Mebendazole, a drug already used for the treatment of parasitic infections, has shown in a study that it can mainly prevent metastases. The drug is also believed to have beneficial effects in all stages of cancer.
Pancreas Image Courtesy of Blausen Medical
About 60,430 people are diagnosed with pancreatic cancer in the US each year of which 48,220 will die. This cancer is particularly aggressive and has a poor prognosis because it is often detected late. Researchers from Johns Hopkins School of Medicine are offering new hope to sufferers. In a study published in the journal Oncotarget, they explain that Mebendazole an anti-parasitic treatment is effective in treating this form of cancer. Mebendazole has promising effects on the development and progression of cancer and on the formation of metastases.
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Its effect on tumors is similar to that on parasites
Professor Gregory Riggins, professor of neurosurgery and oncology, and his team reached this conclusion by conducting experiments on mice. They were genetically modified to develop pancreatic cancer. They then tested the effects of mebendazole. This anti-parasitic drug is commonly used to fight different types of parasites by preventing the formation of tubulin, a substance in cells. “The drug enters the parasite’s gut and breaks down the tubulin, causing the parasite to starve”, the researchers explain. This study suggests that mebendazole may also have a similar effect on pancreatic cancer by breaking down the structure of cancer cells and also through other mechanisms such as reducing inflammation.
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Further studies on humans are needed
Following these convincing results in mice, the researchers want to continue their work in humans. We believe mebendazole may be relevant at all stages,” says Professor Riggins. It was particularly effective in the early stages of pancreatic cancer. He says the drug can be used at an early stage to slow the growth of cancer. If the disease is more advanced, surgery can be avoided.
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References
Mebendazole disrupts stromal desmoplasia and tumorigenesis in two models of pancreatic cancer
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