Fenbendazole is a widely used anti-parasitic drug with potential cancer-related activity. However, its effect on cell cycle and mitosis is complex, and its mode of action is unclear. Inhibition of tubulin polymerization is thought to interfere with cyclin B1 binding to CDK1 and trigger mitotic catastrophe, but the precise mechanism of action is unknown. To address this issue, we tested the effects of fenbendazole on cell-cycle progression in a mouse tumor model. We found that three daily i.p. injections of fenbendazole did not inhibit the growth of either unirradiated or irradiated EMT6 tumors, and the growth curve was indistinguishable from that of controls. In addition, fenbendazole did not alter the radiation dose-response curve of unirradiated tumors or docetaxel in combination with fenbendazole.
Focus group interviews were conducted with 21 lung cancer patients undergoing treatment for cancer stages one to four and divided into three categories: 1) acquisition channel of general and false information, 2) quality of obtained information and 3) perception toward information. Results showed that patients acquired information from a variety of channels step by step, but the majority of the false and general information came from TV followed by YouTube. They were more likely to actively search for complementary and alternative medicine information, but perceived that this information needed to be verified by experts before it could be deemed credible.
The hypoxic sensitivity of EMT6 cells was examined by treating the cultures with fenbendazole for 2 or 24 h, then irradiating them under aerobic or hypoxic conditions and assaying cell survival using a colony formation assay. Survivals (yield-corrected surviving fraction) were shown to be significantly reduced in the hypoxic culture treated for 24 h with fenbendazole, but this reduction was not seen in the 2-h fenbendazole treatment. fenbendazole cancer