Sunday, April 02, 2017

Media distorted cancer cause study, duh

An example of how the media serves the corporate world that pays for ads is the recent claim by the news media that most cancers do not have an environmental cause, are just "bad luck". This is a misinterpretation of the data. And it ignores the fact that pollutants are so widespread that we don't know what the cancer rate would be w/o them. Even this article from Scientific American which corrects the media distortions contains the same kind of click-bait headline. Such headlines are usually not created by the writers of the article, but by those who are concerned with getting reader clicks & advertiser dollars.

https://www.scientificamerican.com/article/most-cancer-cases-arise-from-bad-luck/

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Now the authors of that 2015 paper are back. In a study published on Thursday in Science, they double down on their original finding but also labor mightily to correct widespread misinterpretations of it. This time, using health records from 69 countries, they conclude that 66 percent of cancer-causing genetic mutations arise from the “bad luck” of a healthy, dividing cell making a random mistake when it copies its DNA. [Don't stop reading or you will get the wrong impression.]

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Separate research has shown that roughly 42 percent of cancers are preventable by, for instance, not smoking, maintaining a healthy weight, and not being exposed to cancer-causing pollutants.

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The original “bad luck” study as well as this one compared how rates of cancer in different tissues relate to the frequency with which healthy cells in those tissues — lung, bone, brain, and more — divide.

They found a very close correlation. Cells of the large intestine divide frequently, and 5 percent of people develop cancer in that tissue. Cells of the small intestine divide rarely, and only 0.2 percent of people develop cancer there. Because dividing cells do not always copy their DNA perfectly, every division is an opportunity for a cancer-causing mutation to arise; more divisions, more cancers, the Hopkins team argued.

Overall, they found, about two-thirds of the difference in cancer rates from one kind of tissue to another is due to differences in the rates of cell division in those tissues. That conclusion echoes the one in their previous, US-only study, and held for all 17 cancer types and all 69 countries they analyzed.

That doesn’t mean that two-thirds of cancers are caused by unforced errors in DNA copying, however. The high or low rate of cell divisions account for two-thirds of the differences in cancer rates from one kind of tissue to another. For instance, the “cause” of the Himalayas is the Indian tectonic plate smashing into the Eurasian Plate. That has produced more than a dozen peaks reaching above 26,000 feet. But the difference between K2’s 28,251 feet and Annapurna’s 26,545 feet is nevertheless partly due to random factors, from wind erosion to the angle of the rock strata underlying each mountain.

Similarly, the cause of many cancers might be environmental factors. But the difference in cancer rates in different tissues can still be the result of different underlying rates of cell division. That’s what the Hopkins scientists found.

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Several mutations are required for cancer. Therefore, if two out of three required mutations arise from copying mistakes, but the third comes from an environmental carcinogen, then avoiding that carcinogen prevents the cancer.

This time the Hopkins team agrees. There is a difference between how cancer-causing mutations come about and whether that cancer is preventable, they acknowledge. For instance, 65 percent of mutations in lung cancers arose randomly but 89 percent of those cancers are preventable by avoiding smoking, Tomasetti said.

Their critics argue that the environment’s effect on cancer goes beyond mutations, in which case prevention might have an even bigger role to play. Whether a few malignant cells form a dangerous tumor depends on, among other things, levels of inflammation, insulin, and obesity. Those influences don’t show up in genomic analyses like those the Hopkins researchers did but are affected by lifestyle and environmental factors, said Ross Prentice, a renowned cancer biostatistician at Fred Hutchinson Cancer Center in Seattle.

“Environmental exposures can influence cancer risk in many ways,” he said, including whether cells repair cancer-causing mutations and whether the immune system destroys tumor cells before they cause actual disease.

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Surely environmental factors affect how often cancer-causing mutations come about during cell division. The same rate of environmental causation would be totally expected to result in more mutations in tissue with more cell divisions. Just like the same death rate in a population would result in more deaths in a large city than in a small town.

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