A new study has revealed that fenbendazole, an anthelmintic, may reactivate the p53 gene in cancer cells. The p53 gene is a tumor suppressor and prevents cancer from growing.
However, fenbendazole hasn’t been tested in humans and doesn’t have any FDA approval for treating cancer. A specialist cancer information nurse told Full Fact that Tippens’ claim is untrue.
Inhibition of glucose uptake
The cancer-fighting drug fenbendazole inhibits glucose uptake, which helps prevent the formation of tumors. This is a good thing, because cancer cells need more glucose than normal cells to survive. The drug acts by binding to b-tubulin microtubules, which disrupts their polymerization. This is how it kills parasites, and it may also inhibit the growth of cancer cells.
Cells need energy for a variety of functions, including growth and cell division. Cells establish their shape and structure through a protein scaffold called the cytoskeleton, which is made up of microtubules. These microtubules are derived from the tubulin protein. Several drugs act by targeting microtubules, including paclitaxel, vincristine, and doxorubicin. However, these drugs have limited efficacy and can result in resistance. A new drug called fenbendazole may overcome this resistance by affecting multiple cellular targets.
In experiments in cultured tumor cells, fenbendazole inhibited glucose uptake and reduced the growth of two different types of human cancers. It also reduced the number of cancer cells and the ability of these cells to evade chemotherapy drugs. In addition, fenbendazole interfered with the process of mitosis, which is necessary for even separation of chromosomes during cell division.
While fenbendazole has been approved for use in animals, it is not yet known if it works in humans. The drug is a benzimidazole compound that is partially absorbed from the gastrointestinal tract and converted to its active forms, fenbendazole sulfone and oxifendazole. It is not known whether these compounds are safe or effective in humans, although a randomized placebo-controlled phase 1 clinical trial is underway.
Inhibition of microtubules
Fenbendazole is an antiparasitic drug that acts by binding to b-tubulin microtubule subunits and inhibiting their polymerization. This drug has also been shown to suppress the growth of cancer cells in cell culture and animal models. However, there is not enough evidence to support the claims that fenbendazole can cure cancer in humans. Tippens’ anecdotal experience may not be typical, and randomized controlled trials involving human patients would need to be performed before this could happen.
The benzimidazole carbamates inhibit microtubule assembly, which is critical for the mitotic cycle of cell division. They do so by binding to the acetylation sites on mammalian tubulin, resulting in reduced microtubule stability. This is similar to the effect of Vinca alkaloids, which are approved drugs used in cancer chemotherapy.
To investigate the effects of fenbendazole on cell-cycle progression, researchers treated H460 and A549 cells with varying concentrations of fenbendazole. They found that treatment with fenbendazole inhibited glucose uptake by cancer cells, which is important for the maintenance of their energy source. It also interfered with the progression of cyclin B1 into mitosis, a process that is necessary for progression from G2 to anaphase.
In addition, the treatment caused a decrease in glycogen stores and ATP formation in cancer cells. Moreover, fenbendazole inhibited the mitotic spindle, which is required for even separation of chromosomes during anaphase.
Inhibition of p53 gene
Fenbendazole is a chemical compound that has been shown to inhibit the growth of cancer cells in cell cultures and animals. It appears to do this by inhibiting the p53 tumor suppressor gene. This interaction promotes RAB-coupling protein (RCP)-dependent recycling of cell surface receptors and prevents the activation of apoptosis, which is dependent on p53.
The drug interferes with the normal growth of microtubules, which essentially give structure to all cells. It also interferes with the mitotic spindle, a structure that separates and divides chromosomes during cell division. This process is essential for the healthy functioning of a cell, so drugs that block the activity of these microtubules are considered anti-cancer agents.
Previous studies have shown that fenbendazole has minimal toxicity in normal human cells, even at high doses. However, it is not a selective microtubule destabilizer and has little effect on normal cell viability at doses that approach the limit of solubility. The researchers studied the effects of 2- and 24-h treatments of fenbendazole on the viability of EMT6 tumor cells. Both treatments had a similar toxicity profile, with a steep decrease in cell viability at low drug concentrations and a plateau at higher doses.
Cancer Research UK tells Full Fact that there is insufficient evidence to show that fenbendazole cures cancer in humans. The dog wormer ingredient is not an approved cancer treatment, and it hasn’t gone through any clinical trials to test its effectiveness in humans. The nonprofit organization also says that Tippens’ anecdotal claim about his remission isn’t reliable, as it doesn’t take into account conventional cancer treatments he received.
Inhibition of tumor growth
The claim that fenbendazole can cure cancer is often based on anecdotal evidence from patients with atypical tumors, as well as the work of some self-proclaimed “cancer doctors.” While studies using cells in a laboratory setting suggest that fenbendazole might help treat certain types of cancer, these results do not apply to humans. In addition, many people with atypical tumors also receive conventional cancer treatments in a clinical trial.
The researchers investigated the effects of fenbendazole in human cancer cells and found that it caused partial alteration of microtubule networks around the cell nucleus and enhanced cell death-inducing activity in p53 mutant lung cancer cells. They also found that the drug inhibited the RAS-related signaling pathway. They then tested fenbendazole in mice, which are known to be sensitive to the drug. The mice were administered 1 mg/mouse of fenbendazole every second day for 12 days, and their tumors showed a significant reduction in size and weight.
The research was conducted at the City of Hope in California and was published in Scientific Reports. A press release from the hospital said that fenbendazole works by blocking cancer cells from growing in the body. It is a member of the benzimidazole carbamate family, which includes mebendazole, albendazole, and flubendazole. Other anthelmintic drugs of this type have also shown anticancer effects in animals and mice. fenbendazole for humans cancer