Cancer

Abstract

Despite discrepancies both within and between data from human patient populations and mouse models of altered GH induced signaling, abrogation of this signaling via mutation of the GHR appears to protect both mice and humans from cancer development and progression. While research on this phenomenon has been hindered by the low prevalence of Laron syndrome in the human population, research in the GHR-/- mouse is more extensive. The GHR-/- mouse exhibits statistically significant reductions in the overall incidence of malignancy (Ikeno et al. 2009), particular breast cancer (Zhang et al. 2007), lung cancer (Ikeno et al. 2009), lymphoma (Ikeno et al. 2009), and pituitary adenoma (Kineman et al. 2001) either under normal conditions or after carcinogen challenge as compared to control mice. While many of these phenotypes have not been confirmed in LS individuals, ongoing work has demonstrated that Laron patients exhibit resistance to malignancies (Shevah and Laron 2007). Continuing clinical and experimental work in both human patients and using the GHR-/- mouse shall further elucidate the intricacies and, hopefully, the mechanisms behind these phenotypes. © Springer-Verlag Berlin Heidelberg 2011.