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Pathogenesis of ECL cell tumors in humans.

In ECL cell tumors developed in the setting of hypergastrinemic conditions (ECL cell carcinoids type 1 and 2), hypergastrinemia is the dominant agent acting as a promoter in all steps (hyperplasia-dysplasia-neoplasia) of the tumorigenic sequence. In contrast, it apparently lacks transforming propert...

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Detalles Bibliográficos
Autores principales: Bordi, C., D'Adda, T., Azzoni, C., Ferraro, G.
Formato: Texto
Lenguaje:English
Publicado: Yale Journal of Biology and Medicine 1998
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2578995/
https://www.ncbi.nlm.nih.gov/pubmed/10461358
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author Bordi, C.
D'Adda, T.
Azzoni, C.
Ferraro, G.
author_facet Bordi, C.
D'Adda, T.
Azzoni, C.
Ferraro, G.
author_sort Bordi, C.
collection PubMed
description In ECL cell tumors developed in the setting of hypergastrinemic conditions (ECL cell carcinoids type 1 and 2), hypergastrinemia is the dominant agent acting as a promoter in all steps (hyperplasia-dysplasia-neoplasia) of the tumorigenic sequence. In contrast, it apparently lacks transforming properties as shown by the absence of ECL cell carcinoids in patients exposed to hypergastrinemia alone, i.e., those with sporadic Zollinger-Ellison syndrome. The potential transforming factors include: the allelic loss of the MEN-1 suppressor gene in the genetically predisposed MEN-1 patients, an alteration that may induce ECL cell tumors even in the absence of hypergastrinemia; the still unknown factor(s) associated with atrophic corporal gastritis; agents whose role in the induction of human ECL cell tumors is still unclarified, such as basic Fibroblast Growth Factor, human Chorionic Gonadotropin-alpha and Transforming Growth Factor-alpha; and agents having a favoring role on the ECL exposure to mitogens such as BCL-2. No information is currently available on the pathogenesis of gastrin-independent, sporadic ECL cell carcinoids (type 3) or of gastric neuroendocrine carcinomas.
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spelling pubmed-25789952008-11-05 Pathogenesis of ECL cell tumors in humans. Bordi, C. D'Adda, T. Azzoni, C. Ferraro, G. Yale J Biol Med Research Article In ECL cell tumors developed in the setting of hypergastrinemic conditions (ECL cell carcinoids type 1 and 2), hypergastrinemia is the dominant agent acting as a promoter in all steps (hyperplasia-dysplasia-neoplasia) of the tumorigenic sequence. In contrast, it apparently lacks transforming properties as shown by the absence of ECL cell carcinoids in patients exposed to hypergastrinemia alone, i.e., those with sporadic Zollinger-Ellison syndrome. The potential transforming factors include: the allelic loss of the MEN-1 suppressor gene in the genetically predisposed MEN-1 patients, an alteration that may induce ECL cell tumors even in the absence of hypergastrinemia; the still unknown factor(s) associated with atrophic corporal gastritis; agents whose role in the induction of human ECL cell tumors is still unclarified, such as basic Fibroblast Growth Factor, human Chorionic Gonadotropin-alpha and Transforming Growth Factor-alpha; and agents having a favoring role on the ECL exposure to mitogens such as BCL-2. No information is currently available on the pathogenesis of gastrin-independent, sporadic ECL cell carcinoids (type 3) or of gastric neuroendocrine carcinomas. Yale Journal of Biology and Medicine 1998 /pmc/articles/PMC2578995/ /pubmed/10461358 Text en
spellingShingle Research Article
Bordi, C.
D'Adda, T.
Azzoni, C.
Ferraro, G.
Pathogenesis of ECL cell tumors in humans.
title Pathogenesis of ECL cell tumors in humans.
title_full Pathogenesis of ECL cell tumors in humans.
title_fullStr Pathogenesis of ECL cell tumors in humans.
title_full_unstemmed Pathogenesis of ECL cell tumors in humans.
title_short Pathogenesis of ECL cell tumors in humans.
title_sort pathogenesis of ecl cell tumors in humans.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2578995/
https://www.ncbi.nlm.nih.gov/pubmed/10461358
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