Cancers are caused by mutations in human DNA. A few lines of genetic code are removed or mixed up and this change allows cells to proliferate and develop in an abnormal manner. Sometimes these DNA changes are genetic – people inherit them from their parents – but sometimes they’re caused by environmental factors. Understanding the DNA of a tumor can help create targeted gene therapies to fight it.
For years, epidemiological studies have shown that thyroid cancer is particularly common in people exposed to radioactive iodine, especially in people exposed as children. In high enough doses, radioactive iodine kills thyroid cells and can in fact be used as treatment for thyroid cancer and other thyroid conditions. But the radiation from Chernobyl was not enough to kill the cells. Instead, Morton says, exposure for several months to lower doses caused changes in the cells that resulted in tumors.
In his article, Morton and his colleagues were able to take a closer look at the tumors of people who lived near Chernobyl, studying the DNA of more than 350 people who developed thyroid cancer after being exposed to radiation during their time. youth. They created a complete molecular picture of these tumors. Then, to see how they differed from thyroid cancers caused by other factors, the researchers compared these tumors to tissues of 81 people born near Chernobyl after 1986 who developed thyroid cancer but who didn’t. have never been exposed to radiation. They also compared the tumors to data from the Cancer Genome Atlas, which characterized the genomes of thousands of cancers.
They found that cancer cases caused by exposure to radioactive iodine after the fusion had mutated genes by breaking both strands of DNA and breaking them. In contrast, thyroid cancers in the Atlas of the Cancer Genome and in the control group of 81 unexposed people from the region were more likely to be caused by point mutations, where a single base pair of the DNA is changed.
After the disaster, scientists monitored many communities near Chernobyl, as well as workers responsible for cleaning up and enclosing the radioactive reactor in a steel and concrete sarcophagus. The researchers also conducted in-depth interviews with residents about their indirect exposure. For example, the radioactive isotopes from the reactor fell into the surrounding fields and were eaten by grazing cows, transmitting the radiation to their milk and subsequently to people who drank it. Thus, information on the consumption of dairy products offered clues as to how much radiation a person had been exposed to. Physicists and epidemiologists worked together to reconstruct all of these direct and indirect measurements into a reconstruction of the doses of radiation that the people who donated the tissue samples would have received. “This is a unique circumstance where we know a lot about the exhibit,” says Chanock. “Most of the large genome landscape studies do not contain any information about the places and objects to which people have been exposed.”
This gave researchers the opportunity to take a close look at how this cancer process works. They found that the more radiation a person was exposed to, and the younger they were at the time of exposure, the more double-stranded DNA breaks they would have.
Finally, the team looked at the drivers of cancer, the specific genes whose mutations were responsible for tumor growth. They found that the molecular characteristics of radiation-induced cancers were not that different from what was seen in random thyroid cancers. It was only the cause – those double-stranded DNA breaks – that was different. “That’s what really gave us insight into how radiation causes cancer,” Morton says.
There were no special biomarkers marking these cells as having been mutated by radiation, indicating to scientists that the effect of radiation occurred early in the carcinogenic process and that the biomarkers – if there were any – were lost or eliminated as the cancer grew. This molecular similarity indicates that these cases do not require further treatment. “These cancers really do look, at the end of the day, like typical thyroid cancers, so there are no specific implications for taking a different treatment approach,” she says.