Serum cholecystokinin and neurotensin during follow-up of pancreas, prostate and medullary thyroid tumors

Background: Growth of pancreatic carcinoma cells is stimulated by cholecyst okinin (CCK) and neurotensin (NT). Prostatic carcinoma cells can secrete ne urotensin. The CCK gene has bem described in thyroid medullary carcinomas ( MCT). Methods: Serum CCK and NT were measured by RIAs during monitoring of 19 pancreas tumours, 10 prostate adenocarcinomas and 10 thyroid, medullary cancers (MCT). Results: No correlations were found between CCK and NT in th e three tumour types, nov with CA 19.9, PSA, CEA or calcitonin. In pancreas adenocarcinomas (n = 72), initial median CCK was >8pg/ml (non significant differences between stages T, N or M). Median NT was >80 pg/ml in all but M O and stages I-II cases, and significantly higher in M1 and stages N (P = 0 .002). Non significant differences were found for CCK and NT according to c linical stages. In prostate cancers, median CCK was significantly more elev ated after relapse (P = 0.040). Median NT was significantly more elevated i n disease-free patients (P = 0.04). In MCT, CCK and NT weve not related to clinical stages. Conclusion: In pancreas and prostate cancers serum CCK may follow tumour load and disease progression. NT was lower in progressive di sease. The contribution of these peptides in human tumour growth, since the y may have therapeutic implication, warrants further investigation.