Search Results
Search for other papers by Reetobrata Basu in
Google Scholar
PubMed
Molecular and Cellular Biology Program, Ohio University, Athens, Ohio, USA
Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, USA
Search for other papers by John J Kopchick in
Google Scholar
PubMed
growth hormone (GH) and the insulin-like growth factor 1 (IGF1) axis. Massive amount of research over the last 70 years have established that GH and IGF1 have both overlapping and mutually exclusive roles in driving multiple aspects of cancer initiation
Search for other papers by Paul C Marker in
Google Scholar
PubMed
Search for other papers by Christopher J Unterberger in
Google Scholar
PubMed
Search for other papers by Steven M Swanson in
Google Scholar
PubMed
Introduction Investigation of the role of growth hormone (GH) and its downstream mediators including insulin-like growth factor 1 (IGF-1) in the initiation and progression of cancer has been motivated by several factors including low cancer
Search for other papers by Cindy H Chau in
Google Scholar
PubMed
Search for other papers by Cathee Till in
Google Scholar
PubMed
Search for other papers by Douglas K Price in
Google Scholar
PubMed
Search for other papers by Phyllis J Goodman in
Google Scholar
PubMed
Search for other papers by Marian L Neuhouser in
Google Scholar
PubMed
Search for other papers by Michael N Pollak in
Google Scholar
PubMed
Search for other papers by Ian M Thompson in
Google Scholar
PubMed
Search for other papers by William D Figg in
Google Scholar
PubMed
between the two may involve crosstalk among hormonal pathways that include sex steroid hormones and the insulin/insulin-like growth factor 1 (IGF1) axis, specifically adiposity-related changes in metabolism and endogenous hormone levels ( Hsing et al
Search for other papers by Cesar Luiz Boguszewski in
Google Scholar
PubMed
Search for other papers by Margaret Cristina da Silva Boguszewski in
Google Scholar
PubMed
Search for other papers by Wouter W de Herder in
Google Scholar
PubMed
time, it was shown that GH action in peripheral tissues could be mediated by another factor, somatomedin-C which was later re-named insulin-like growth factor 1 (IGF1) ( Salmon & Daughaday 1957 ). Figure 1 highlights the main pioneers of the first
Department of Oncology, Medical University of Warsaw, Warsaw, Poland
Search for other papers by Piotr T Wysocki in
Google Scholar
PubMed
Search for other papers by Karol Czubak in
Google Scholar
PubMed
Search for other papers by Anna A Marusiak in
Google Scholar
PubMed
Search for other papers by Monika Kolanowska in
Google Scholar
PubMed
Department of Immunology, Medical University of Warsaw, Warsaw, Poland
Search for other papers by Dominika Nowis in
Google Scholar
PubMed
for each insert. Insulin-like growth factor 1 (IGF1)-induced chemotaxis assays were performed identically, except that the serum-starvation step was omitted, and the lower compartments of the chambers were filled with serum-free RPMI-1640 medium
Search for other papers by Lena Lapkina-Gendler in
Google Scholar
PubMed
Search for other papers by Itai Rotem in
Google Scholar
PubMed
Search for other papers by Metsada Pasmanik-Chor in
Google Scholar
PubMed
Yoran Institute for Human Genome Research, Tel Aviv University, Tel Aviv, Israel
Search for other papers by David Gurwitz in
Google Scholar
PubMed
Search for other papers by Rive Sarfstein in
Google Scholar
PubMed
Search for other papers by Zvi Laron in
Google Scholar
PubMed
Yoran Institute for Human Genome Research, Tel Aviv University, Tel Aviv, Israel
Search for other papers by Haim Werner in
Google Scholar
PubMed
Introduction The growth hormone (GH)–insulin-like growth factor-1 (IGF1) axis has a fundamental role in growth and development throughout life ( Rosenfeld 2005 ). As originally postulated by Salmon et al . in the mid-1950s, anabolic actions
Search for other papers by W Patricia Bandettini in
Google Scholar
PubMed
Department of Pediatrics, Georgetown University Hospital, Washington, District of Columbia, USA
Search for other papers by Alexander S Karageorgiadis in
Google Scholar
PubMed
Search for other papers by Ninet Sinaii in
Google Scholar
PubMed
Search for other papers by Douglas R Rosing in
Google Scholar
PubMed
Search for other papers by Vandana Sachdev in
Google Scholar
PubMed
