Recent studies suggest that acromegaly might predispose to an increased risk of benign and malignant neoplasms, thus influencing the final outcome of the disease. The exact mechanism of neoplastic events in acromegaly has not been completely clarified. Several studies indicate an autocrine-paracrine role for growth hormone (GH) and insulin-like growth factor-I (IGF-I) in the proliferation of normal and neoplastic cells. The paper reviews the results of molecular, clinical and epidemiological data supporting a role for GH-IGF-I action in colon, prostate, breast and lung carcinogenesis inpatients with acromegaly.