Vitamin C May Help Kill Blood Cancer Cells
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.
Vitamin C may help genes to kill blood cancer stem cells
- Vitamin C tell stem cells in the bone marrow to mature and die normally
- Study revolves around the relationship between TET2 and cytosine
- High-dose vitamin C treatment induced stem cells to mature
"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," said corresponding study author Benjamin G Neel MD, PhD, professor in the Department of Medicine and director of the Perlmutter Cancer Center.
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. They also suppressed the growth of leukemia cancer stem cells from human patients implanted in mice.
First study author Luisa Cimmino said "Interestingly, we also found that vitamin C treatment had an effect on leukemic stem cells that resembled damage to their DNA."
Cimmino added "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."
Corresponding author Iannis Aifantis, PhD, professor and chair of the Department of Pathology at NYU Langone Health said "Our team is working to systematically identify genetic changes that contribute to risk for leukemia in significant groups of patients."
"This study adds the targeting of abnormal TET2-driven DNA demethylation to our list of potential new treatment approaches."
The findings appear in journal Cell.