Mj. Ramirez et al., Multicolour FISH detection of radioactive iodine-induced 17cen-p53 chromosomal breakage in buccal cells from therapeutically exposed patients, CARCINOGENE, 21(8), 2000, pp. 1581-1586
Simultaneous labelling of 17cen and the p53 locus by multicolour FISH was u
sed to monitor radioactive iodine-induced structural and numerical chromoso
me abnormalities in buccal cells from 29 hyperthyroidism and thyroid cancer
patients sampled before and after therapeutic treatment. This novel method
ology allowed the efficient detection of 17p deletions leading to p53 allel
ic deletions, 17p gains and whole chromosome 17 numerical abnormalities in
epithelial cells. Highly significant increases in the frequency of cells wi
th (i) 17p abnormalities (1.8-fold; P < 0.001), including p53 monoallelic d
eletions (2.1-fold; P < 0.001) and 17p gains (3.5-fold; P < 0.001); (ii) ch
romosome 17 numerical abnormalities (2-fold; P < 0.001); and (iii) simultan
eous 17p breakage and chromosome 17 numerical abnormalities (2.3-fold; P <
0.001), were observed after radioactive iodine treatment. As expected, the
major contribution to these increases was detected in hyperthyroidism patie
nts compared with thyroid cancer patients who suffered thyroidectomy before
radioactive iodine exposure and, therefore, experienced a rapid eliminatio
n of the radioisotope, Considering that both the genetic endpoints and the
target tissue are extremely relevant in carcinogenesis, it is suggested tha
t the observed genetic damage could contribute to the reported increase in
cancer risk of people therapeutically or accidentally exposed to radioactiv
e iodine.