Search for other papers by Marie Helene Schernthaner-Reiter in
Google Scholar
PubMed
Department of Pediatrics, Georgetown University Hospital, Washington, District of Columbia, USA
Search for other papers by Evgenia Gourgari in
Google Scholar
PubMed
Search for other papers by Georgios Z Papadakis in
Google Scholar
PubMed
Search for other papers by Meg F Keil in
Google Scholar
PubMed
Search for other papers by Charalampos Lyssikatos in
Google Scholar
PubMed
Search for other papers by J Aidan Carney in
Google Scholar
PubMed
Search for other papers by Andrew E Arai in
Google Scholar
PubMed
Search for other papers by Maya Lodish in
Google Scholar
PubMed
Search for other papers by Constantine A Stratakis in
Google Scholar
PubMed
primary and recurrent tumors ( Stratakis et al . 2001 ). A number of studies have suggested that both GH and insulin-like growth factor 1 (IGF-1), such as in patients with acromegaly, may play a role in increasing the risk for certain cancers ( Ron et
Search for other papers by Kjell Öberg in
Google Scholar
PubMed
Search for other papers by Steven W J Lamberts in
Google Scholar
PubMed
growth factor 1 (IGF-1) by the liver, resulting in a proliferation of bone, cartilage and soft tissue. As the onset of physical changes is insidious, diagnosis can be delayed for up to 10 years in some patients ( Rajasoorya et al . 1994 ), leading to
Search for other papers by Zvi Laron in
Google Scholar
PubMed
Search for other papers by Haim Werner in
Google Scholar
PubMed
The growth hormone–insulin-like growth factor endocrine system The growth hormone (GH)–insulin-like growth factor-1 (IGF-1) endocrine system plays an essential role in the regulation of multiple metabolic and growth processes throughout life
Search for other papers by Thomas Cuny in
Google Scholar
PubMed
Search for other papers by Caroline Zeiller in
Google Scholar
PubMed
Search for other papers by Martin Bidlingmaier in
Google Scholar
PubMed
Search for other papers by Céline Défilles in
Google Scholar
PubMed
Search for other papers by Catherine Roche in
Google Scholar
PubMed
Search for other papers by Marie-Pierre Blanchard in
Google Scholar
PubMed
Search for other papers by Marily Theodoropoulou in
Google Scholar
PubMed
APHM Timone, Department of Neurosurgery, Marseille, France
Search for other papers by Thomas Graillon in
Google Scholar
PubMed
Search for other papers by Morgane Pertuit in
Google Scholar
PubMed
Search for other papers by Dominique Figarella-Branger in
Google Scholar
PubMed
APHM, Conception, Laboratory of Molecular Biology, Marseille, France
Search for other papers by Alain Enjalbert in
Google Scholar
PubMed
APHM Conception, Department of Endocrinology, Marseille, France
Search for other papers by Thierry Brue in
Google Scholar
PubMed
APHM, Conception, Laboratory of Molecular Biology, Marseille, France
Search for other papers by Anne Barlier in
Google Scholar
PubMed
Pegvisomant (PEG), an antagonist of growth hormone (GH)-receptor (GHR), normalizes insulin-like growth factor 1 (IGF1) oversecretion in most acromegalic patients unresponsive to somatostatin analogs (SSAs) and/or uncontrolled by transsphenoidal surgery. The residual GH-secreting tumor is therefore exposed to the action of circulating PEG. However, the biological effect of PEG at the pituitary level remains unknown. To assess the impact of PEG in vitro on the hormonal secretion (GH and prolactin (PRL)), proliferation and cellular viability of eight human GH-secreting tumors in primary cultures and of the rat somatolactotroph cell line GH4C1. We found that the mRNA expression levels of GHR were characterized in 31 human GH-secreting adenomas (0.086 copy/copy β-Gus) and the GHR was identified by immunocytochemistry staining. In 5/8 adenomas, a dose-dependent inhibition of GH secretion was observed under PEG with a maximum of 38.2±17% at 1μg/mL (P<0.0001 vs control). A dose-dependent inhibition of PRL secretion occurred in three mixed GH/PRL adenomas under PEG with a maximum of 52.8±11.5% at 10μg/mL (P<0.0001 vs control). No impact on proliferation of either human primary tumors or GH4C1 cell line was observed. We conclude that PEG inhibits the secretion of GH and PRL in primary cultures of human GH(/PRL)-secreting pituitary adenomas without effect on cell viability or cell proliferation.
