Interest in investigating the role of the growth hormone/insulin-like growth factor 1 axis in the initiation and progression of experimentally induced carcinomas has arisen due to several observations in the human population. First, subjects with Laron Syndrome who lack growth hormone signaling have significantly lower rates of cancer than people who have normal growth hormone signaling. Second, epidemiologic studies have found strong associations between elevated circulating insulin-like growth factor 1 and the incidence of several common cancers. Third, women who bear children early in life have a dramatically reduced risk of developing breast cancer, which may be due to differences in hormone levels including growth hormone. These observations have motivated multiple studies that have experimentally altered activity of the growth hormone/insulin-like growth factor 1 axis in the context of experimental carcinoma models in mice and rats. Most of these studies have utilized carcinoma models for four organ systems: the mammary gland, prostate gland, liver, and colon that are also frequent sites of carcinomas in humans. This review focuses on these studies and describes some of the most common genetic models used to alter activity of the growth hormone/insulin-like growth factor 1 axis in experimentally induced carcinomas. A recurring theme that emerges from these studies is that manipulations that reduce the activity of growth hormone or mediators of growth hormone action also inhibit carcinogenesis in multiple model systems.
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