B-6 and Leukemia
Leukemia, a kind of blood cancer that mainly affects children and older adults, is the tenth most frequent type of cancer in the United States, accounting for 3.5 percent of all new cancer cases. The National Cancer Institute reports that the illness is also the sixth leading cause of cancer mortality in the United States. According to statistics, an estimated 22,840 individuals died of leukemia in 2019.
Acute myeloid leukemia (AML) is the disease’s second most prevalent subtype. AML spreads rapidly, resulting in a poor survival rate. Less than a third of patients diagnosed with AML survive five years following diagnosis. AML’s malignant cells divide at a rate that exceeds the rate at which the present therapy can eradicate them. Developing a novel treatment that is more effective in targeting these cells is critical for long-term survival.
Cancer cells employ metabolic alterations —numerous activated or accelerated cell activities — to grow and spread at an abnormal rate. One of the most distinguishing characteristics of a leukemic cell is its altered metabolic pathways to promote aberrant cell proliferation.
The function of Vitamin B-6
The mechanism through which AML cells divide so rapidly has been uncovered. Surprisingly, it is centered on a certain vitamin.
Vitamin B-6 is required for optimal bodily function. It is entirely derived from a person’s food and aids in cell development and metabolism and the production of neurotransmitters and red blood cells.
A study team discovered over 230 distinct genes active in leukemic cells by extracting genes from AML’s malignant white blood cells. The researchers examined each one using CRISPR gene editing techniques to inhibit each gene’s activity.
Cancer utilizes and abuses
The scientists sought and discovered a gene that inhibited the spread of malignant cells. A gene that encodes a metabolic enzyme called pyridoxal kinase (PDXK).
PDXK regulates vitamin B-6 use by synthesizing proteins that convert the vitamin to its active form. When cells are healthy, they do not require vitamin B-6 continuously. When the moment is perfect for cells to divide, the enzyme activates it. However, the researchers discovered that the enzyme boosted this vitamin in quickly proliferating malignant cells.
This resulted in the proliferation of AML cells, perhaps resulting in the disease’s continued development and dissemination. Pyridoxal kinase has been demonstrated to be required for leukemic cell proliferation. Vitamin B-6 is required by leukemic cells, rendering a susceptibility to the disease.
Cancer researchers were previously aware that vitamin B-6 regulated various enzymes essential for synthesizing the building blocks necessary for cell growth and proliferation. Research showed that the vitamin B-6 route might be necessary for cancer survival.
Achieving a more effective therapy
Most significantly, this enzyme-vitamin combination may represent a potential target for a new, more successful kind of treatment. It would not be as straightforward as just lowering patients’ vitamin B-6 consumption, as this might impair critical B-6 functions throughout the body, including the brain and the rest of the central nervous system.
Rather than that, medicinal chemists are developing a medication that inhibits the PDXK enzyme. Inhibiting PDXK prevents leukemic cells from using vitamin B-6 to their advantage. Not only might this approach slow or stop the spread of leukemia, but it could also spare healthy cells that rely on vitamin B-6 for life.
B vitamins and their role in cancer immune regulation
Chronic inflammation can result in cancer through epigenetic modification. Infection and irritation can induce chronic inflammatory states that promote genomic lesions and tumor start, activate oncogenes, and impair tumor suppressor activity, all of which contribute to cancer formation.
Inflammation-induced genetic changes efficiently equip cancer cells with a mechanical mechanism of survival. Current scientific thinking on inflammation and cancer progression is centered on identifying ways to mitigate inflammation to prevent the formation of cancer and give a potential cure.
Numerous clinical and epidemiological investigations have established a strong link between inflammation and the development of cancer. Indeed, people with inflammatory bowel disorders such as ulcerative colitis or Crohn’s disease have a tenfold increased risk of developing colorectal cancer.
By contrast, it has been demonstrated that malignancies of the gastrointestinal tract, prostate, and liver arise from areas of persistent inflammation. Additionally, several studies in the literature show vitamin B’s function in regulating immune responses and inflammation.
Inadequate B vitamin levels can significantly change immune response by impairing nucleic acid and protein synthesis, limiting immune cell function, and interfering with metabolic processes such as methylation, serine, glycine, and purine cycles.
Inadequate methylation can result in hyperhomocysteinemia, a condition in which the body has an abnormally high homocysteine level. This results in widespread and vascular inflammation, which leads to the development of various illnesses. Numerous molecular consequences of vitamin B deficiency are associated with cancer growth characteristics.
The current level of research about B vitamins and inflammation is mostly focused on the impact of vitamin B deficient states and the pathologies associated with these deficiencies. There is a wealth of data demonstrating the critical function of B vitamins in immunity. It is widely acknowledged that an inadequate diet has a detrimental effect on immune cells.
Globally, chronic malnutrition is the leading cause of immune insufficiency, and chronic illnesses result from even minor deficiencies; vitamins B2, B6, and B9 are critical components of the immune system’s nutritional support. Inadequate levels of these may significantly impair immune function by interfering with nucleic acid and protein synthesis, impairing immune cell activity, interfering with metabolic processes such as methylation, and contributing to oxidative stress.
Hyperhomocysteinemia is caused by inefficient methylation, which contributes to disease pathogenesis by triggering systemic and vascular inflammation. Immune dysfunction at the cellular level can manifest as abnormal antigen presentation, dysregulated cytokine production, unmodulated autoimmune responses, immune cell function abnormalities, and inefficient virus clearance.
Additionally, vitamin B2 is critical for the immune system because it is connected with mucosal-associated invariant T lymphocytes involved in autoimmune, inflammatory, and cancer disorders. B2, B6, and B9 play critical roles in DNA and protein synthesis, cell maintenance, and proliferation, all of which affect how deficient conditions influence the immune system.
B vitamin shortage impairs both cell-mediated and humoral immunity, with varying effects on immune cells. Numerous studies have demonstrated that B vitamin supplementation enhances the immune response in both animal and human models. However, some studies have indicated that excessive supplementation may have a detrimental effect on immunological function.