Blood Cancer: High Doses of Vitamin C Could Encourage Stem Cells to Die
December 2017

According to new research, a diet that contains high levels of vitamin C could prove effective in battling cancer.

The study was carried out by researchers around the world, working together on the project funded by many sources including the Leukaemia & Lymphoma Society, and the Chemotherapy Foundation. The results, published in the journal CellPress, showed that vitamin C may in fact cause blood cancer stem cells to die by activating the TET2 function, an enzyme that encourages stem cells to mature and eventually die as opposed to multiplying. When used in conjunction with other cancer treatments such as chemotherapy, the results could help to cure certain kinds of blood cancers such as leukaemia.

According to Professor Benjamin Neel, one of the study’s corresponding authors, the future use of Vitamin C as a successful cancer treatment looks promising. “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,” he writes.



TET2, or Tet Methylcytosine Dixoygenase 2, produces a protein that forms in stem cells located in bone marrow.


TET2 tends to act as a tumour suppressor, and so the loss of TET2 function can cause mutations that frequently causes blood cancers along with other blood disorders such as anaemia. According to Professor Neel, reduced rates of TET2 function present in 10 per cent of patients living with acute myeloid leukaemia (AML), in 30 per cent of patients with myelodysplastic syndrome (pre-leukaemia), and in almost half the patients suffering with chronic myelomonocytic leukaemia. In the study, researchers set out to learn more about TET2 and leukaemia stem cells by treating genetically engineered mice with injections of Vitamin C. The team wanted to assess whether the injections would restore the normal function of TET2 and therefore stop the progression of leukaemia.



The results revealed that when the “function” of TET2 was switched off, the stem cells behaved abnormally, but that the behaviour corrected once the TET2 was switch back on.


This was achieved by administering vitamin C intravenously into the mice that were experiencing a TET2 deficiency. As the stem cells matured, the leukaemia cancer stem cells were suppressed, pointing researchers towards the conclusion that vitamin-C could indeed be used to help treat types of blood cancer. In the report, researchers concluded: “We have found that targeted restoration of Tet2 is sufficient to block aberrant self-renewal of pre-leukemic stem cells. Similarly, vitamin C, by enhancing the activity of TET family dioxygenases, acts as a pharmacologic mimic of Tet2 restoration. Moreover, genetic or pharmacological restoration of TET activity confers an emergent vulnerability in leukemia cells, rendering them more sensitive to PARP inhibitors. Together, these results suggest new therapeutic strategies for clonal hematopoiesis, MDS and AML.”

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