Gastric endocrine tumours (gastric carcinoids) usually grow from enterochromaffin-like (ECL) cells. Three types of tumour may be distinguished on the basis of the background gastric pathology: type 1, which develops in atrophic body gastritis (ABG); type 11, which is associated with multiple endocrine neoplasia and Zollinger-Ellison syndrome; and the sporadic type 111, which is not associated with any background pathology. This classification plays a major role in determining the optimal approach to these diseases. In fact, type I carcinoids can be considered to be benign lesions, with exceptional risk of metastases. Type 11, in contrast, may be associated with distant metastases, which are also common in type III carcinoids. The therapeutic approach is based mainly on endoscopic excision and somatostatin analogues in types I and 11, or on surgical resection in type Ill. Both types I and 11 grow under the stimulus of hypergastrinaemia through a well-described sequence. However, gastrin is sufficient to cause ECL cell hyperplasia and dysplasia, but not transformation, which is due to menin defects in MEW patients, or to other unknown alterations in ABG. Several other candidates-including Bc12, p53 and MMP9-have been linked with carcinoid initiation and progression. The biology of type Ill tumours which are not associated with hypergastrinaemia is still poorly understood.

Endocrine tumours of the stomach / DELLE FAVE, Gianfranco; Gabriele, Capurso; Massimo, Milione; Francesco, Panzuto. - In: BAILLIERE'S BEST PRACTICE & RESEARCH. CLINICAL GASTROENTEROLOGY. - ISSN 1521-6918. - 19:5 SPEC. ISS.(2005), pp. 659-673. [10.1016/j.bpg.2005.05.002]

Endocrine tumours of the stomach

DELLE FAVE, Gianfranco;Francesco Panzuto
2005

Abstract

Gastric endocrine tumours (gastric carcinoids) usually grow from enterochromaffin-like (ECL) cells. Three types of tumour may be distinguished on the basis of the background gastric pathology: type 1, which develops in atrophic body gastritis (ABG); type 11, which is associated with multiple endocrine neoplasia and Zollinger-Ellison syndrome; and the sporadic type 111, which is not associated with any background pathology. This classification plays a major role in determining the optimal approach to these diseases. In fact, type I carcinoids can be considered to be benign lesions, with exceptional risk of metastases. Type 11, in contrast, may be associated with distant metastases, which are also common in type III carcinoids. The therapeutic approach is based mainly on endoscopic excision and somatostatin analogues in types I and 11, or on surgical resection in type Ill. Both types I and 11 grow under the stimulus of hypergastrinaemia through a well-described sequence. However, gastrin is sufficient to cause ECL cell hyperplasia and dysplasia, but not transformation, which is due to menin defects in MEW patients, or to other unknown alterations in ABG. Several other candidates-including Bc12, p53 and MMP9-have been linked with carcinoid initiation and progression. The biology of type Ill tumours which are not associated with hypergastrinaemia is still poorly understood.
2005
atrophic body gastritis; gastric carcinoids; gastric endocrine tumours; hypergastrinaemia; multiple endocrine neoplasia type i; zollinger-ellison syndrome
01 Pubblicazione su rivista::01a Articolo in rivista
Endocrine tumours of the stomach / DELLE FAVE, Gianfranco; Gabriele, Capurso; Massimo, Milione; Francesco, Panzuto. - In: BAILLIERE'S BEST PRACTICE & RESEARCH. CLINICAL GASTROENTEROLOGY. - ISSN 1521-6918. - 19:5 SPEC. ISS.(2005), pp. 659-673. [10.1016/j.bpg.2005.05.002]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/95508
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