Fenbendazole For Cancer

Fenbendazole for cancer is a new treatment method that has been developed by scientists in California. It works by disrupting cellular processes that cancer cells and many viruses use to grow and spread. This approach could help prevent the recurrence of some tumors and reduce the amount of chemotherapy needed to treat them. The research has been published in Science Translational Medicine.

Social media has made it easy for nonmedical individuals to disseminate information, including medical facts. However, the lack of quality control on social media sites makes it possible for unproven and potentially dangerous information to be circulated. This is particularly true when it comes to anticancer treatments. A case study reported in Scientific Reports illustrates the danger of social media-related health care misinformation.

A 80-year-old patient with advanced nonsmall cell lung cancer received pembrolizumab monotherapy and experienced severe liver injury 9 months later. The patient revealed to her family that she had self-administered fenbendazole for a month on the basis of online reports suggesting that it has antitumor activity. The patient discontinued the self-administration of fenbendazole and her liver function recovered.

Researchers have found that fenbendazole, a broad-spectrum benzimidazole anthelmintic drug, has potential to be repurposed as an anticancer agent. It is widely used to treat parasitic worms in animals such as horses. It binds to b-tubulin microtubule subunits, inhibiting their polymerization, and exerts anthelmintic effects. It also has antitumor activity in animal models.

To investigate its anticancer effect, fenbendazole was treated with 5-fluorouracil-resistant colorectal cancer (CRC) cell lines and assessed by cell viability, Western blot and flow cytometry assays. It was observed that fenbendazole caused G2/M arrest and apoptosis in both 5-FU-sensitive and resistant cells. Moreover, it induced autophagy in both cells through Beclin-1 expression. Additionally, it triggered ferroptosis and necroptosis in the resistant cells.

In order to understand the mechanism behind fenbendazole-induced cell death, researchers performed a proteomic analysis of colorectal cancer cells that were either mock treated or exposed to fenbendazole for 3 days. They identified a number of proteins that were affected by fenbendazole, and found that the drug induced apoptosis, cell cycle arrest, ER stress, phosphorylation of JNK and GTP-binding protein, and necroptosis in the cells. These results suggest that fenbendazole may be able to overcome resistance to conventional chemotherapy in CRC by enhancing apoptosis, necroptosis, and autophagy. Furthermore, apoptosis and necroptosis were augmented in cells with wild-type p53, whereas apoptosis was reduced in p53 mutant cells. Thus, a combination of p53-mediated apoptosis and ER stress induced autophagy might be more effective in treating colorectal cancer. However, further studies are needed to determine if this is the case in human patients. Currently, the most common treatment for CRC is chemotherapy. New approaches are needed to develop novel treatment strategies. These include the development of new compounds and combinations of existing ones. These should be evaluated in clinical trials to determine their effectiveness and safety in humans. Hopefully, these research findings will encourage doctors to consider alternative treatments as part of a comprehensive therapy regimen for their patients with this disease.

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