This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Farrand, K. Articles by Grebe, S. K. G. Search for Related Content PubMed PubMed Citation Articles by Farrand, K. Articles by Grebe, S. K. G.

High Resolution Loss of Heterozygosity Mapping of 17p13 in Thyroid Cancer: Hurthle Cell Carcinomas Exhibit a Small 411-Kilobase Common Region of Allelic Imbalance, Probably Containing a Novel Tumor Suppressor Gene

Departments of Medicine (X.W., B.M., I.D.H.), Biochemistry and Molecular Biology (N.L.E.), and Laboratory Medicine and Pathology (J.R.G., S.K.G.G.), Mayo Clinic and Foundation, Rochester, Minnesota 55905; and Department of Pathology and Molecular Medicine, Wellington School of Medicine (K.F., B.D., S.K.G.G.), Wellington, New Zealand

Address all correspondence and requests for reprints to: Dr. Stefan K. G. Grebe, Department of Laboratory Medicine and Pathology, Mayo Clinic and Foundation, 200 1st Street SW, Rochester, Minnesota 55905. E-mail: grebs{at}mayo.edu.

Abstract

There is strong evidence in many tumor types, including thyroid cancer, for a novel tumor suppressor gene (TSG) at 17p13. To identify the putative thyroid 17p13 TSG we mapped thyroid tumor loss of heterozygosity (LOH) at high resolution within this region. We examined 20 typical follicular thyroid carcinomas (FTC), 19 Hurthle cell carcinomas (HCC), 15 papillary thyroid carcinomas (PTC), and 7 follicular adenomas (FA) for LOH at 17p13 using 18 probes. Complete clinical follow-up data were available for all patients. We confirmed a high 17p13 LOH rate in FTC (18 of 20) and HCC (13 of 19) and showed an association between 17p13 LOH and advanced tumor grade. Only 4 of 15 PTC and 1 of 7 FA displayed 17p13 LOH. In the HCC we identified a narrow minimal common deleted region between D17S1308 (285 kb from the p-telomer) and D17S695 (696 kb from the p-telomer). This region was flanked centromerically by a breakpoint cluster, further suggesting nonrandom deletion. All but 1 of the PTC and FA with 17p LOH and 50% of the affected FTC also showed LOH in this region.

These data suggest that a TSG, involved in HCC pathogenesis, is contained within the D17S1308-D17S695 interval. There are several potential candidate TSGs in this region that are worthy of further study.

This article has been cited by other articles:

				E. M Pinto, A. E. C. Billerbeck, M. C. B. V. Fragoso, B. B. Mendonca, and A. C. Latronico Deletion Mapping of Chromosome 17 in Benign and Malignant Adrenocortical Tumors Associated with the Arg337His Mutation of the p53 Tumor Suppressor Protein J. Clin. Endocrinol. Metab., May 1, 2005; 90(5): 2976 - 2981. [Abstract] [Full Text] [PDF]

				E. M. Reis, E. P.B. Ojopi, F. L. Alberto, P. Rahal, F. Tsukumo, U. M. Mancini, G. S. Guimaraes, G. M.A. Thompson, C. Camacho, E. Miracca, et al. Large-scale Transcriptome Analyses Reveal New Genetic Marker Candidates of Head, Neck, and Thyroid Cancer Cancer Res., March 1, 2005; 65(5): 1693 - 1699. [Abstract] [Full Text] [PDF]

				F. Weber, M. A. Aldred, C. D. Morrison, C. Plass, A. Frilling, C. E. Broelsch, K. A. Waite, and C. Eng Silencing of the Maternally Imprinted Tumor Suppressor ARHI Contributes to Follicular Thyroid Carcinogenesis J. Clin. Endocrinol. Metab., February 1, 2005; 90(2): 1149 - 1155. [Abstract] [Full Text] [PDF]