FRIDAY, Aug. 29 (HealthDay News) -- Some Japanese survivors of the World War II atomic bomb blasts in Hiroshima and Nagasaki experienced key genetic changes that may have sparked the onset of a form of thyroid cancer, new research indicates.
Papillary thyroid cancer (PTC) is typically linked to a particular genetic mutation involving the so-called BRAF gene. But Japanese researchers say that among Japanese atom bomb survivors, a different and relatively rare disease trigger -- involving the chromosomal rearrangement of the RET/PTC gene -- seems to be to blame.
Though both mechanisms spur activation of the same enzyme-signaling pathway that leads to PTC, "the RET/PTC rearrangements were more common among cancers from individuals with higher (radiation exposure) doses, cancers that occurred earlier after the A-bomb exposure, and cancers among those who were at younger ages at A-bomb exposure," noted study lead author Kiyohiro Hamatani.
Hamatani is chief of the laboratory of cell biology in the department of radiobiology/molecular epidemiology at the Radiation Effects Research Foundation (RERF), in Hiroshima. He and his colleagues reported their findings in the Sept. 1 issue of Cancer Research.
The finding is just the latest from a decades-long tracking of 120,000 Japanese atom bomb survivors. It comes on the heels of an analysis released this past spring that revealed that young children exposed to radioactive atomic fallout in the blasts faced a greater risk of adult cancers than those exposed to radiation while still in the womb.
With respect to radiation-associated PTC, the authors noted that other studies have uncovered evidence of similar (but not identical) chromosomal rearrangements among childhood survivors of the 1986 Chernobyl nuclear power plant accident in Russia who later developed PTC.
In their study, Hamatani's team found that between 1958 and 1998, there were 63 cases of thyroid cancer attributable to A-bomb radiation exposure, of which 90 percent were of the papillary variety.
They also extracted genetic material called RNA from thyroid tissue samples supplied by 50 patients who had been exposed to atomic bomb radiation, along with 21 patients who were not exposed.
The comparative genetic profiles revealed that younger men and women who lived close to the bomb site when exposed to radioactive fallout, and who went on to develop PTC, were more likely to have the less frequent chromosomal rearrangement.
Hamatani cautioned, however, that he and his colleagues still do not know exactly how radiation exposure might have contributed to the onset of RET/PET rearrangements. It's even possible that radiation exposure may not have played a role in the development of PTC among patients who had the chromosomal rearrangement before they were diagnosed with the disease. Hamatani noted that, among childhood PTC cases in particular, such chromosomal shifts are relatively common, regardless of whether a child has been exposed to radiation or not.
Because of this, Hamatani stressed that any link between radiation and chromosomal changes, "needs to be confirmed with additional PTC patients in the future".
In the meantime, Dr. Alfred I. Neugut, a professor of medicine and epidemiology at Columbia University College of Physicians and Surgeons, and co-director of cancer prevention at New York Presbyterian Hospital, in New York City, said the association "makes biological sense."