GH1 and neoplasm: Moreover, a model to explain neoplastic colon growth has been proposed in which high endocrine or autocrine GH levels – for instance, as a result of acromegaly or colonic DNA damage and inflammation – inactivate tumor-suppressor genes, suppress apoptosis, and stimulates epithelial to mesenchymal transition, leading to changes in the intestinal mucosal field that favor malignant transformation [52].