Loss of Heterozygosities in Five Tumor Suppressor Genes (FHIT Gene, p16, pRb, E-Cadherin and p53) in Thyroid Tumors
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Objectives. To evaluate the loss of heterozygosities (LOH) of chromosomes 3p14 (FHIT gene), 9p21 (p16), 13q21 (pRb), 6q22 (E-cadherin) and 17p13 (p53) in various thyroid tumors. Methods. Eighty thyroid tumor cases (20 follicular adenomas, 10 follicular carcinomas, and 50 papillary carcinomas) have been analyzed for the presence of LOH in chromosomes 3p14, 9p21, 13q21, 6q22, and 17p13 allelic loss, using mic- rosatellite markers and DNA obtained from formalin-fixed paraffin-embedded archival tissues. Results. LOH on 3p14 was found in 10.5%, 33.3%, and 30.4% of follicular adenomas, follicular carcinomas, and papillary carcinomas, respectively. LOH on 9p21 was detected in 6%, 44.4%, and 47.8%, respectively. LOH on pRb gene was found in 5.3%, 20.0%, and 35.4%, respectively. LOH on E-cadherin gene was found in 5.3%, 22.2%, and 43.8%, respectively. LOH on 17p13 was detected in 0%, 40%, and 45.8%, respectively. LOH in FHIT gene, p16, pRb, E- cadherin, and p53 genes were more frequently identified in follicular carcinoma and papillary carcinoma than in fol- licular adenoma. Conclusion. LOH results of the five tumor suppressor genes (FHIT gene, p16, pRb, E-cadherin, and p53) showed statistical differences between benign tumor and malignant tumor. Among papillary carcinoma, LOH in p16, E-cadherin and p53 genes well correlated with poorly differentiated grade, and LOH of E-cadherin was associated with lymph node metastasis.
Abstract
Objectives. To evaluate the loss of heterozygosities (LOH) of chromosomes 3p14 (FHIT gene), 9p21 (p16), 13q21 (pRb), 6q22 (E-cadherin) and 17p13 (p53) in various thyroid tumors. Methods. Eighty thyroid tumor cases (20 follicular adenomas, 10 follicular carcinomas, and 50 papillary carcinomas) have been analyzed for the presence of LOH in chromosomes 3p14, 9p21, 13q21, 6q22, and 17p13 allelic loss, using mic- rosatellite markers and DNA obtained from formalin-fixed paraffin-embedded archival tissues. Results. LOH on 3p14 was found in 10.5%, 33.3%, and 30.4% of follicular adenomas, follicular carcinomas, and papillary carcinomas, respectively. LOH on 9p21 was detected in 6%, 44.4%, and 47.8%, respectively. LOH on pRb gene was found in 5.3%, 20.0%, and 35.4%, respectively. LOH on E-cadherin gene was found in 5.3%, 22.2%, and 43.8%, respectively. LOH on 17p13 was detected in 0%, 40%, and 45.8%, respectively. LOH in FHIT gene, p16, pRb, E- cadherin, and p53 genes were more frequently identified in follicular carcinoma and papillary carcinoma than in fol- licular adenoma. Conclusion. LOH results of the five tumor suppressor genes (FHIT gene, p16, pRb, E-cadherin, and p53) showed statistical differences between benign tumor and malignant tumor. Among papillary carcinoma, LOH in p16, E-cadherin and p53 genes well correlated with poorly differentiated grade, and LOH of E-cadherin was associated with lymph node metastasis.
참고문헌 (15)
- Zou M, "FHIT gene abnormalities in both benign and malignant thyroid tumours", Eur J Cancer, 35(3), pp.467~472 (1999)
- Roque L, "Chromosome imbalances in thyroid follicular neoplasms: a comparison between follicular adenomas and carcinomas", Genes Chromosomes Cancer, 36(3), pp.292~302 (2003)
- Kitamura Y, "Association of allelic loss on 1q, 4p, 7q, 9p, 9q, and 16q with postoperative death in papillary thyroid carcinoma", Clin Cancer Res, 6(5), pp.1819~1825 (2000)
- Grebe SK, "Frequent loss of heterozygosity on chromosomes 3p and 17p without VHL or p53 mutations suggests involvement of unidentified tumor suppressor genes in follicular thyroid carcinoma", J Clin Endocrinol Metab, 82(11), pp.3684~3691 (1997)
- Semczuk A, "Loss of heterozygosity of the retinoblastoma gene is correlated with the altered pRb expression in human endometrial cancer", Virchows Arch, 441(6), pp.577~583 (2002)
- Naito A, "Clinical significance of E-cadherin expression in thyroid neoplasms", J Surg Oncol, 76(3), pp.176~180 (2001)
- Huiping C, "Analysis of the fragile histidine triad (FHIT) gene in lobular breast cancer", Eur J Cancer, 36(12), pp.1552~1557 (2000)
- Lee SH, "Altered expression of the fragile histidine triad gene in primary gastric adenocarcinomas", Biochem Biophys Res Commun, 284(3), pp.850~855 (2001)
- Weinberger PM, "Molecular classification identifies a subset of human papillomavirus: associated oropharyngeal cancers with favorable prognosis", J Clin Oncol, 24(5), pp.736~747 (2006)
- Nakashima R, "Alteration of p16 and p15 genes in human uterine tumours", Br J Cancer, 80(3-4), pp.458~467 (1999)
- Gold KA, "Role of molecular markers and gene profiling in head and neck cancers", Curr Opin Oncol, 21(3), pp.206~211 (2009)
- Scott N, "p53 in colorectal cancer: clinicopathological correlation and prognostic significance", Br J Cancer, 63(2), pp.317~319 (1991)
- Soares P, "E-cadherin gene alterations are rare events in thyroid tumors", Int J Cancer, 70(1), pp.32~38 (1997)
- Franchi A, "Prediction of occult neck metastases in laryngeal carcinoma: role of proliferating cell nuclear antigen, MIB-1, and E-cadherin immunohistochemical determination", Clin Cancer Res, 2(10), pp.1801~1808 (1996)
- Lee SH, "Loss of heterozygosity of tumor suppressor genes (p16, Rb, E-cadherin, p53) in hypopharynx squamous cell carcinoma", Otolaryngol Head Neck Surg, 145(1), pp.64~70 (2011)