World Journal of Endocrine Surgery

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VOLUME 8 , ISSUE 1 ( January-April, 2016 ) > List of Articles

RESEARCH ARTICLE

Oral Presentation VIII

Jia Liu, Guang Chen

Citation Information : Liu J, Chen G. Oral Presentation VIII. World J Endoc Surg 2016; 8 (1):47-54.

DOI: 10.5005/wjoes-8-1-47

License: CC BY-NC 4.0

Published Online: 01-04-2016

Copyright Statement:  Copyright © 2016; Jaypee Brothers Medical Publishers (P) Ltd.


Abstract

BACKGROUND AND AIMS

Activin, a member of the transforming growth factor beta protein family, was originally isolated from gonadal fluids and stimulates the release of pituitary follicle-stimulating hormone (FSH). Activin has numerous functions in both normal and neoplastic cells. Although it was suggested that gonadal tissue is the primary site of activin production, several extragonadal sources have subsequently been identified, including human thyrocytes.

METHODS

In our study, serum levels of activin A were measured by chemiluminescence, and the expression of receptors of activin A in thyroid tissue was detected by immunohistochemistry in female patients with thyroid papillary cancer [stage I (n = 60), stage II (n = 60), stage III (n = 60), stage IV (n = 60)] and in normal controls (n = 60).

RESULTS

The serum levels of activin A were no significantly different between patients with thyroid papillary cancer and normal controls as well as different stages. But the expressions of receptors of activin A were greater in patients with thyroid papillary cancer than in normal controls. And the positive rates of receptor expression were significantly more in stage III and IV than in stage I and II.

CONCLUSION

In conclusion, this study demonstrates that serum levels of activin A undergo no significant changes when thyroid papillary cancer occurs. The thyroid gland is not the predominant source of activin A. The expressions of receptors of activin A were significantly greater in patients with thyroid papillary cancer than in normal controls. And the positive rates of receptor expressions were associated with the severity of cancer. Because activin A may exert negative action on thyrocyte proliferation, it is conceivable that the increase in the receptor of activin A in thyroid papillary cancer might represent a counteracting mechanism.


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