Thyroid cancer susceptibility and THRA1 and BAT-40 repeats polymorphisms

Although genetic and environmental factors have been identified in the etiology of thyroid cancer, the specific genetic implications in sporadic thyroid tumors are poorly understood but, as in other common cancers, low-penetrance susceptibility genes are believed to be crucial in the tumorigenesis p...

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Bibliographic Details
Published in:Cancer epidemiology, biomarkers & prevention biomarkers & prevention, 2005-03, Vol.14 (3), p.638-642
Main Authors: BAIDA, Aida, FARRINGTON, Susan M, GALOFRE, Pere, MARCOS, Ricard, VELAZQUEZ, Antonia
Format: Article
Language:English
Subjects:
Adult
Biological and medical sciences
Case-Control Studies
Endocrinopathies
Female
Genetic Predisposition to Disease
Humans
Male
Medical sciences
Middle Aged
Non tumoral diseases. Target tissue resistance. Benign neoplasms
Odds Ratio
Polymorphism, Genetic
Thyroid Hormone Receptors alpha - genetics
Thyroid Neoplasms - etiology
Thyroid Neoplasms - genetics
Thyroid. Thyroid axis (diseases)
Tumors
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Summary:Although genetic and environmental factors have been identified in the etiology of thyroid cancer, the specific genetic implications in sporadic thyroid tumors are poorly understood but, as in other common cancers, low-penetrance susceptibility genes are believed to be crucial in the tumorigenesis processes. Here, we have carried out a case-control study to investigate whether there is an association between THRA1 CA repeat or BAT-40 A repeat polymorphisms and thyroid cancer risk. The THRA1 repeat resides in the thyroid hormone receptor-alpha1 gene, which is associated with thyroid cancer and whose expression depends on the THRA1 repeat size. We also analyzed the BAT-40 repeat that maps to chromosome 1, a region known to be involved in thyroid cancer. This repeat is located in the 3-beta-hydroxysteroid dehydrogenase gene that is associated with prostate cancer susceptibility. The THRA1 repeat was genotyped in 212 thyroid cancer patients and 141 controls of a Spanish population. From these individuals, 207 patients and 138 controls were also analyzed for the BAT-40 marker. No significant difference in the THRA1 allele distribution between patients and controls was found, although short alleles (
ISSN:1055-9965
1538-7755
DOI:10.1158/1055-9965.EPI-04-0424