Vitamin C may stop leukemia from progressing
Vitamin C may stop leukemia from progressing:- Since the 1970s, researchers have taken an interest in high-dose vitamin C and its therapeutic potential for treating cancer. New research shows how vitamin C might stop leukemic stem cells from multiplying, and thus block some forms of blood cancer from advancing.
The evidence for vitamin C as an effective treatment for cancer remains controversial. Several studies have shown that it works against a wide variety of cancers, including pancreatic cancer, liver cancer, colon cancer, and ovarian cancer. Other studies, however, have suggested that it might make chemotherapy less effective.
New research – conducted by scientists at the Perlmutter Cancer Center at New York University (NYU) Langone Health in New York City – investigates the effect of vitamin C on blood cancer.
The first author of the study is Luisa Cimmino, Ph.D., an assistant professor in the Department of Pathology at NYU Langone Health, and the findings were published in the journal Cell.
The role of the enzyme TET2 in leukemia
An enzyme called Tet methylcytosine dioxygenase 2 (TET2) is known to have the ability to make stem cells – which are undifferentiated cells that have not yet gained a specific identity and function – differentiate into mature, normal blood cells that end up dying similarly to any other normal cell.
This is beneficial to patients with leukemia, in which blood stem cells are not “told” to mature, so instead, they regenerate themselves and multiply ad infinitum. This stops the body from producing normal white blood cells, which our immune system needs to fight infection.
Genetic changes can influence this enzyme’s beneficial action. The authors note in their study that 10 percent of acute myeloid leukemia patients, 30 percent of patients with a type of pre-leukemia called myelodysplastic syndrome, and 50 percent of those with chronic myelomonocytic leukemia have a genetic malfunction that reduces TET2.
Therefore, Prof. Cimmino and colleagues set out to examine how this enzyme can be genetically stimulated, and whether or not vitamin C can be used to do so.
Switching the TET2 gene on and off
The researchers genetically engineered mice to lack the enzyme, having designed mouse models with the TET2 gene “switched on” and “off.” When the gene was off, the researchers found that stem cells started to malfunction. When the researchers turned the gene back on, these malfunctions were reversed.
It was known to the researchers that, in leukemia and other blood diseases that depend on TET2 genetic malfunctions, only one of the two copies of the TET2 gene is altered.
So, they hypothesized that a high dose of vitamin C administered intravenously might compensate for the faulty copy of the gene by amplifying the action of the copy that still functions normally.
Vitamin C, PARP inhibitors block cancer cells
The study confirmed the researchers’ hypothesis. They found that high-dose vitamin C promoted a genetic mechanism that restored TET2 function. This mechanism is called DNA demethylation – a process that, simply put, activates genes that “tell” stem cells to mature and evolve toward death, as normal. This process does not work properly in patients with TET2 genetic mutations.
The new study, however, gives such patients hope, as the researchers found that intravenous treatment with vitamin C promoted DNA demethylation, “telling” stem cells to mature and die. The treatment also stopped leukemia cancer stem cells that had been transplanted from human patients to mice from growing in the rodents.
The results prompted the researchers to see what would happen if they combined the therapeutic potential of vitamin C with a class of anticancer drugs called PARP inhibitors. These are “a drug type known to cause cancer cell death by blocking the repair of DNA damage, and [are] already approved for treating certain patients with ovarian cancer,” explains Prof. Cimmino.
The researchers found that this combination boosted the efficacy of the vitamin C treatment, making it even more difficult for the leukemic stem cells to self-renew.
Source:-Â http://www.medicalnewstoday.com/articles/319017.php
