Vitamin C May Help Leukemia Treatment

Researchers from New York University has found that high-dose Vitamin C may be helpful in leukemia treatment. Simply speaking , a portion of patients with certain leukemias are lack of an enzyme called TET2 in their body. TET2 works to encourage stem cells to belcome mature blood cells and eventually die. High-dose of vitamin C can activate TET2 funciton, and inhibit the growth of leukemia cancer stem cells. High dose of vitamin C can work with other target therapy to treat certain types of leukemia, and vitamin C is a very safe treatment option.

Below are the details about the research.

Vitamin C can “tell” defective stem cells in the bone marrow to mature and die normally, rather than doubling blood cancer. This was the discovery of a study led by researchers at the Langone Health Perlmutter Cancer Center at New York University and published in the journal Cell.

The authors say that certain genetic changes in many patients with certain leukemias are known to reduce the ability of the enzyme called TET2 to encourage stem cells to become mature blood cells and eventually die. New research found that vitamin C can activate TET2 function in mice lacking enzymes.

The corresponding research author Benjamin G. Neel said: “High-dose vitamin C may be a safe treatment for blood diseases caused by TET2-defective leukemia stem cells, and we are most excited about the prospect of combining with other targeted therapies.”

Changes in the genetic code (mutations) that reduce TET2 function were found in 10% of patients with acute myeloid leukemia (AML), 30% of patients with a preleukemic form of myelodysplastic syndrome, and nearly 50% Chronic bone marrow monocytic leukemia. Such cancers cause anemia, risk of infection, and bleeding because abnormal stem cells multiply in the bone marrow until they interfere with blood cell production, and as the number of people increases, the number of cases increases.

The authors believe that with the development of these diseases, new test results indicate that about 2.5% of all cancer patients in the United States (ie, approximately 42,500 new patients each year) may have TET2 mutations (including lymphomas and solid tumors).

The results revolve around the relationship between TET2 and cytosine, which is one of the four nucleic acid “letters” that contain the genetic DNA code. Each cell type has the same gene, but each cell type has different instructions to open only those needed in the background of a given cell.

These “epidemic” regulatory mechanisms include DNA methylation, the attachment of small molecules called methyls to cytosine bases, which shut down the effect of the genes that contain them.

The attachment and removal of methyl groups can also regulate gene expression in stem cells. Stem cells can mature, specialize and multiply into muscle, bone, nerve or other cell types. But bone marrow will also keep the stem cell pool mature and ready to become a replacement cell as needed. In leukemia, blood stem cells are usually told to mature signals, so that they continue to multiply and “self-renewal” rather than produce normal white blood cells that are offset by infection.

The enzyme studied in this report, Tet methyl cytosine dioxygenase 2 (TET2), changes the molecular structure (oxidation) of methyl groups and these methyl groups are removed from cytosine. This “demethylation” causes the stem cells to directly mature genes and begins to reverse self-destruction as part of normal work. Neel said that this is an anti-cancer safety mechanism that is destroyed in TET2-mutated blood cancer patients.

To determine the effect of mutations that reduce TET2 function in abnormal stem cells, the team genetically engineered mice to allow scientists to turn the TET2 gene on or off.

Similar to the naturally occurring effects of TET2 mutations in mice or humans, molecular biology techniques can be used to shut off TET2 in mice causing abnormal stem cell behavior. It is worth noting that these changes are reversed when TET2 expression is restored by genetic techniques. Previous work showed that vitamin C stimulates the activity of TET2 and its relatives TET1 and TET3. Since only one copy of two copies of the TET2 gene in each stem cell is usually affected in TET2 mutant blood diseases, the authors hypothesized that high doses of vitamin C can only be injected intravenously, possibly reversing the effects of TET2 deficiency and increasing the remaining functional genes .

In fact, they found that vitamin C functions the same as genetically restoring TET2. By promoting DNA demethylation, high-dose vitamin C treatment induces stem cell maturation and also inhibits the growth of leukemia cancer stem cells in human patients implanted in mice.

“Interestingly, we also found that vitamin C treatment has similar DNA damage effects on leukemia stem cells,” said lead investigator Dr. Luisa Cimmino. “So we decided to combine vitamin C with a PARP inhibitor (a drug that is known to block the death of cancer cells by blocking DNA damage repair) and has been approved for the treatment of certain patients with ovarian cancer.”

The researchers found that this combination has an increased effect on leukemic stem cells, further shifting from self-renewal to maturation and cell death. The results also show that Cimmino said that vitamin C may drive the death of leukemia stem cells without TET2 mutations because it can make any TET2 activity in place.

Corresponding author Dr. Iannis Aifantis, professor and director of the Department of Health Pathology at Langkorn, New York University, said: “Our team is working hard to systematically identify genetic changes that will contribute to the treatment of patients with leukemia. “This study will aberrant TET2-driven DNA. Demethylated targets were added to our list of potential new treatments. ”

* The Content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.