[Gastrointestinal carcinoid tumors: cellular biology, molecular expression and physiopathological consequences of an enigmatic neoplasia].
Gastrointestinal carcinoid tumors arise from cells of the diffuse neuroendocrine system localized in the digestive trace and represent more than 70% of all carcinoid tumors in humans. The present article reviews the following topics: 1) The biological profile of these tumors (histopathology, cytokine markers, metabolic alterations, storage of neuroamines and hormonal proteins, cytodynamic behavior, and biological behavior according to embryological origin). 2) The etiological circumstances (exceptional hereditary factors, association of gastric carcinoid tumors with autoimmune gastritis, little-known exogenous factors). 3) Pathogenic aspects (persistent mitogenesis of endocrine cells associated with hypergastrinemia, inactivation of some putative tumor suppressor genes, the doubtful participation of oncogenes, autocrine action of some cellular growth-stimulating proteins). 4) The repercussions of certain physiopathological events (peritumoral desmoplastic reaction causing the "mass effect" on the digestive tube, the "kidnapping" of dietary tryptophan by tumoral cells toward an abnormal metabolic pathway; the easy metastatic dissemination coexisting with low tumoral aggressivity, and the release into the bloodstream of stored secretory products leading to "carcinoid syndrome" and some endocrine hyperfunction syndromes. Finally, it should be remembered that gastrointestinal carcinoid tumors represent only a proportion of the neoplasms classified as neuroendocrine tumors.
Servicio de Aparato Digestivo, Fundación Jiménez Díaz, Universidad Autónoma, Avenida Reyes Católicos 2, Madrid, Spain. Palomasanchezfayos@wanadoo.es
Paloma
P
Sánchez-Fayos Calabuig
María Jesús
MJ
Martín Relloso
Agustina
A
González Guirado
Juan Carlos
JC
Porres Cubero
D002276:Carcinoid Tumor / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D005770:Gastrointestinal Neoplasms / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006801:Humans