由于在人群中出现了几个观察结果，对于研究生长激素/胰岛素样生长因子1轴在实验性诱导癌的起始和进展中的作用引起了兴趣。首先，缺乏生长激素信号的拉龙综合症患者患癌症的比率显著低于具有正常生长激素信号的人群。其次，流行病学研究发现，循环胰岛素样生长因子1水平升高与多种常见癌症发病率强烈关联。第三，早期生育的妇女患乳腺癌的风险显著降低，可能是由于激素水平（包括生长激素）的差异所导致的。这些观察结果激发了多项研究，这些研究在小鼠和大鼠的实验性癌症模型中实验性地改变了生长激素/胰岛素样生长因子1轴的活性。其中，大多数研究利用乳腺腺体、前列腺腺体、肝脏和结肠这四种器官系统的癌症模型，这些器官系统在人类中也经常发生癌症。本综述重点介绍了这些研究，描述了一些用于改变实验性诱导癌的生长激素/胰岛素样生长因子1轴活性的最常见的基因模型。这些研究中经常出现的主题是，降低生长激素活性或生长激素作用介质的干预也能在多种模型系统中抑制癌变过程。

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.