Genetic changes in chromosomes 1p and 17p in thyroid cancer progression

Little is known about the genetic alterations that occur during the progres sion of thyroid neoplasms. To understand better the biology of thyroid tumo rs, we investigated several genetic loci in benign and malignant thyroid ne oplasms. Forty-one thyroid tumors (6 adenomas, 16 papillary, 14 follicular, and 5 anaplastic carcinomas) were studied. Normal and tumor cells were mic rodissected from paraffin-embedded tissues. DNA was used for polymerase cha in reaction-based loss of heterozygosity (LOH) analysis with the following markers: D1S243 (1p35-36), D1S165 (1p36) and D1S162 (1p32), TP53 (17p13), a nd INT-2 (11q13). Immunohistochemistry for Ki-67 was performed. The Ki-67 l abeling index (LI) was the percentage of positive tumor cells. LOH at Ip wa s seen in 2 of 5 (40%) informative cases of anaplastic carcinoma (2 of 2 at D1S162 and 1 of 2 at D1S165) and in 2 of 11 (18%) informative cases of fol licular carcinoma (2 of 7 at D1S243, 2 of 7 at D1S165, and 1 of 6 at D1S162 ). One anaplastic (20%) and two follicular carcinomas (14%) had LOH in at l east two of the Ip loci analyzed. None of the adenomas and papillary carcin omas had LOH at these loci. LOH at 17p and 11q13 were infrequent. Ki-67 LI was 1.4, 7, 16, and 65% in adenomas, papillary, follicular, and anaplastic carcinomas, respectively. Allelic loss at Ip may occur in aggressive types of thyroid carcinoma and may be a marker of poor prognosis. LOH at Ip may r epresent a late genetic event in thyroid carcinogenesis. LOH at 17p and 11q 13 (MEN gene locus) is uncommon in thyroid neoplasms.