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Growth hormone and cancer
- Source :
- Current Opinion in Endocrinology, Diabetes & Obesity. 20:307-313
- Publication Year :
- 2013
- Publisher :
- Ovid Technologies (Wolters Kluwer Health), 2013.
-
Abstract
- Purpose of review Animals born with a deficiency in the cell surface receptor for growth hormone (GH) have a significantly reduced risk of developing cancer. Conversely, increased expression levels of GH and the GH receptor (GHR) are detectable in a variety of different human cancers. Here we discuss recent literature contributing to our understanding of the field. Recent findings In addition to animal evidence, studies of individuals with Laron syndrome suggest that congenital GHR deficiency may also protect humans against cancer. GH expression in certain malignancies is correlated with clinicohistopathological parameters and may contribute the therapeutic resistance. Other recent studies have identified novel aspects of the GH signal transduction pathway, including receptor crosstalk and the involvement of microRNA in endocrine regulation of GH. Summary Substantial evidence suggests the GH/insulin-like growth factor-1 axis initiates and promotes progression of cancer. However, important questions remain unanswered regarding the therapeutic utility of GH or GHR antagonism in cancer. Further clinical studies regarding the clinical association of GH expression with human malignancies and translational studies investigating GHR antagonism in animal models of human cancer are critical.
- Subjects :
- Nutrition and Dietetics
business.industry
Endocrinology, Diabetes and Metabolism
Cancer
Growth hormone receptor
Bioinformatics
medicine.disease
Growth hormone
Endocrinology
Cell surface receptor
Growth Hormone
Neoplasms
microRNA
Internal Medicine
medicine
Laron syndrome
Animals
Humans
Endocrine system
Insulin-Like Growth Factor I
Signal transduction
business
Signal Transduction
Subjects
Details
- ISSN :
- 1752296X
- Volume :
- 20
- Database :
- OpenAIRE
- Journal :
- Current Opinion in Endocrinology, Diabetes & Obesity
- Accession number :
- edsair.doi.dedup.....36e269fc554b0e8270ce31f8216adb0c