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Loss of dependence on IGF-1 for proliferation of human thyroid adenoma cells..pdf (879.25 kB)

Loss of dependence on IGF-1 for proliferation of human thyroid adenoma cells.

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journal contribution
posted on 2016-12-13, 15:51 authored by D. W. Williams, E. D. Williams, D. Wynford-Thomas
The proliferative responses to IGF-1 (Somatomedin C) and TSH, as assessed by 3H-thymidine (3H-TdR) incorporation and autoradiographic labelling index (LI), of suspension and monolayer cultures of human thyroid follicular epithelium derived from both normal and adenoma tissue have been compared. In cultures of normal follicles, whilst neither TSH nor IGF-1 alone produced any effect, a combination of TSH (0.1 mU ml-1) together with IGF-1 (10 ng ml-1) induced a highly significant proliferative response as shown by a peak of 3HTdR incorporation and LI, 4-5 days after growth factor addition. The TSH concentration-effect curve was bell-shaped, a higher concentration of TSH (10 mU ml-1) resulting in a reduced response. In cultures derived from adenoma tissue, however, TSH alone at 0.1 mU ml-1 was sufficient to permit a highly significant proliferative response (equivalent to, or greater than the normal) in 4 out of 5 adenomas examined; again a higher concentration of TSH (10 mU ml-1) resulted in a diminished response. Addition of IGF-1 (10 ng ml-1) produced no significant change in the response to TSH (0.1 mU ml-1) in 3 of these 4 adenomas, and significantly inhibited the response in the fourth adenoma. It is concluded that escape from the requirement for an exogenous source of IGF-1 may be a key step in the development of human thyroid epithelial (follicular cell) neoplasia.

Funding

We are grateful to the Cancer Research Campaign for grant support.

History

Citation

British Journal of Cancer, 1988, 57 (6), pp. 535-539

Author affiliation

/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGY/School of Medicine

Version

  • VoR (Version of Record)

Published in

British Journal of Cancer

Publisher

Cancer Research UK, Nature Publishing Group

issn

0007-0920

eissn

1532-1827

Available date

2016-12-13

Publisher version

http://www.nature.com/bjc/journal/v57/n6/abs/bjc1988124a.html

Language

en

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