The Progression of Leukemia may be stopped by Vitamin-C

The Progression of Leukemia may be stopped by Vitamin-C
Since the 1970s, researchers have been interested in the therapeutic potential of vitamin C for the treatment of cancer. Now, research by scientists at the Perlmutter Cancer Center at New York University shows how vitamin C can prevent leukemia stem cells from multiplying and blocking their progress.

It is known that an enzyme called Tet methylcytosine dioxygenase 2 (TET2) has the ability to produce stem cells, undifferentiated cells that have not yet gained a specific identity and function, a circumstance that can be exploited for patients with leukemia, since in Instead of maturing and dying like any other cell, they regenerate and multiply infinitely, hence the body is unable to produce normal white blood cells, which our immune system needs to fight infection.

According to experts, 50% of patients who have chronic myelomonocytic leukemia also has a genetic malfunction that reduces TET2, hence they will focus on finding out how this enzyme could be genetically stimulated and whether vitamin C would play an important role or do not.

Leukemia is a disease of the blood in which the bone marrow produces abnormal white blood cells.

Activation and deactivation of the TET2 gene

In leukemia and other diseases of the blood that depend on TET2, only one of the copies of the gene is altered.
When tested for intravenous administration of a high dose of vitamin C to the modified rodents, they found that vitamin C promoted a genetic mechanism (DNA demethylation) that restored TET2 function; That is, the defective copy of the gene was compensated by amplifying the copy action that does function normally in the TET2 gene.

The researchers used mice genetically modified to lack this enzyme and designed mouse models with the possibility of "turning on" and "turning off" the TET2 gene through optogenetics. By turning off this gene, experts discovered that stem cells started to malfunction. When the gene was activated, this dysfunction was reversed.

The study confirmed without a doubt the hypothesis of the researchers. By promoting DNA demethylation, vitamin C "told" stem cells to mature and die. Not only that. The treatment also stopped the leukemia cancer cells that had been transplanted from human patients to growing mice.

Combining the therapeutic potential of vitamin C with anticancer drugs - inhibitors of PARP -, the effectiveness of vitamin C treatment was enhanced, making it even more difficult for leukemic stem cells to reproduce.
"We also planned additional preclinical studies to test the effects of high doses of vitamin C in combination with PARP [inhibitors] on more models of acute myeloid leukemia and in samples from primary patients," concludes Neel.