Fenbendazole For Humans Cancer

Fenbendazole is a broad-spectrum antiparasitic agent which acts by blocking the synthesis of mitotic spindles and preventing the polymerization of tubulin, the component of microtubules that make up the cytoskeleton and give shape to cells. Microtubules are a target of a number of cytotoxic and radiosensitizing agents, including the vinca alkaloids (vinblastine, vindesine, and vinorelbine) and the taxanes (paclitaxel and docetaxel).

A patient with advanced nonsmall cell lung cancer received information about the antitumor effects of self-administration of fenbendazole from social media and, on this basis, decided to supplement her chemotherapy regimen with this anthelmintic drug. However, self-administration of this drug may increase the risk of adverse events.

Social networking sites facilitate the rapid spread of medical information, including unproven therapies, to large numbers of individuals. This has the potential to contaminate medical practice and may result in patients receiving unnecessary and potentially harmful treatments.

The use of fenbendazole, a member of the benzimidazole family, as an alternative or supplementary treatment for cancer has been reported in several studies, but clinical trials are rare. One study reported that fenbendazole significantly reduced tumor growth and decreased metastasis when administered with chemotherapy to patients with metastatic colon cancer and hepatocellular carcinoma (HCC). However, these data have not been confirmed in other studies and this approach is controversial.

Another study reported that fenbendazole, in combination with paclitaxel, significantly improved the survival of patients with metastatic HCC who received doxorubicin and cyclophosphamide as first-line therapy. This improvement was associated with the increased sensitivity of the cancer to paclitaxel and to a reduction in the rate of chemotherapy-related neutropenia.

Our laboratory recently evaluated the radiosensitizing effects of fenbendazole in the EMT6 mouse mammary tumor in cell culture and as solid tumors in mice. Treatment of these tumors with fenbendazole in the absence and in the presence of radiation resulted in dose-dependent increases in cell death, and the effect was maintained when cultures were exposed to hypoxia.

In addition, fenbendazole did not alter the radiation dose-response curves of aerobic or hypoxic cells when the cells were treated with graded doses of radiation in the presence and absence of fenbendazole and assayed for clonogenicity. This observation was consistent with our earlier findings that fenbendazole does not modify the radiation response of aerobic or hypoxic cells in cell culture.

We also examined the effects of fenbendazole on the radiation responses of EMT6 cells in vitro and as solid tumors in mice after irradiation. These experiments showed that fenbendazole, at concentrations up to 10 mM, did not alter the radiation dose-response of cells when exposed to hypoxia and when combined with docetaxel in maximally intensive regimens. The survival curves for these two drugs were superimposed and, when normalized to account for the toxicity of fenbendazole, indicated that fenbendazole and docetaxel produced additive toxicities. This additive toxicity was confirmed by isobologram analyses. These data suggest that the benzimidazole anthelmintic drug fenbendazole has potential as an alternative or supplementary radiosensitizer in cancer therapy, especially in conditions of severe hypoxia. fenbendazole for humans cancer

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