Chromosomal Analysis of Anaplastic Thyroid Carcinomas by Comparative Genomic Hybridization.
10.3803/jkes.2005.20.4.362
- Author:
Mi Kyoung KIM
1
;
Chang Hun LEE
;
Jin Mi SONG
;
Kyung Yub GONG
;
Yong Ki KIM
Author Information
1. Department of Internal Medicine, Wallace Memorial Baptist Hospital, USA.
- Publication Type:Original Article
- Keywords:
Anaplastic Thyroid Carcinoma;
Comparative Genomic Hybridization;
Cyclin D1
- MeSH:
Base Sequence;
Carcinogenesis;
Comparative Genomic Hybridization*;
Cyclin D1;
Cytogenetic Analysis;
DNA;
Genes, Tumor Suppressor;
Neoplasm Metastasis;
Oncogenes;
Thyroid Gland*;
Thyroid Neoplasms*
- From:Journal of Korean Society of Endocrinology
2005;20(4):362-374
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Compared with common well-differentiated thyroid carcinomas, the genetic alterations underlying the development and progression of anaplastic thyroid carcinomas(ATC) are still uncharacterized. Comparative genomic hybridization(CGH) is a cytogenetic technique that can identify gains and losses in the DNA sequence copy number in tumors. METHODS: The authors studied the changes in the DNA copy number due to CGH in paraffin-embedded tissue blocks of 17 ATC cases, and tried to ascertain whether the genomic changes correlate with the clinicopathological parameters including patients' age, sex, primary tumor size, lymphovascular invasion, extrathyroid extension, regional node metastasis and immunohistochemical expression of cyclin D1. RESULTS: Fourteen of the 17 samples(82.4%) showed chromosomal changes, with a mean number of gains or losses per carcinoma of 3.6(range 2~6; 30 gains and 21 losses). The most frequently detected imbalance was the gain of chromosome 1q, which was seen in 35.7% of cases, particularly commonly in ATC associated with a papillary thyroid carcinoma. Other commonly occurring gains were present in 11q13 and 19(28.6%, respectively). Genomic amplification was detected in all four cases showing the 11q13 gain. Genomic losses were commonly noted in 3q, 6q, 18q andchi(21.4%, respectively). When numerical CGH alterations were compared to the clinicopathological parameters, there were no significant correlations(P>0.05). Cyclin D1 expression was noted in sixteen of the 17 cases(94.1%), but the extent of cyclin D1 expression was not correlated with the numerical CGH alterations(P>0.05). CONCLUSION: Taken together, the aberrations of 1q, 3q, 6q, 11q13 and 18q are relatively common in ATC, and may play an important role it developement. These findings should lead to the characterization of tumor suppressor genes and oncogenes that are potentially involved in the carcinogenesis of ATC. The amplification of 11q13 is characteristically found, but cyclin D1 in this region may be innocent of the aggressiveness of these carcinomas.
