Risk of neoplasia in pediatric patients receiving growth hormone therapy - A report from the pediatric endocrine society drug and therapeutics committee Journal Article
| Authors: | Raman, S.; Grimberg, A.; Waguespack, S. G.; Miller, B. S.; Sklar, C. A.; Meacham, L. R.; Patterson, B. C. |
| Article Title: | Risk of neoplasia in pediatric patients receiving growth hormone therapy - A report from the pediatric endocrine society drug and therapeutics committee |
| Abstract: | Context: GH and IGF-1 have been shown to affect tumor growth in vitro and in some animal models. This report summarizes the available evidence on whether GH therapy in childhood is associated with an increased risk of neoplasia during treatment or after treatment is completed. Evidence Acquisition: A PubMed search conducted through February 2014 retrieved original articles written in English addressing GH therapy and neoplasia risk. Subsequent searches were done to include additional relevant publications. Evidence Synthesis: In children without prior cancer or known risk factors for developing cancer, the clinical evidence does not affirm an association between GH therapy during childhood and neoplasia. GH therapy has not been reported to increase the risk for neoplasia in this population, although most of these data are derived from postmarketing surveillance studies lacking rigorous controls. In patients who are at higher risk for developing cancer, current evidence is insufficient to conclude whether or not GH further increases cancer risk. GH treatment of pediatric cancer survivors does not appear to increase the risk of recurrence but may increase their risk for subsequent primary neoplasms. Conclusions: In children without known risk factors for malignancy, GH therapy can be safely administered without concerns about an increased risk for neoplasia. GH use in children with medical diagnoses predisposing them to the development of malignancies should be critically analyzed on an individual basis, and if chosen, appropriate surveillance for malignancies should be undertaken. GH can be used to treat GHdeficient childhood cancer survivors who are in remission with the understanding that GH therapy may increase their risk for second neoplasms. Copyright © 2015 by the Endocrine Society. |
| Keywords: | signal transduction; cancer survival; event free survival; protein expression; leukemia; janus kinase 2; cancer recurrence; cancer growth; treatment duration; brain tumor; protein domain; cell proliferation; cell survival; cancer susceptibility; breast cancer; protein protein interaction; incidence; cell fate; cell differentiation; phosphatidylinositol 3 kinase; protein p53; risk factor; cancer mortality; acute lymphoblastic leukemia; childhood cancer; growth hormone deficiency; short stature; cancer survivor; animalia; dna strand breakage; systematic review; medulloblastoma; phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase; neurofibromin; malignant neoplastic disease; familial cancer; hormonal therapy; craniopharyngioma; meningioma; somatomedin c; wt1 protein; gene dosage; von hippel lindau disease; leukemia relapse; stat5 protein; postmarketing surveillance; growth hormone receptor; neurofibroma; apc protein; von hippel lindau protein; protein tyrosine phosphatase shp 2; hamartoma; receptor binding; somatomedin binding protein 3; leukemia remission; craniospinal irradiation; polyposis; neurofibromatosis type 1; noonan syndrome; somatomedin binding protein 2; inflammatory bowel disease; recombinant growth hormone; non melanoma skin cancer; human; priority journal; article; 6 mercaptopurine derivative; denys drash syndrome; frasier syndrome |
| Journal Title: | Journal of Clinical Endocrinology and Metabolism |
| Volume: | 100 |
| Issue: | 6 |
| ISSN: | 0021-972X |
| Publisher: | Oxford University Press |
| Date Published: | 2015-06-01 |
| Start Page: | 2192 |
| End Page: | 2203 |
| Language: | English |
| DOI: | 10.1210/jc.2015-1002 |
| PROVIDER: | scopus |
| PUBMED: | 25839904 |
| PMCID: | PMC5393518 |
| DOI/URL: | |
| Notes: | Export Date: 2 July 2015 -- Source: Scopus |
