LifeSmart - "Doctor, what is the cause of my cancer?" For doctors, this question is often confusing. Some of the population risk factors are known, but with regard to specific cases, only assumptions can be given. Even so, scientists have an increasing understanding of the mechanisms underlying tumor development. Although some are still very polemical.
Two US researchers have recently sparked controversy with their research on the role of "fate" in cancer. Their latest article is published in the prestigious March issue of the journal Science. The researchers, Christian Tomasetti and Bert Vogelstein of Johns Hopkins University in Baltimore, point out that the disease is less dependent on heredity (a genetic predisposition) and environmental risks (such as smoking, or exposure to asbestos) than in random mutations (such as errors DNA replication) that arise spontaneously in cells when splitting and reproducing throughout our lives.
In other words, "luck" has much to do with it. In a 2015 article, also in Science magazine, they have been researching the frequency of cancer in different tissues in the human body. For example, the lifetime risk of lung cancer is 6.9%, compared with 1.08% risk of thyroid cancer, even less risk for brain cancer and other cancers.
In other words, "luck" has much to do with it. In a 2015 article, also in Science magazine, they have been researching the frequency of cancer in different tissues in the human body. For example, the lifetime risk of lung cancer is 6.9%, compared with 1.08% risk of thyroid cancer, even less risk for brain cancer and other cancers.
Cancer is more common in the colon than the small intestine
These differences are generally associated with greater exposure to specific tissues against various risk factors such as tobacco, alcohol, and ultraviolet light. But this does not explain why in the digestive system, for example, the colon is more often exposed than other organs. In fact, the small intestine (between the stomach and the large intestine) is much more exposed to substances that cause mutation than brain cells, but cerebral tumors are three times more prevalent.
This paradox also applies to hereditary malignancies. Although the same genetic mutation is responsible for colorectal tumors and intestinal tumors, the latter is much more rare. However, in mice with mutations, the tendency is reversed: they develop tumors in the small intestine more often than in the colon.
Hence Tomasetti and Vogelstein put forward the hypothesis that the cause may lie in spontaneous mutations that take place during stem cell division (undifferentiated cells). In humans, stem cells are updated at a higher rate in the colon than in the small intestine, whereas in mice the opposite is true. The more often the cells divide, the higher the risk of errors in the process of copying DNA. This could explain the difference in cancer frequency in organs that are equally exposed to heredity and environmental risk.
This paradox also applies to hereditary malignancies. Although the same genetic mutation is responsible for colorectal tumors and intestinal tumors, the latter is much more rare. However, in mice with mutations, the tendency is reversed: they develop tumors in the small intestine more often than in the colon.
Hence Tomasetti and Vogelstein put forward the hypothesis that the cause may lie in spontaneous mutations that take place during stem cell division (undifferentiated cells). In humans, stem cells are updated at a higher rate in the colon than in the small intestine, whereas in mice the opposite is true. The more often the cells divide, the higher the risk of errors in the process of copying DNA. This could explain the difference in cancer frequency in organs that are equally exposed to heredity and environmental risk.
The rate of tissue update associated with higher cancer risk
Their study of the alleged link between the number of stem cell divisions in a particular tissue throughout life and the risk of cancer in the area shows a strong correlation. The higher the rate of stem cell renewal, the higher the cancer risk in the tissue. These results, based on data from the American population, are supported by a second study published in March this year, which found the same average correlation in 69 countries.
The two researchers then began to isolate the effects of spontaneous mutations from other, derivative and environmental risk factors. They point out that the majority of cancers are caused by "bad luck" -in other words, by random spontaneous mutations. "Luck" even plays a significant role in cancer where environmental causes are so believed, such as the causes associated with smoking.
The results of the research have caused quite a bit of controversy because it can encourage us to believe that encouraging citizens to behave in a healthy way - such as quitting smoking and eating lots of vegetables and fruit - is not as important as we think it has been. The data of the two researchers were even reviewed by a separate team, which found luck did not play such an important role.
The two researchers then began to isolate the effects of spontaneous mutations from other, derivative and environmental risk factors. They point out that the majority of cancers are caused by "bad luck" -in other words, by random spontaneous mutations. "Luck" even plays a significant role in cancer where environmental causes are so believed, such as the causes associated with smoking.
The results of the research have caused quite a bit of controversy because it can encourage us to believe that encouraging citizens to behave in a healthy way - such as quitting smoking and eating lots of vegetables and fruit - is not as important as we think it has been. The data of the two researchers were even reviewed by a separate team, which found luck did not play such an important role.
The effects of oxidative stress on DNA
Keep in mind that scientific literature in microbiology, directly related to cancer research or not, offers an abundance of articles on DNA mutations and damage. In an article published in 2000, American scientist Lawrence Marnett analyzed the effects of oxidative stress (attacks on our cells by reactive oxygen species, or "free radicals") and found these effects far more significant than those associated with carcinogenic substances. And, oxidative stress is not the only cause of DNA damage, as can be seen in a 2004 summary of Roel De Bont and Nicolas Van Larebeke.
