Cancer and DNA

     Excessive alcohol consumption, highly processed sugary foods, vitamin D deficiency and toxic substance poisoning are the main causes of cancer and most of them can be prevented or controlled. Even genetic risk can be controlled with a healthy lifestyle, especially if it is personalized according to DNA. Based on our DNA, we can discover which strategies will adapt to our lifestyle to effectively prevent this disease.

    The enzyme dihydrofolate reductase catalyses the conversion of dihydrofolate (DHF) into tetrahydrofolate (THF), a methyl group shuttle required for the synthesis of purines, thymidine and nucleic acids - precursors to DNA and RNA. The action of DHFR on folic acid (synthetic folate) absorbed in the liver is slower than on dietary folate absorbed in the intestine. Anti-folate drugs such as methotrexate target DHFR to deplete cells of reduced folate resulting in the suppression of purine and pyrimidine precursor synthesis. Variants on the DHFR gene may down regulate or up regulate activity. Lower activity may protect against certain cancers (colorectal cancer and childhood leukaemia), similar to the action of methotrexate, however, the consequent deficiency of folate can increase susceptibility to megaloblastic anaemia, neural tube defects and spina bifida. Higher enzyme activity can deplete 5,10 Methylene-THF and 5-MTHF required for synthesis of SAMe (the master methyl donor) and may tilt the balance in favour of DNA synthesis at the expense of methyl supply which can lead to aberrant DNA methylation and instability. High intake of folic acid (synthetic folate) has been linked to higher DHFR activity and increased risk of breast cancer in DHFR 19-bp deletion carriers. The DHFR A16352G polymorphism shows decreased DHFR activity, which may result in reduced folate absorption. The presence of a 19bpDEL deletion in DHFR is associated with up to 2.4x greater expression of DHFR and increased enzymatic activity. This can deplete the 5,10-methylene-THF pool, the critical substrate for DNA synthesis and remethylation of homocysteine that provides the methyl donor (SAMe) for reactions of methylation, which can lead to instability in the methylation of DNA. This genotype has also been associated with increased (up to 2x) liver toxicity from methotrexate treatment. High intake of folic acid (synthetic folate) for this genotype increases the risk of adverse health effects.

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