In reply
Anand raises two interesting points pertinent to the pathogenesis of gastrointestinal cancer in patients with acromegaly.
First, the possibility that the occurrence of growth hormone secreting pituitary tumor and digestive cancer could be the result of common genetic alterations. Alternatively, the sustained growth hormone hypersecretion could act as a promoter of neoplastic growth in an appropriate genetic background.
Second, the importance of the sensitivity of target tissues, in this case the gastrointestinal mucosa, to circulating growth factors. There is, indeed, general agreement in the literature that the occurrence of colonic cancer in acromegaly does not merely reflect the entity of growth hormone or insulinlike growth factor—I secretion, and we also argued on this point.1 It is conceivable that the expression of growth hormone or insulinlike growth factor—I receptors in the gastrointestinal mucosa (genetically determined?) is the key to the neoplastic growth.