The Testing Evidence for Using Ivermectin for Treating Brain Tumor in Dogs

Executive Summary

• This article covers the evidence I could find for Ivermectin as a treatment for Brain Tumor in Dogs.

Introduction

This article provides an overview covering the evidence for Ivermectin versus Brain Tumor in Dogs.

In many articles on this site, such as the article How Ivermectin Is Useful for Treating Cancer we covered the evidence for the benefits of Ivermectin for cancer. However, the topic of which specific cancers Ivermectin has been proven effective is a constant source of questions.

There are a lot of quotes in this article, but I have a short one for each cancer type. The article uses the term “IVM” to mean Ivermectin.

About the Brightwork Research Treatment Database

A bit about us -- we have a subscription website that provides people with everything they need to know about using Ivermectin for several diseases. Cancer is just one of our most researched areas.

Article Indexes

• Open this link to see just one example Ivermectin article index.
• Open this link to see the full article index. 

Cancer Type #5: Brain Tumor in Dogs

These results showed that IVM had the potential to resist tumor angiogenesis and tumor metastasis. However, here, we must emphasize that because IVM cannot effectively pass the blood-brain barrier, the prospect of the use of IVM in the treatment of gliomas is not optimistic.

Glioma is the most common cerebral tumor and approximately 100,000 people worldwide are diagnosed with glioma every year. Glioblastoma is the deadliest glioma, with a median survival time of only 14-17 months [61,62]. Experiments showed that IVM inhibited the proliferation of human glioblastoma U87 and T98 G cells in a dose-dependent manner and induced apoptosis in a caspase-dependent manner [63]. This was related to the induction of mitochondrial dysfunction and oxidative stress. Moreover, IVM could induce apoptosis of human brain microvascular endothelial cells and significantly inhibit angiogenesis. These results showed that IVM had the potential to resist tumor angiogenesis and tumor metastasis. In another study, IVM inhibited the proliferation of U251 and C6 glioma cells by inhibiting the Akt/mTOR pathway [64]. – NIH

The Importance of The NIH Stopping Any Funding For Ivermectin Studies

Notice that none of the studies on Ivermectin were performed in the US. The US has by far the largest national medical research budget in the world, and so if the US is not performing studies, this is not only a negative but tells us something peculiar about what the NIH is deciding not to fund in the area of cancer research.

Zero is the number of studies funded by the NIH on Ivermectin. The NIH will not fund studies into generic drugs, as the NIH is controlled by pharmaceutical companies and they have deep financial ties to them. Funding research into generic drugs could end up showing those drugs as effective, which is a threat to pharmaceutical profits, which the NIH is dedicated to maximizing. 

Testing Evidence for Ivermectin

The following quotes are from the article Ivermectin, a potential anticancer drug derived from an antiparasitic drug.

Impact #1: Inhibiting Proliferation of Tumor Cells

Recently, ivermectin has been reported to inhibit the proliferation of several tumor cells by regulating multiple signaling pathways.

The Ivermectin blocking of PAK1 proteins, aka activated kinase, is a reason for this.

The instrumentality of PAK1 in cancer growth is explained in the following quotation from the article Ivermectin: enigmatic multifaceted ‘wonder’ drug continues to surprise and exceed expectations.

In human ovarian cancer and NF2 tumor cell lines, high-dose ivermectin inactivates protein kinase PAK1 and blocks PAK1-dependent growth.

PAK proteins are essential for cytoskeletal reorganization and nuclear signaling, PAK1 being implicated in tumor genesis while inhibiting PAK1 signals induces tumor cell apoptosis (cell death).

PAK1 is essential for the growth of more than 70% of all human cancers, including breast, prostate, pancreatic, colon, gastric, lung, cervical and thyroid cancers, as well as hepatoma, glioma, melanoma, multiple myeloma and for neurofibromatosis tumors.

PAK1 becomes hyperactive in cancer cells for reasons that are not yet understood.

Ivermectin can be viewed as a PAK1 restrictor or modulator (I say modulator as PAK1 is present in normal healthy cells, but an overage of PAK is a prime cause of cancer.)

This means that Ivermectin interferes with a precursor to cancer. This modulating influence on PAK is another reason Ivermectin is effective against many types of cancer.

PAK1 is implicated in multiple cancers if found in the quotation from the article Effect of P21-activated kinase 1 (PAK-1) inhibition on cancer cell growth, migration, and invasion.

Previous studies showed that PAK-1 mediated the growth of prostate PC-3 cell tumor xenografts in athymic nude mice as well as the transforming growth factor-β (TGFβ)-induced prostate cancer cell epithelial-mesenchymal transition (EMT). These studies suggested that PAK-1 plays a major role in prostate cancer progression and is a potential target for prostate cancer therapy. PAK-1 has also been suggested to be involved in the early stages of breast cancer and may partially participate in the mechanisms mediating the transformation of mammary epithelial cells into mesenchymal malignant cells.

Hyperactive PAK1 and Cancer

This is explained in the quotation from P21 Activated Kinase-1 (Pak1) Promotes Prostate Tumor Growth and Microinvasion via Inhibition of Transforming Growth Factor β Expression and Enhanced Matrix Metalloproteinase 9 Secretion.

Even though Pak1 has been identified in normal prostatic epithelial cells and cancer cells, its specific role in the development of prostate cancer remains unclear. We report here that highly invasive prostate cancer cells express significantly higher levels of Pak1 protein compared with non-invasive prostate cancer cells. Furthermore, prostate tumor tissues and prostate cancer metastasized to lungs showed a higher expression of Pak1 compared with normal tissues.

This appears to match the experience with other cancers, but they have not performed sufficient studies to say for sure.