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High Rates of ras Codon 61 Mutation in Thyroid Tumors in an Iodide-deficient Area

Thyroid Research Laboratory [Y. S., M. Z., H. S., N. R. F.] and Department of Pathology [D. R.], Health Sciences Centre, St. John's, Newfoundland, Canada A1B 3V6, and II Department of Surgery [F. J.] and Blood Bank [V. S.], Debrecen, Hungary

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.

¹ To whom requests for reprints should be addressed, at Department of Medicine, King Faisal Specialist Hospital and Research Centre, P.O. Box 3354, Riyadh 11211, Saudi Arabia.

Received 11/ 8/90. Accepted 3/ 1/91.

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