By IANS,
Washington : Radiation from the atomic bomb detonations in Hiroshima and Nagasaki in 1945 possibly rearranged chromosomes in some survivors who later developed papillary thyroid cancer as adults, according to a research.
Papillary thyroid cancer forms in follicular cells in the thyroid and grows in small finger-like shapes. It grows slowly, is more common in women than in men, and often occurs before age 45. It is the most common type of thyroid cancer.
The scientists reported that subjects who stayed close to the blast sites, were comparably young at the time and developed the cancer quickly once they reached adulthood and were likely to have a chromosomal rearrangement known as RET/PTC that is otherwise not very frequent in adults who develop the disease.
“Thyroid cancer is associated with exposure to external or internal ionising radiation. Elucidation of mechanisms of radiation-induced cancer in humans, especially early steps and pathways, has potential implications for epidemiological risk analyses, early clinical diagnosis, and chemo-preventive interventions,” said the study’s co-author, Kiyohiro Hamatani, lab chief at the Radiation Effects Research Foundation (RERF) in Hiroshima.
He added that there are several irradiated populations worldwide that have been shown to have an increase in thyroid cancer, and that children exposed to radioactive fallout from the 1986 Chernobyl nuclear power plant accident who develop papillary thyroid cancer have also been found to have RET/PTC rearrangements, although they are slightly different.
This study is part of the foundation’s long running follow-up research on 1,20,000 atomic bomb survivors. During 1958 to 1998, the study found about 470 thyroid cancer cases of which the estimated number of excess cases attributable to radiation is 63. About 90 percent of thyroid cancer among the survivors is of the papillary type.
Researchers looked at the genetic profile of cancer patients in the RERF’s follow-up study — 50 patients who were exposed to atomic bomb radiation and 21 patients who were not.
The researchers do not know exactly how radiation is involved in the occurrence of RET/PTC rearrangements. “It could be either by direct DNA damage or by other pathways such as a result of radiation-induced genomic instability,” Hamatani said.
These findings are scheduled for publication in September 1 issue of Cancer Research.