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Cancer is caused by mutations in human DNA. Some lines of the genetic code are deleted or confused and this change allows the cells to proliferate and grow abnormally. Sometimes these DNA changes are genetic — people receive them from their parents — but sometimes they are caused by environmental factors. Understanding the DNA of a tumor can help create the right genetic therapies to combat it.
Over the years, epidemiological studies they have shown that thyroid cancer it is particularly common among people exposed to radioactive iodine, especially among those who suffered when they were small. At relatively high doses, radioactive iodine kills thyroid cells and can actually be used as treatment for thyroid cancer and other thyroid conditions. But Chernobyl radiation was not enough to kill the cells. Instead, Morton says, monthly exposure to lower doses caused changes in the cells that caused the tumor.
In his paper, Morton and his colleagues were able to closely examine the tumors of people living near Chernobyl by examining the DNA of 350 people who developed thyroid cancer who had been exposed to radiation as children. They created a comprehensive molecular image of these tumors. Then, to look at the differences in thyroid cancer caused by other factors, the researchers compared the tissues of 81 people who were born around 1986 in Chernobyl and developed thyroid cancer but never had radiation. Tumors have been compared with data from the Cancer Genome Atlas, which has characterized the genomes of thousands of cancers.
They were found to be mutated genes of cancer caused by exposure to radioactive iodine after dissolution, breaking and shattering the twin strands of DNA. In contrast, thyroid cancer in the Atlas of the Cancer Genome and in the control group of 81 unexplained people in the area were usually caused by single-point mutations where only one base pair of DNA changes.
After the disaster, scientists monitored many communities near Chernobyl, as well as workers responsible for cleaning and collecting the radioactive reactor in a steel and concrete sarcophagus. The researchers conducted extensive interviews with residents about indirect exposure. For example, the radioactive isotopes in the reactor fell into the surrounding fields and the cows who fed the cows ate the radiation they transmitted to their milk and then drank. So the information on dairy consumption provided clues as to how much radiation someone had been exposed to. Physicists and epidemiologists worked together to reconstruct the doses of radiation that would be received by people who donated one hundred samples to all of these direct and indirect measurements. “It’s the only circumstance we know a lot about exposure,” Chanock says. “Most studies of large genome landscapes have no information on where and what people were exposed to.”
This allowed the researchers to study in detail how this cancer process works. They found that the more radiation a person was exposed to, and the younger they were during exposure, the more double-stranded DNA would break.
Finally, the group studied the agents of cancer, the specific genes that were responsible for the growth of the tumor. They found that the molecular characteristics of radiation-induced cancers were not as different as those seen in randomly occurring thyroid cancers. The cause was different (those double-stranded DNA fractures). “That really gave us a sense of how radiation causes cancer,” Morton says.
There were no special biomarkers that labeled these cells mutated as radiation, which told scientists that the radiation effect occurred at the beginning of the carcinogenic process and that the biomarkers – if any – were lost or cleared as the cancer grew. . This molecular similarity indicates that these cases do not require new treatment. “These cancers only look like typical thyroid cancers in the end, so there are no specific consequences for taking a different approach to treatment,” he says.
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