Since the 1970s, researchers have been interested in the therapeutic potential of vitamin C for the treatment of cancer. Now, research by scientists at New York University’s Perlmutter Cancer Center shows how vitamin C can prevent leukemia stem cells from multiplying, thus blocking their progression.
It is already 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 used 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 have a genetic malfunction that reduces TET2, hence they focused on finding out how this enzyme could be genetically stimulated and if vitamin C would play an important role or not.
Activation and deactivation of the TET2 gene
The researchers used mice genetically modified to lack this enzyme and designed mouse models with the ability to “turn on” and “off” the TET2 gene using optogenetics. By turning off this gene, the experts discovered that the stem cells began to malfunction. By activating the gene, this dysfunction was reversed.
In leukemia and other TET2-dependent blood diseases, only one of the copies of the gene is altered.
When trying to administer a high dose of vitamin C intravenously to 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 action of the copy that does function normally in the TET2 gene.
The study clearly confirmed the researchers’ hypothesis. By promoting DNA demethylation, vitamin C “told” stem cells to mature and die . Not only that. The treatment also stopped leukemia cancer cells that had been transplanted from human patients to growing mice.
By combining the therapeutic potential of vitamin C with anticancer drugs – PARP inhibitors – the efficacy of vitamin C treatment was enhanced, making it even more difficult for leukemic stem cells to reproduce.
“Our results suggest that the high dose of vitamin C – and it is important to note that this means that the doses to be administered intravenously – could have therapeutic benefits in TET2 mutant myelodysplastic syndrome”, explains Benjamin Neel, co-author of the work.
“We also plan additional preclinical studies to test the effects of high doses of vitamin C in combination with PARP [inhibitors] in more acute myeloid leukemia models and in primary patient samples,” Neel concludes.
Referencia: Restoration of TET2 Function Blocks Aberrant Self-Renewal and Leukemia Progression. NYU Langone Health / NYU School of Medicine. Agosto 2017. Cell.DOI: http://dx.doi.org/10.1016/j.cell.2017.07.032
