Abstract
Although clinical trials have not been completed, it has already been confirmed that mebendazole, a well-known anti-parasitic drug widely used in the tropical areas, inhibits cancer cell growth. Preclinical studies show that mebendazole notably impedes the growth of malignant and metastatic tumors such as osteosarcoma and soft tissue sarcoma, melanoma, carcinoma (lung, colorectal, breast, ovarian, hepatocellular and adrenocortical), acute myeloid leukaemia, glioblastoma multiforme and meduloblastoma. Mebendazole can induce the depolymerization of microtubules in neoplasms and newly formed vasculature, stopping tumor growth and neoangiogenesis, along with other proposed mechanisms of action.Keywords: Anthelmintic, Mebendazole, Cancer treatment, Antimicrotubullar effect, Antineoangiogenesis
Highlights
Numerous early-stage laboratory experiments, clinical studies and epidemiological research have documented promising anticancer properties of many existing medications that millions of people take safely every day for other indications [1,2,3]
Clinical trials are essential for determining whether repurposed drugs are applicable and better than the regular care, and for which patient groups
Mebendazole effectively inhibited Hh signalling, even in cell clones that became resistant to vismodegib due to the mutated gene which encodes Smoothened protein [47]
Summary
Numerous early-stage laboratory experiments, clinical studies and epidemiological research have documented promising anticancer properties of many existing medications that millions of people take safely every day for other indications [1,2,3]. Microtubules in the lung cancer culture were effective targets for anticancer therapy with mebendazole This therapy blocked mitosis, induced apoptosis of lung cancer cells, activated caspase and released cytochrome c [23]. Mebendazole strongly suppressed Hh signalling and decreased the proliferation of Hh-controlled medulloblastoma human cell lines at concentrations achievable in clinical conditions [47]. Mebendazole effectively inhibited Hh signalling, even in cell clones that became resistant to vismodegib due to the mutated gene which encodes Smoothened protein [47]. The mebendazole and vismodegib combination has an additive inhibitory effect on Hh signalling [47] Some antimicrotubular drugs, such as mebendazole, can induce the depolymerization of microtubules in tumor blood vessels and as such target vasculature to decrease neoangiogenesis and the nutrient provision of neoplasms [35]. Mebendazole treatment could provide the following advantages: oral treatment (no need for infusion), lower toxicity (no special equipment for toxicities required), less frequent visits, potentially fewer blood tests and a low cost - so less cost for the patient and better compliance
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