The Testing Evidence for Using Mebendazole for Treating Acute Myeloid Leukemia
Executive Summary
- This article covers the evidence I could find for Mebendazole as a treatment for Acute Myeloid Leukemia.
Article Summary
Studies demonstrate that Mebendazole is effective against cancer, we then cover how Mebendazole works against cancer by explaining the mechanisms of action, and then the impacts of Mebendazole on cancer.
Introduction
This article provides an overview covering the evidence for Mebendazole and related drugs versus Acute Myeloid Leukemia.
Many articles on this website cover the evidence for the benefits of Mebendazole for cancer. But the question of which specific cancers Mebendazole has been proven effective is a constant source of questions.
The most common Benzimidazoles are Fenbendazole, Mebendazole and Albendazole. In our analysis, we include research for all three drugs together in articles as they are very similar to one another and it improves the ability to tie together different studies. You may see the following terms/acronyms used.
- FZ or FBZ means Fenbendazole
- MBZ means Mebendazole
- AZ means Albendazole
Cancer Type #5: Acute Myeloid Leukemia
The following quote is from the article Mebendazole exhibits potent anti-leukemia activity on acute myeloid leukemia.
Here through screening more than 1,000 drugs approved by the Food and Drug Administration (FDA) of United States, the anthelmintic drug mebendazole (MBZ) was found to inhibit the growth of AML cell lines (THP-1, U937, NB4 and K562) and bone marrow mononuclear cells (BM-MNCs) from AML patients at pharmacologically achievable concentrations. In contrast, similar concentration of MBZ had little inhibitory effect on the growth of normal peripheral blood mononuclear cells (PBMC) or human umbilical vein endothelial cells (HUVEC). In addition, MBZ induced mitotic arrest and mitotic catastrophe in AML cells based on nuclear morphology, cell cycle distribution, mitotic marker analyses and the number of multinucleated cells and apoptotic cells. Furthermore, MBZ treatment inhibited activation of Akt and Erk in AML leukemic cells. Finally, MBZ repressed the progression of leukemic cells in vivo and prolonged survival in AML xenograft mouse model. Taken together, our results suggest that MBZ could be a potential new therapeutic agent for the treatment of AML patients.
The following quote is from the article Inhibition of Wnt Signaling in Colon Cancer Cells via an Oral Drug that Facilitates TNIK Degradation.
We identify dimaprit and mebendazole as a drug combination which induces myeloid differentiation. In the second approach, we show that genetic manipulation of specific Mogrify®-identified TFs (MYC and IRF1) leads to co-operative induction of APL differentiation, as does pharmacological targeting of these TFs using currently available compounds. We also show that loss of IRF1 blunts ATRA-mediated differentiation, and that MYC represses IRF1 expression through recruitment of PML-RARα, the driver fusion oncoprotein in APL, to the IRF1 promoter.
Finally, we demonstrate that these drug combinations can also induce differentiation of primary patient-derived APL cells, and highlight the potential of targeting MYC and IRF1 in high-risk APL. Thus, these results suggest that Mogrify® could be used for drug discovery or repositioning in leukaemia differentiation therapy for other subtypes of leukaemia or cancers.
Adding up the Studies of Mebendazole Versus Cancer
There are many studies of Fenbendazole, Mebendazole, Albendazole, and other Benzimidazole derivatives versus cancer.
Due to the success of these studies and the information published in the study publications, the specific mechanisms by which these Benzimidazole-based Anthelmintics work against cancer are at this point well understood. There has not been a study published for every cancer type using one of the Benzimidazole derivatives. There are a very large number of different cancer types and limited funding for this type of research.
How Many Major Cancer Types Are There Studies For?
When I completed my analysis, I found 18 different types of cancer types which demonstrated effectiveness versus cancer. In many cases, these different cancer types had multiple cancer studies testing the different Benzimidazole derivatives.
Cancer centers do not apply the large body of published studies on the effectiveness of Benzimidazole derivatives to include as part of their treatment offerings. This is true even though Fenbendazole has been demonstrated to improve chemotherapy outcomes.
To understand the mechanisms by which Benzimidazole derivatives work against cancer, see the following few examples. To see all of the known mechanisms that I have compiled from all of the studies see the article on the mechanisms listed below.
The Multiple Mechanisms by Which Mebendazole Works Against Cancer
There are many ways in which Mebendazole works against cancer including.
- Reducing metastasis
- Increase autophagy
- Increase cancer cell death or apoptosis
- and much more
This topic is covered in the article By How Many Different Mechanisms Does Menbendazole Fight Cancer?