tuladar, Dorothy B. Wakefield, Linus Chuang
Conclusions: The incidence of BM among patients with gynecologic malignancies is rare and associated with poor survival. For select patients, SRS may be associated with prolonged survival.
(Hubrecht Institute) Researchers from the group of Hans Clevers at the Hubrecht Institute have modeled the development and progression of high-grade serous ovarian cancer in mini-versions, or organoids, of the female reproductive organs of the mouse. They found that the cells of the oviduct, the equivalent of fallopian tubes in humans, are more prone to develop into tumors than the ovarian surface epithelium, the outer layer of the ovaries. This may influence future changes in preventive treatment.
We report that the loss of 4.1N correlated with progress in clinical stage, as well as poor survival in EOC patients. The loss of 4.1N induces EMT in adherent EOC cells and its expression inhibits anoikis resistance and EMT by directly binding and accelerating the degradation of 14-3-3 in suspension EOC cells. Furthermore, the loss of 4.1N could increase the rate of entosis, which aggravates cell death resistance in suspension EOC cells. Moreover, xenograft tumors in nude mice also show that the loss of 4.1N can aggravate peritoneal dissemination of EOC cells. Single-agent and combination therapy with a ROCK inhibitor and ...
Volume 48, Issue 1, December 2020, Page 824-833 .