In an article published earlier this year, Anthony Tubbs and Andre Nussenzweig stressed that every human cell's DNA experiences about 70,000 wounds per day. We will not live long if the body has no way of correcting those mistakes, especially if all those errors encourage us to develop tumors. It is important to remember that tumors only appear after several control mechanisms fail.
At first, the normal repair process of damaged DNA cells must fail. Then, it can reproduce in a haphazard way, meaning it in principle must have influenced the genes responsible for cell duplication, or that governs the duplication. Damaged cells also must pass the programmed self-destruction is naturally known as apoptosis) and the vigilance of the immune system, whose job is to eliminate foreign elements and elements of other disfungional.
Cell contact with external or internal mutagen is thus only one step in the long sequence of failures that must occur before a tumor can develop.
In an article published earlier this year, Anthony Tubbs and Andre Nussenzweig stressed that every human cell's DNA experiences about 70,000 wounds per day. We will not live long if the body has no way of correcting those mistakes, especially if all those errors encourage us to develop tumors. It is important to remember that tumors only appear after several control mechanisms fail.
At first, the normal repair process of damaged DNA cells must fail. Then, it can reproduce in a haphazard way, meaning it in principle must have influenced the genes responsible for cell duplication, or that governs the duplication. Damaged cells also must pass the programmed self-destruction is naturally known as apoptosis) and the vigilance of the immune system, whose job is to eliminate foreign elements and elements of other disfungional.
Cell contact with external or internal mutagen is thus only one step in the long sequence of failures that must occur before a tumor can develop.
The role of stress
In the discussion phase of the role of "bad luck" in the appearance of this cancer, it is appropriate to notice the special role played by individual stress, the subject of my work Stress and Cancer: When we attach Plays Tricks on Us (De Boeck). Every step towards cancerous cells is sensitive to stress and stress hormones. Hence chronic psychological stress, which is currently primarily caused by psychological stress, can be considered a direct cause of cancer. I need to add, however, there are still open disagreements on this issue.
Chronic psychological stress in fact does accelerate cell reproduction, including telomere shortening, "hood" that protects our chromosomes from wear. This phenomenon is revealed by the research of Elizabeth Blackburn, who won the Nobel Prize in Medicine for discovering telomerase. The more these differentiated cells multiply, the higher the risk of random mutations of their DNA. In addition, more and more differentiated cells grow old and die, the more stem cells divide to make new cells, heightening the risk of developing cancer.
But that's not all. Through the neuroendocrine process, psychological stress also affects oxidative metabolism, DNA repair, oncogen expression and production growth factors. This raises common problems associated with chronic inflammation and loss of effective immune function, as can be seen in the studies cited in my book.
Controversy "bad luck" that surrounds and Vogelstein Tomasetti study provide new food for thought. They point out that, according to the Cancer Research UK organization, 42% of cancers can be avoided by changing the environment and lifestyle. In France, the national cancer institute reported a similar ratio to preventable cancers. This number is high and not as low as expected. Does this mean there is nothing to do with about 60% of other cases?
What is clear, Tomasetti and Vogelstein suggests ways to fight the "bad luck". They suggest, among other things, the use of antioxidants in cancer prevention. Given the dangerous process run by stress, protecting one's psychological health is also an effective weapon to fight cancer.
Chronic psychological stress in fact does accelerate cell reproduction, including telomere shortening, "hood" that protects our chromosomes from wear. This phenomenon is revealed by the research of Elizabeth Blackburn, who won the Nobel Prize in Medicine for discovering telomerase. The more these differentiated cells multiply, the higher the risk of random mutations of their DNA. In addition, more and more differentiated cells grow old and die, the more stem cells divide to make new cells, heightening the risk of developing cancer.
But that's not all. Through the neuroendocrine process, psychological stress also affects oxidative metabolism, DNA repair, oncogen expression and production growth factors. This raises common problems associated with chronic inflammation and loss of effective immune function, as can be seen in the studies cited in my book.
Controversy "bad luck" that surrounds and Vogelstein Tomasetti study provide new food for thought. They point out that, according to the Cancer Research UK organization, 42% of cancers can be avoided by changing the environment and lifestyle. In France, the national cancer institute reported a similar ratio to preventable cancers. This number is high and not as low as expected. Does this mean there is nothing to do with about 60% of other cases?
What is clear, Tomasetti and Vogelstein suggests ways to fight the "bad luck". They suggest, among other things, the use of antioxidants in cancer prevention. Given the dangerous process run by stress, protecting one's psychological health is also an effective weapon to fight cancer.
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