Zinc: The Wonder Drug for the Treatment of Carcinomas

Abstract

Evidence is evolving that support the relationship that all carcinomas exhibit the following important relationships: The malignant cells exhibit a significant decreased zinc compared to the normal cells. The higher zinc levels that exist in the normal cells are cytotoxic in the malignant cells. The decrease in zinc is due to the down regulation of the ZIP-family zinc uptake transporter. These cells are as "ZIP-deficient/decreased zinc" malignancies. This provides a target for a chemotherapy that can restore the high zinc levels that will manifest cytotoxic effects in the malignant cells. In order to achieve this, a vehicle that facilitates the uptake and accumulation of zinc in the ZIP-deficient cells is required. The zinc ionophore, clioquinol, exhibits the properties that will provide these requirements. This is demonstrated by the treatment of a patient with 3% Clioquinol Cream, which successfully suppressed the progression of androgen-dependent prostate cancer. This treatment should also be efficacious for pancreatic cancer, liver cancer, breast cancer, thyroid cancer, kidney cancer, stomach cancer, gall bladder cancer, and lung cancer; which are carcinomas that exhibit decreased zinc. Thus, it is appropriate to describe that "Zinc is the wonder drug for the treatment of carcinomas".

Keywords: Carcinomas; Clioquinol; Treatment; Zinc.

Figure 1:

List of population reports reveals that all studies have demonstrated a significant decreased zinc in prostate cancer.

Figure 2:

Dithizone stain of prostate tissue sections showing high zinc in normal/BPH acinar cells vs. loss of zinc in malignant cells.

Figure 3:

Energy dispersive x-ray fluorescent measurements of zinc in normal and cancer prostate tissue samples (modified from [5])

Figure 4:

Dithizone stain of liver tissue sections shows marked decreased zinc in malignancy.

Figure 5:

Liver zinc levels show that zinc is always decreased in malignancy.

Figure 6:

Dithizone stain of pancreatic tissue sections shows marked decreased zinc in malignancy.

Figure 7:

Zinc staining and histology to show the localization of zinc in breast tissue components.

Figure 8:

In situ immunohistochemistry of ZIP transporters in prostate, pancreas, and liver tissue sections.

Figure 9:

Effects of two experiments of clioquinol treatment of human prostate tumor growth in xenograft mice.

Figure 10:

A. ZIP3 transporter localized at the plasma membrane in HepG2 liver cells. B. The uptake of zinc and its effect on cell growth.

Figure 11:

A. ZIP3 plasma membrane localization in Panc1 cells. B. The uptake of zinc and its effect on cell growth.

Figure 12:

Zinc promotion of mitochondrial apoptogenesis. 1–4 shows Zn recruitment of Bax to mitochondrial membrane for release of cytochrome c.