The Testing Evidence for Using Fenbendazole for Treating Breast Cancer

Executive Summary

• This article covers the evidence I could find for Fenbendazole as a treatment for Breast Cancer.

Article Summary

Studies demonstrate that Fenbendazole is effective against cancer, we then cover how Fenbendazole works against cancer by explaining the mechanisms of action, and then the impacts of Fenbendazole on cancer.

Introduction

This article provides an overview covering the evidence for Fenbendazole and related drugs versus Breast Cancer.

Many articles on this website cover the evidence for the benefits of Fenbendazole for cancer. But the question of which specific cancers Fenbendazole 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 #3: Breast Cancer

The following quote is from the article Redox-mediated Anticancer Activity of Anti-parasitic Drug Fenbendazole in Triple-negative Breast Cancer Cells.

An increasing number of studies are reporting anticancer activity of widely used antiparasitic drugs and particularly benzimidazoles. Fenbendazole is considered safe and tolerable in most animal species at the effective doses as an anthelmintic.

The experiments were performed on three cell lines: normal breast epithelial cells (MCF-10A) and cancer breast epithelial cells (MCF7 – luminal adenocarcinoma, low metastatic; MDA-MB-231 – triple-negative adenocarcinoma, highly metastatic). Cells were treated with fenbendazole for 48-h and three parameters were analyzed using conventional assays: cell viability and proliferation, level of intracellular superoxide, and level of hydroperoxides.

The data demonstrated that MDA-MB-231 cells were more vulnerable to fenbendazole-induced oxidative stress than MCF-7 cells. In normal breast epithelial cells MCF-10A, fenbendazole significantly suppressed oxidative stress compared to untreated controls.

The following quote is from the article Benzimidazoles Downregulate Mdm2 and MdmX and Activate p53 in MdmX Overexpressing Tumor Cells.

Our findings have several important implications. Benzimidazole derivatives ABZ and FBZ stimulate the activity of p53 in malignant melanoma and breast cancer cells overexpressing MdmX.
Our data provide the first evidence that this enhancement occurs, at least in part, through MdmX and Mdm2 downregulation. This points out the significance of MdmX in p53 regulation in tumors that overexpress this essential negative p53 regulator, such as the majority of malignant melanomas.

The following quote is from the article Anticancer Effect of Benzimidazole Derivatives, Especially Mebendazole, on Triple-Negative Breast Cancer (TNBC) and Radiotherapy-Resistant TNBC In Vivo and In Vitro.

Our findings demonstrated that the four benzimidazole derivatives ALB, FLU, FBZ, and MBZ had anticancer effects, such as reduced colony formation in MDA-MB-231 cells, a TNBC cell line, and RT-R-MDA-MB-231 cells. In particular, MBZ showed the strongest anticancer effect and reduction of lung metastasis in the mouse model; therefore, we further investigated the mechanisms by which MBZ exerts anticancer effects in MDA-MB-231 and RT-R-MDA-MB-231 cells. MBZ induced cell cycle arrest at the G2 / M phase and increased cyclin B1 levels, but not those of cyclin D1, for up to 24 h after treatment, and decreased these levels thereafter.

In addition, tubulin polymerization was inhibited in the MBZ-treated group. These results suggest that MBZ promotes cell cycle progression from G1 to G2-M by increasing cyclin B1 protein levels and then arresting cells at the M phase by inhibiting tubulin polymerization at 24 h. α- and β-tubulins polymerize into microtubules, major constituents of mitotic spindles, and function in many essential processes, including cell division [18]. Drugs that inhibit tubulin polymerization or promote microtubule depolymerization cause mitotic arrest [1,920].

Adding up the Studies of Fenbendazole 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 Fenbendazole Works Against Cancer

There are many ways in which Fenbendazole 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 Fenbendazole Fight Cancer?