Journal
ENDOCRINE-RELATED CANCER
Volume 24, Issue 11, Pages R367-R385Publisher
BIOSCIENTIFICA LTD
DOI: 10.1530/ERC-17-0192
Keywords
thyroid hormones; thyroid hormone receptors; iodothyronine deiodinases; neoplasia; carcinogenesis
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Funding
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brasil [457547/2013-8]
- Fundacao de Amparo a Pesquisa do Rio Grande do Sul (FAPERGS), Brasil [10/0051-9]
- Fundo de Incentivo a Pesquisa do Hospital de Clinicas de Porto Alegre (FIPE), Brasil
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Thyroid hormones (TH) are critical regulators of several physiological processes, which include development, differentiation and growth in virtually all tissues. In past decades, several studies have shown that changes in TH levels caused by thyroid dysfunction, disruption of deiodinases and/or thyroid hormone receptor (TR) expression in tumor cells, influence cell proliferation, differentiation, survival and invasion in a variety of neoplasms in a cell type-specific manner. The function of THs and TRs in neoplastic cell proliferation involves complex mechanisms that seem to be cell specific, exerting effects via genomic and nongenomic pathways, repressing or stimulating transcription factors, influencing angiogenesis and promoting invasiveness. Taken together, these observations indicate an important role of TH status in the pathogenesis and/or development of human neoplasia. Here, we aim to present an updated and comprehensive picture of the accumulated knowledge and the current understanding of the potential role of TH status on the different hallmarks of the neoplastic process.
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