Advances in molecular and cellular biology have generated a clearer understanding of the putative biological mechanisms interrelated in the genesis of inflammation and neoplasia. The worldwide incidence of chronic pancreatitis is 3%, with alcohol etiologically responsible for approximately two thirds of cases. The incidence of pancreatic cancer, steadily increasing over the past 60 years, is presently 2%. Risk factors epidemiologically correlated with the development of pancreatic cancer include smoking, diet, coffee, diabetes mellitus, and previous peptic ulcer surgery. A strong causal association exists for smoking and previous peptic ulcer surgery, while the relationship to diet, coffee, and diabetes mellitus is dubious. Several epidemiological studies suggest chronic pancreatitis is associated with an increased risk of developing pancreatic carcinoma, citing the risk in this population as 3%. The reports documenting the association are epidemiological in nature, with modest scientific data supporting the relationship. These studies do not demonstrate a convincing correlation between the two diseases. Theoretically, however, support for the association is derived from historical awareness of the effects of the chronic inflammatory state on epithelial tissues. It is likely that a weak association of uncertain relevance exists between chronic pancreatitis and the development of cancer of the pancreas. This observation may represent a correlatable epiphenomenon. This review documents existing epidemiological and experimental studies and suggests the definitive nature of the relationship between chronic pancreatitis and pancreatic carcinoma may be determined through the study of peptide growth factors expressed in normal, inflammatory, and neoplastic pancreatic tissue.