Super-strength vitamin C doses could be a way to fight leukemia, ‘exciting’ early trials suggest. Found in high levels in oranges, peppers, and kale, scientists believe it encourages blood cancer stem cells to die.
Faulty stem cells in bone marrow often multiply, fueling the growth of fatal tumors, but vitamin C tells them to die, scientists claim. But they warned it is impossible to get the required amount through fruit, and that such high quantities would be given intravenously.
By injecting patients with it, sufferers can get up to 500 times the amount than they would through eating fruit and vegetables.
Found in high levels in oranges, peppers, and kale, scientists believe vitamin C encourages blood cancer stem cells to die
This isn’t the first time researchers have studied the cancer-fighting properties of vitamin C – but its effects on leukemia were previously not understood.
What did the scientists discover?
The new Perlmutter Cancer Centre trial discovered vitamin C activated the TE2 function in mice engineered to be deficient in the enzyme.
Some forms of leukemia often involve genetic changes in this enzyme – which stops faulty stem cells from dying naturally. Lead author Professor Benjamin Neel said: ‘We’re excited by the prospect that high-dose vitamin C might become a safe treatment for blood diseases.’
Writing in the journal Cell, he said it would most likely be used in combination with chemotherapy or other conventional forms.
How was the study carried out?
In the studies on mice, turning off the TET2 mechanism caused abnormal stem cell behavior. The changes were reversed when it was restored.
They discovered vitamin C, also called ascorbic acid, did the same thing as restoring the function genetically. The bizarre technique also suppressed the growth of leukemia cancer stem cells from human patients implanted into the mice.
When combining vitamin C with a PARP inhibitor, a drug known to kill cancer cells, they found it had an enhanced effect.
How common is this faulty gene?
Changes in genetic code reduce TE2 function and are known to be present in half of all chronic myelomonocytic leukemia cases. The same faulty process can also be seen in one in 10 acute myeloid leukemia patients, the New York-based researchers added.
Both forms of the disease can lead to anemia and bleeding as abnormal stem cells multiply in the bone marrow and interfere with blood cell production. The researchers said the results revolve around the relationship between TET2 and cytosine, one of four ‘letters’ that comprise the DNA code in genes.