The Testing Evidence for Using Ivermectin for Treating Chronic Leukemia in Dogs

Executive Summary

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

Introduction

This article provides an overview covering the evidence for Ivermectin versus Leukemia 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.

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Article Indexes

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Cancer Type: Leukemia in Dogs

There are many types of leukemias — however, the following study showed effectiveness for Ivermectin versus chronic myeloid leukemia.

This quote is from the article Identification of Ivermectin Induces Apoptosis Through Mitochondrial Dysfunction in CML Cells.

Ivermectin, an antihelminthic, causes apoptosis of chronic myeloid leukemia (CML) cells and CML CD34 stem/progenitor cells through oxidative stress and mitochondrial dysfunction, according to a study published in Biochemical and Biophysical Research Communications.

Treatment with ivermectin resulted in caspase-dependent apoptosis of CD34 and K562 CML cells, but not normal CD34 cells. Apoptosis occurred in about 30% of CML CD34 or K562 CML cells when treated with a TKI or ivermectin monotherapy. The combination of ivermectin and a TKI, however, increased the frequency of apoptosis to about 95%, suggesting that the combination has a synergistic effect.

Ivermectin showed cytotoxicity (the ability to damage or kill) cancer cells.

Ivermectin decreased basal and maximal mitochondrial respiration in CML CD34, K562 CML cells, and normal cells, and decreased the mitochondrial respiratory complex I in CML and normal CD34 cells. Ivermectin also increased levels of ROS and superoxide, both markers of mitochondrial dysfunction.

This means that Ivermectin disrupted the mitochondrial metabolism. This is very important because the immune system identifies cells with dysregulated metabolism for disposal.

The Impact of Ivermectin on Cancer

The different way that Ivermectin impacts cancer is explained in the following items.

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.