IGF-1 is Linked to Cancers, Heart Disease, Type 2 Diabetes and Osteoporosis

Insulin-like growth hormone (IGF-1) is believed to be linked to Cancers, Heart Disease, Type 2 Diabetes and Osteoporosis. It could be used to predict the risk of these disease. OR does it?

The link does exist:

decreases serum IGF-1 concentration by ~40%, protects against cancer and slows aging in rodents.

Source: Aging Cell. 2008 Oct;7(5):681-7. – Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans.

Plasma levels of insulin-like growth factor I (IGF-I) have been associated with risk of several cancers.

Source: Cancer Epidemiol Biomarkers Prev. 2002 Sep;11(9):852-61 – Dietary correlates of plasma insulin-like growth factor I and insulin-like growth factor binding protein 3 concentrations.

Variation in the circulating concentrations of the insulin-like growth factor (IGF) system has been implicated in the etiology of chronic diseases including cancer (prostate, breast, colon, and lung), heart disease, type 2 diabetes, and osteoporosis


The results of this study lend additional support to the hypothesis that circulating IGF-I concentrations increase the risk of prostate, bladder, colorectal, and breast cancer

Source: Cancer Epidemiol Biomarkers Prev. 2003 Aug;12(8):739-46. Determinants of circulating insulin-like growth factor I and insulin-like growth factor binding protein 3 concentrations in a cohort of Singapore men and women.

The insulin-like growth factor (IGF) system has been implicated in the aetiopathogenesis of cancer, cardiovascular disease and diabetes.

Source: Public Health Nutr.  2003 Apr;6(2):175-80.  The influence of dietary intake on the insulin-like growth factor (IGF) system across three ethnic groups: a population-based study.

The above studies can be found here http://www.worldhairresearch.com/?p=154


BMC Med. 2010 Jan 5;8:2.

Basic and clinical significance of IGF-I-induced signatures in cancer.

Werner H, Bruchim I.

Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. hwerner@post.tau.ac.il


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The insulin-like growth factor (IGF) system mediates growth, differentiation and developmental processes; it is also involved in various metabolic activities. Deregulation of IGF system expression and action is linked to diverse pathologies, ranging from growth deficits to cancer development. Targeting of the IGF axis emerged in recent years as a promising therapeutic approach in cancer and other medical conditions. Rational use of IGF-I-induced gene signatures may help to identify patients who might benefit from IGF axis-directed therapeutic modalities. In the accompanying research article in BMC Medicine, Rajski et al. show that IGF-I-induced gene expression in primary breast and lung fibroblasts accurately predict outcomes in breast and lung cancer patients.See the associated research paper by Rajski et al: http://www.biomedcentral.com/1741-7015/8/1.

PMID: 20051101 [PubMed - indexed for MEDLINE]

Source: http://www.ncbi.nlm.nih.gov/pubmed/20051101


Study Links IGF-1 to Prostate Cancer
American Association for the Advancement of Science
January 23, 1998
SECTION: No. 5350, Vol. 279; Pg. 563; ISSN: 0036-8075
Plasma insulin-like growth factor-I and prostate cancer risk: a prospective study.

If our results are confirmed, pharmacological approaches to decreasing IGF-I bioactivity may warrant
investigation as risk-reduction strategies specifically targeted at men at high
risk due to increased IGF-I levels. Partial suppression of the growth hormone
(GH)-IGF-I axis by somatostatin analogs (32) or GH-releasing hormone
antagonists (33) are two possibilities. Finally, our results raise concern that
administration of GH or IGF-I over long periods, as proposed for elderly men to
delay the effects of aging (34), may increase risk of prostate cancer.



Novartis Found Symp. 2004;262:193-9; discussion 199-204, 265-8.
IGF-1 and prostate cancer.

Roberts CT Jr.

Department of Pediatrics, NRC5, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA.


By virtue of their potent proliferative and anti-apoptotic effects, the insulin-like growth factors (IGFs) have been the subject of long-term scrutiny for their role in tumorigenesis. With regard to prostate cancer in particular, IGF-1 has been shown to stimulate the proliferation of human prostate epithelial cells in culture and to be necessary for normal growth and development of the rat and mouse prostate. Epidemiological studies have established a link between high circulating serum IGF-1 levels and the risk of later developing advanced prostate cancer, and overexpression of IGF-1 in the prostate basal epithelial layer of transgenic mice results in prostate adenocarcinoma that is similar to human disease. Thus, IGF-1 action appears to be important for prostate cancer initiation. On the other hand, decreased IGF action, subsequent to the down-regulation of IGF-1 receptor expression, is associated with advanced, metastatic disease. This decrease in IGF-1 receptor may confer a survival advantage to prostate cancer cells that have entered the circulation by making them resistant to the differentiative effects of IGF-1 at metastatic sites such as bone. The molecular mechanisms that effect IGF-1 receptor down-regulation appear to involve novel oncogenic functions of the Wilms’ tumour suppressor, as well as novel actions of the androgen receptor.

PMID: 15562830 [PubMed - indexed for MEDLINE]


Here we see that IGF-1 levels can indicate the aggressiveness of tumors:
Insulin-like growth factor (IGF) 1 and 2 help to predict disease outcome in GIST patients
Accepted January 25, 2008.

We might hypothesize that the IGF system, and in particular IGFR-I in presence of high concentration of IGF1 and IGF2, has an active role in cell proliferation through the activation of MAPK and PI3K bypassing KIT. It is likely that GISTs tend to produce IGFs, which in turn, through a paracrine, autocrine and sometimes an endocrine loop, might create an auto-enhancing stimulation of cell proliferation, causing a more aggressive and malignant behavior of the tumor. This is why we found a stronger expression of IGFs in metastatic GISTs versus localized GISTs, in relapsed versus non-relapsed GISTs and in higher risk GISTs. Our findings regarding the association between weaker IGF2 expression and PDGFRa-mutated GISTs follow this logic, since others [38] and we [39] previously demonstrated that PDGFRa-mutated GISTs have a favorable outcome.

Source: http://annonc.oxfordjournals.org/content/early/2008/03/27/annonc.mdn040.full

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