Washington D.C.: Good news! A study has recently revealed that vitamin C may tell faulty stem cells in the bone marrow to mature and die normally, instead of multiplying to cause blood cancers.
According to researchers, certain genetic changes are known to reduce the ability of an enzyme called TET2 to encourage stem cells to become mature blood cells, which eventually die, in many patients with certain kinds of leukemia.
The new study found that vitamin C activated TET2 function in mice engineered to be deficient in the enzyme.
Corresponding study author Benjamin G. Neel said, “We’re excited by the prospect that high-dose vitamin C might become a safe treatment for blood diseases caused by TET2-deficient leukemia stem cells, most likely in combination with other targeted therapies.”
The results suggested that changes in the genetic code (mutations) that reduce TET2 function are found in 10 percent of patients with acute myeloid leukemia (AML), 30 percent of those with a form of pre-leukemia called myelodysplastic syndrome, and in nearly 50 percent of patients with chronic myelomonocytic leukemia.
The study results revolve around the relationship between TET2 and cytosine, one of the four nucleic acid “letters” that comprise the DNA code in genes.
To determine the effect of mutations that reduce TET2 function in abnormal stem cells, the team genetically engineered mice such that the scientists could switch the TET2 gene on or off.
The findings indicated that vitamin C did the same thing as restoring TET2 function genetically. By promoting DNA demethylation, high-dose vitamin C treatment induced stem cells to mature, and also suppressed the growth of leukemia cancer stem cells from human patients implanted in mice.
“Interestingly, we also found that vitamin C treatment had an effect on leukemic stem cells that resembled damage to their DNA,” said first study author Luisa Cimmino.
“For this reason, we decided to combine vitamin C with a PARP inhibitor, a drug type known to cause cancer cell death by blocking the repair of DNA damage, and already approved for treating certain patients with ovarian cancer,” Cimmino added.
The findings appear in journal Cell.