The evidence for vitamin C as an effective treatment for cancer remains controversial. Several studies have shown that it works against a wide variety of cancers, including pancreatic cancer, liver cancer, colon cancer and ovarian cancer.
The role of the TET2 enzyme in leukemia:
New research by scientists at the Perlmutter Cancer Center at New York University (NYU) Langone Health on the effect of vitamin C against blood cancer.
The first author of the study is Luisa Cimmino, Assistant Professor in the Department of Pathology at NYU Langone Health, and the results were published in the journal Cell.
An enzyme called Tet methylcytosine dioxygenase 2 (TET2) is known to have the ability to make stem cells (undifferentiated cells that have not yet acquired a specific identity and function), turning into mature and normal blood cells that eventually die similarly to normal cells.
This is beneficial for leukemia patients, whose blood stem cells are not “mature”, they regenerate themselves and multiply endlessly. This stops the body from producing normal white blood cells, which the immune system needs to fight the infection. Genetic changes can influence the beneficial action of this enzyme.
Activation and deactivation of the TET2 gene:
The researchers genetically engineered the mice so they didn’t have the enzyme, having designed mouse models with the TET2 gene “on” and “off.” When the gene was turned off, the researchers found that the stem cells started to malfunction. When the researchers reactivated the gene, these dysfunctions were reversed.
Researchers have recognized that in leukemia and other blood diseases that depend on TET2 genetic dysfunctions, only one of the two copies of the TET2 gene is changed.
Thus, they hypothesized that a high dose of vitamin C administered intravenously could compensate for the defective copy of the gene by enhancing the action of the copy which still functions normally.
PARP inhibitors block cancer cells:
The study confirmed the researchers’ hypothesis. They found that the high dose of vitamin C promotes a genetic mechanism that restored TET2 function.
This mechanism is called demethylation of DNA, a process that activates genes that cause stem cells to mature and progress to death. This process does not work properly in patients with TET2 genetic mutations.
The new study, however, gives these patients hope, as the researchers found that intravenous treatment with vitamin C promotes DNA demethylation, “pushing” stem cells to maturity and die.
The results prompted the researchers to see what would happen if they combined the therapeutic potential of vitamin C with a class of anticancer drugs called PARP inhibitors. These are a type of medicine known to cause the death of cancer cells by blocking the repair of DNA damage, and are already approved to treat certain patients with ovarian cancer.