High rates of ras codon 61 mutation in thyroid tumors in an iodide-deficient area.
Using polymerase chain reaction and sequence-specific oligonucleotide hybridization, the frequency of three ras oncogene mutations (N-ras, Ha-ras, and K-ras) in thyroid tumors (25 adenomas, 16 follicular carcinomas, and 22 papillary carcinomas) was investigated in both iodide-deficient and iodide-sufficient areas. The ras oncogene mutation rate was significantly higher in the iodide-deficient area, being 85 versus 17% in the adenomas, and 50 versus 10% in the follicular carcinomas. No mutations were found in papillary carcinomas. The most common mutation site was Ha-ras codon 61 with Gln----Arg substitution. Two ras mutations at codon 61 (Gln----Lys in N-ras and Gln----Arg in Ha-ras) were found in a microfollicular adenoma specimen from Eastern Hungary. We conclude that dietary iodine may modulate ras oncogene mutations, and that in the iodide-deficient area, ras oncogene activation may play a more important role in the initiation and/or maintenance of follicular tumors. Additional factors are, however, necessary to initiate carcinogenesis.
Shi
Y F
YF
Thyroid Research Laboratory, Health Sciences Centre, St. John's, Newfoundland, Canada.
Zou
M J
MJ
Schmidt
H
H
Juhasz
F
F
Stensky
V
V
Robb
D
D
Farid
N R
NR
D000230:Adenocarcinoma / Q000209:etiology / Q000235:genetics*; D000236:Adenoma / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D002291:Carcinoma, Papillary / Q000209:etiology / Q000235:genetics*; D003062:Codon / Q000235:genetics*; D011905:Genes, ras; D006801:Humans; D006814:Hungary; D007455:Iodine / Q000172:deficiency*; D009154:Mutation; D013964:Thyroid Neoplasms / Q000209:etiology / Q000235:genetics* / Q000473:pathology
D003062:Codon; D007455:Iodine