Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Correspondence
  • Published:

Pituitary hormone receptors and tumorigenesis

Nature Reviews Cancer volume 7, page 722 (2007)Cite this article

A Correspondence to this article was published on 01 September 2007

Access through your institution
Buy or subscribe

We read with interest the Review 'G-protein-coupled receptors and cancer' by Dorsam and Gutkind published in Nature Reviews Cancer1. In table 1 the authors state inaccurately that thyrotropin secreting hormone (TSH) and adrenocorticotropin hormone (ACTH) receptors (TSHR and ACTHR, respectively) cause pituitary tumours.

The pituitary gland secretes six polypeptide hormones — ACTH, TSH, growth hormone (GH), gonadotropins (follicle stimulating hormone (FSH) and luteinizing hormone (LH)) and prolactin. These trophic hormones act at their respective target glands (adrenals, thyroid, cartilage, gonads and breast) to regulate peripheral hormone secretion and glandular growth and differentiation2.

This is a preview of subscription content, access via your institution

Access options

Access through your institution

Buy this article

  • Purchase on SpringerLink
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

References

  1. Dorsam, R. T. & Gutkind, J. S. G-protein-coupled receptors and cancer. Nature Rev. Cancer 7, 79–94 (2007).

    Article  CAS  Google Scholar 

  2. Melmed, S. Mechanisms for pituitary tumorigenesis: the plastic pituitary. J. Clin. Invest. 112, 1603–1618 (2003).

    Article  CAS  Google Scholar 

  3. Lania, A. G., Mantovani, G. & Spada, A. Mechanisms of disease: mutations of G proteins and G-protein-coupled receptors in endocrine diseases. Nature Clin. Pract. Endocrinol. Metab. 2, 681–693 (2006).

    Article  CAS  Google Scholar 

  4. Davies, T. F., Ando, T., Lin, R. Y., Tomer, Y. & Latif, R. Thyrotropin receptor-associated diseases: from adenomata to Graves disease. J. Clin. Invest. 115, 1972–1983 (2005).

    Article  CAS  Google Scholar 

  5. Krohn, K. et al. Molecular pathogenesis of euthyroid and toxic multinodular goiter. Endocr. Rev. 26, 504–524 (2005).

    Article  CAS  Google Scholar 

  6. Parma, J. et al. Somatic mutations in the thyrotropin receptor gene cause hyperfunctioning thyroid adenomas. Nature 365, 649–651 (1993).

    Article  CAS  Google Scholar 

  7. Fuhrer, D., Wonerow, P., Willgerodt, H. & Paschke, R. Identification of a new thyrotropin receptor germline mutation (Leu629Phe) in a family with neonatal onset of autosomal dominant nonautoimmune hyperthyroidism. J. Clin. Endocrinol. Metab. 82, 4234–4238 (1997).

    CAS  PubMed  Google Scholar 

  8. Rodien, P. et al. Familial gestational hyperthyroidism caused by a mutant thyrotropin receptor hypersensitive to human chorionic gonadotropin. N. Engl. J. Med. 339, 1823–1826 (1998).

    Article  CAS  Google Scholar 

  9. Abramowicz, M. J., Duprez, L., Parma, J., Vassart, G. & Heinrichs, C. Familial congenital hypothyroidism due to inactivating mutation of the thyrotropin receptor causing profound hypoplasia of the thyroid gland. J. Clin. Invest. 99, 3018–3024 (1997).

    Article  CAS  Google Scholar 

  10. Sunthornthepvarakui, T., Gottschalk, M. E., Hayashi, Y. & Refetoff, S. Brief report: resistance to thyrotropin caused by mutations in the thyrotropin-receptor gene. N. Engl. J. Med. 332, 155–160 (1995).

    Article  Google Scholar 

  11. Collu, R et al. A novel mechanism for isolated central hypothyroidism: inactivating mutations in the thyrotropin-releasing hormone receptor gene. J. Clin. Endocrinol. Metab. 82, 1561–1565 (1997).

    CAS  PubMed  Google Scholar 

  12. Clark, A. J., McLoughlin, L. & Grossman, A. Familial glucocorticoid deficiency associated with point mutation in the adrenocorticotropin receptor. Lancet 341, 461–462 (1993).

    Article  CAS  Google Scholar 

  13. Reincke, M et al. Deletion of the adrenocorticotropin receptor gene in human adrenocortical tumors: implications for tumorigenesis. J. Clin. Endocrinol. Metab. 82, 3054–3058 (1997).

    CAS  PubMed  Google Scholar 

  14. Reincke, M. Mutations in adrenocortical tumors. Horm. Metab. Res. 30, 447–455 (1998).

    Article  CAS  Google Scholar 

  15. Beuschlein, F., Fassnacht, M., Klink, A., Allolio, B. & Reincke, M. ACTH-receptor expression, regulation and role in adrenocortial tumor formation. Eur. J. Endocrinol. 144, 199–206 (2001).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Department of Medicine, Cedars Sinai Medical Center, UCLA School of Medicine, Los Angeles, California, USA

    Anat Ben-Shlomo & Shlomo Melmed

Authors
  1. Anat Ben-Shlomo
    View author publications

    Search author on:PubMed Google Scholar

  2. Shlomo Melmed
    View author publications

    Search author on:PubMed Google Scholar

Corresponding author

Correspondence to Shlomo Melmed.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Ben-Shlomo, A., Melmed, S. Pituitary hormone receptors and tumorigenesis. Nat Rev Cancer 7, 722 (2007). https://doi.org/10.1038/nrc2069-c1

Download citation

  • Issue date:

  • DOI: https://doi.org/10.1038/nrc2069-c1

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing