Abstract
The adaptive changes of hypertrophy and hyperplasia are diffuse and reversible responses of the pancreas to growth promoting stimuli. Early stages of neoplastic growth in the pancreas have been studied in carcinogen treated animals and preneoplastic lesions including atypical acinar cell foci and nodules, tubular ductal complexes and intraductal hyperplasia were identified. Neoplastic growth is clonal rather than diffuse and involves multiple steps through preneoplastic stages to produce a tumour. The individual steps are commonly regarded as reflecting a series of changes in the genome of the cells. Although the changes are likely to be irreversible, completion of the sequence usually requires a major portion of the lifespan of the host. The rate of progression of preneoplastic lesions to cancer may be modulated by the same factors that control adaptive growth. It follows that such factors will influence the probability that a carcinoma will develop. Cholecystokinin (CCK) seems to provide one example of a hormone/growth factor that can stimulate normal, adaptive, and neoplastic growth, and it is to be expected that other such hormones will be identified.