Cancer cells don’t develop resistance to fenbendazole.
There are additional characteristics that make fenbendazole a remarkable anti-cancer strategy and cancer-fighting tool.
What’s interesting, cancer cells cannot evade this de-wormer drug and adapt to its presence. This means that it can be taken constantly and remain effective. Unfortunately, advanced cancer can develop chemo-resistance to many chemotherapy and biological therapy medications, making them ineffective in time.
One of the main mechanisms of chemo-resistance in cancer cells is the adaptation of excreting the anti-cancer drugs to the outside via special drug efflux pumps called P-glycoproteins. Fenbendazole is not a target for p-glycoproteins, so it cannot be excreted out of cancer cells once it gets inside.
Therefore, the tumors don’t develop resistance against fenbendazole. It will still remain effective and kill cancer cells, which does not seem to be the case with a lot of chemotherapy drugs once chemo-resistance is developed. *https://www.nature.com/articles/s41598-018-30158-6
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Fenbendazole could sensitize tumors to radiotherapy.
The dog-dewormer could be a considerable option before and during radiation treatment. It sensitizes the cancer cells to the treatment in a similar way like chemotherapy agents from the taxane group. *https://www.nature.com/articles/s41598-018-30158-6
The website Fenbendazole.org has some nice, easy-to-understand info and graphics on how fenbendazole works.
https://www.fenbendazole.org/fenbendazole-information/how-fenbendazole-works/
p53
Activating p53, a tumor suppressor gene.
3. Reactivation of the p53 Gene
This mechanism is still controversial, and more studies are needed to confirm that fenbendazole causes this action. However, an increasing number of studies suggest that fenbendazole might enhance the activity of p53, the strongest tumor suppressor in our bodies.
Interestingly, elephants have 20 copies of the p53 gene in their genome, while humans have only one. This might explain why elephants get cancer less frequently than humans, despite having larger bodies, more cells, and a higher potential for genetic mutations. However, there is an increasing number of studies that confirm the fact that fenbendazole might truly increase the strongest tumor suppressor in our bodies.
Mrkvová Z, Uldrijan S, Pombinho A, Bartůněk P, Slaninová I. Benzimidazoles Downregulate Mdm2 and MdmX and Activate p53 in MdmX Overexpressing Tumor Cells. Molecules. 2019;24(11):2152. Published 2019 Jun 7. doi:10.3390/molecules24112152 *https://pubmed.ncbi.nlm.nih.gov/31181622/
Tumor cell lines with wild-type p53 show enhanced sensitivity to FZ induced apoptosis.
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Simultaneously, it[fenbendazole] caused mitochondrial translocation of p53 and effectively inhibited glucose uptake, expression of GLUT transporters as well as hexokinase (HK II) - a key glycolytic enzyme that most cancer cells thrive on. It blocked the growth of human xenografts in nu/nu mice model when mice were fed with the drug orally. The results, in conjunction with our earlier data, suggest that FZ is a new microtubule interfering agent that displays anti-neoplastic activity and may be evaluated as a potential therapeutic agent because of its effect on multiple cellular pathways leading to effective elimination of cancer cells.
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These results suggest that FZ inhibits tumor cell growth in vivo by inducing apoptosis of tumor cells. When tumor sections were further examined for p53 protein expression, a number of p53 positive tumour cells were visible in FZ treated mice suggesting p53 induced cell death (Fig. 9h ii & v). Moreover, FZ treated A549 tumours showed very few CD31 positive endothelial cells in xenografts (Fig. 9h iii & vi). These data are in good agreement with our in vitro analysis of FZ mediated cell death.
*Scientific Reports Published online: 09 August 2018 https://www.nature.com/scientificreports