There is no foolproof method, or plan, with which one can prevent cancer. But, one neat way of doing it, perhaps, is by asking the cells in our body not to divide – a gigantic task, but a scientific reality of the future.
Another huge possibility, according to Bruce Ames, Co-Director of the National Foundation for Cancer Research [NFCR] Center for Genomics and Nutrition, University of California, US, is: “Reverse the process, and look at human cells in culture, deficient in one nutrient, and see what happens.”
Deficiencies of vitamins B12, B6, or folic acid, are suggested to replicate our DNA into components that are not congenial to healthy outcomes. In other words, they lead to shortfalls that can “crack” our chromosomes and cause cancer.
Selenium, a micronutrient, is said to protect against cancer. Also beta carotene, the vitamin A precursor, and anti-oxidant, which keeps cell activity in tact and specialised. New research also evidences that vegetables rich in this nutrient reduces the risk of cancer substantially. There are others too, such as vitamin C and E, which have known anti-oxidant properties.
Cancer research and therapy is geared to meet a long-standing, major challenge, all right: malignancy. Drugs to prevent occurrence or inhibit the growth of a precursor lesion is, therefore, the focus, and the basis of chemoprevention. This includes a host of “ammos,” such as nutrients and phytochemicals [nutraceuticals] – e.g., dietary fibre, soy-genistein, curcumin, green tea etc., – that are all useful in preventative cancer care and management.
Signal the risk
One quick way to hit upon cancer risk, according to emerging research, are biomarkers that monitor precancerous tissues [e.g., intestinal polyps, or oral lesions], and pinpoint a cancerous invasion. Another is the use of newer, and safer, chemopreventive medications, acceptable to discerning consumers. According to Michael Sporn, Oscar M Cohn Professor of Pharmacology and Toxicology at Dartmouth Medical School, US: “People say, ‘how dare we treat healthy people with drugs that subject them to risk?’ But, how dare we not treat someone who we know has a high risk, when we have something to diminish that risk. We can identify people at high risk using genetic [and, cancer] markers, and start to think about intervening earlier.” This is half of the battle won.
Sceptics, however, say that the thoughtful idea carries a double-edged sword. Because, on the one hand, it can prevent cancer and, on the other, it can lead to drug-induced problems. For example, most adenomas [benign cancer states] do not progress to cancer. Also, long-standing use of aspirin, a cancer-pharmaceutical, for instance, can sometimes result in life-threatening complications.
Further along the road of chemoprevention, what with its encouraging results, are selective oestrogen receptor modulators [SERMs] in breast cancer – to highlight one example. Tamoxifen, a SERM, given to women with oestrogen receptor-positive disease, is suggested to prevent cancer in the unaffected breast.
This brings us to one important perspective – that cancer prevention has to work at multiple levels, keeping in mind the awesome possibilities of one tumour developing over a long period of time, more so in the wake of a trillion cell divisions taking place in our body. This is, again, a tough call, because, for all of this and more to happen, over decades at a stretch, it is possible for just one cell to develop the changes needed for a tumour to grow – a tumour that cannot be whisked away by natural mechanisms!
The bottom line, therefore, is simple and complex: it is imperative for new research to slow down the progression of cancer in its tracks with more potent and less harmful therapies – preventative and therapeutic. It’s a prospect that holds the key to stall a disease that is as dangerous as it sounds.
Unmasking our genetic roots, therefore, promises to be a more practical and utilisable option to manage cancer.
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