The Testing Evidence for Using Ivermectin for Treating Transitional Cell Carcinoma in Dogs

Executive Summary

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

Introduction

This article provides an overview covering the evidence for Ivermectin versus Transitional Cell Carcinoma 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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Cancer Type #2: Transitional Cell Carcinoma in Dogs

These quotes are from the article Ivermectin suppresses tumor growth and metastasis through degradation of PAK1 in oesophageal squamous cell carcinoma.

We demonstrated that ivermectin significantly inhibited cell viability and colony formation, and induced apoptosis through a mitochondrial‐dependent manner in ESCC cells. Ivermectin also abrogated ESCC cell migration, invasion, as well as the protein levels of MMP‐2 and MMP‐9. Mechanistically, ivermectin strongly inhibited the expression of PAK1; by further gain‐ and loss‐of‐function experiments, we confirmed that PAK1 played a crucial role in ivermectin‐mediated inhibitory effects on ESCC cells.

These same things have all been found in other studies of Ivermectin versus different cancers.

The results showed that ivermectin effectively suppressed ESCC cell growth in vitro and in vivo, and induced apoptosis. Moreover, ivermectin diminished the abilities of migration and invasion, and the metastasis in nude mice.

That means Ivermectin suppressed cancer cell growth and increased the ability of the immune system to kill cancerous cells.

More importantly, our data also showed that ivermectin had a high antitumour activity against tumour growth and metastasis in nude mouse models.

The Mechanisms by Which Ivermectin Works Against Cancer

Confidence in Ivermectin being effective for many cancer types also comes from understanding the specific mechanisms by which Ivermectin works against cancer. I cover this topic in detail in the article By How Many Different Mechanisms Does Ivermectin Fight Cancer?

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.