Morphological, molecular, and prognostic aspects of gastric endocrine tumors

Solcia, Enrico; Rindi, Guido; Larosa, Stefano; Capella, Carlo

doi:10.1002/(sici)1097-0029(20000315)48:6<339::aid-jemt4>3.0.co;2-d

Cited by 43 publications

(29 citation statements)

References 70 publications

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“…The histo-pathological classification (WHO 2000) differentiates three entities according to size, rate of proliferation and malignancy [2][3][4][5][6] (Table 1). In addition gastric NET are classified clinically ( …”

Section: Classificationmentioning

confidence: 84%

Diagnosis and treatment of gastric neuroendocrine tumours

Plöckinger

2007

Wien Klin Wochenschr

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Gastric neuroendocrine tumours (NET) are rare. Clinically they are classified in tumours type 1 to 3. The histological classification is according to the WHO 2000 classification for endocrine tumours. NET type 1 occur in coincidence with chronic atrophic gastritis, as single or multiple small tumours. The prognosis of type 1 tumours is excellent, with no tumour related death reported during follow-up. NET type 2 are part of the MEN-1 syndrome. These tumours may be more aggressive and even develop metastasis. However, in most patients with MEN-1 the prognosis is due to other manifestations of the disease as duodenal or pancreatic neuroendocrine tumours. Gastric neuroendocrine tumours type 3 are sporadic tumours without relationship to other gastric pathology. They tend to occur earlier, without sex preference. These tumours may develop an aggressive course, with metastatic disease and an overall poor prognosis. Thus, aggressive surgical therapy is recommended.

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Section: Classificationmentioning

confidence: 84%

Diagnosis and treatment of gastric neuroendocrine tumours

Plöckinger

2007

Wien Klin Wochenschr

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“…To this end, we carefully selected 3 groups of patients with CRCs showing distinct clinicopathologic and molecular profiles as well as different overall survival rates. In particular, we included 18 colorectal PDNECs that are a rare and distinct clinicopathologic entity in this site exhibiting a highly aggressive biologic behavior and poor outcome [18,25,26]. In addition, a total of 60 exocrine CRCs were selected for the study, including both tumors with high frequency of microsatellite instability and MSS colorectal carcinomas.…”

Section: Discussionmentioning

confidence: 99%

“…This finding can be explained by the observation that increased synthesis and stabilization of HIF-1α were mainly observed in poorly differentiated tumors such as PDNEC and MSI-H CRCs that are also the tumor classes showing the most different clinical behavior in this site (Fig. 4A) although they have in common a high proliferation rate [18,30]. These data clearly suggest that the detection of high levels of HIF-1α in colorectal cancer is mainly associated with a high tumor proliferation rate providing, in itself, limited information about progression and prognosis in CRCs.…”

Section: Discussionmentioning

confidence: 99%

“…Microsatellite instability (MSI) screening in these tumors was previously performed in our laboratory (unpublished data) by PCR amplification of the 5 markers recommended by the National Cancer Institute, according to Bethesda guidelines [17]. The third tumor class analyzed consisted of 18 colorectal poorly differentiated neuroendocrine carcinomas (PDNECs) characterized by an aggressive biologic behavior and poor outcome (Table 1) [18]. The selection of the cases was based on the availability of sufficient tumor samples for histopathologic, immunohistochemical, and molecular analysis.…”

Section: Patient Selectionmentioning

confidence: 91%

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Up-regulation of the hypoxia-inducible factor–1 transcriptional pathway in colorectal carcinomas

et al. 2008

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“…Hypergastrinemia as consequence of hypoacidity is thought to play a pivotal role in the development of these lesions. However, additional relevant factors that are related to atrophic gastritis rather than hypergastinemia were postulated [19,73]. Morphologically, endocrine nodules in atrophic gastric corpus mucosa resemble in some aspects islets of Langerhans in the pancreas.…”

Section: Intestinal Metaplasiamentioning

confidence: 99%

Immunological and morphogenic basis of gastric mucosa atrophy and metaplasia

Faller¹,

Kirchner²

2004

Virchows Arch

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Chronic gastritis with gastric mucosa atrophy, intestinal metaplasia and endocrine cell hyperplasia are alterations with an increased risk for the development of gastric neoplasias. Immunological studies in autoimmune gastritis, in atrophic Helicobacter pylori gastritis and in studies with transgenic mice point to a central role of the parietal cell in the development of gastric mucosa atrophy. Destruction of gastric epithelial cells alone might not be sufficient for the loss of complete gastric glands. Gastric atrophy, endocrine cell hyperplasia and intestinal and pancreatic metaplasia can be regarded as the result of altered morphogenesis within the gastric mucosa. Impaired expression of the gastric morphogenic factor Sonic Hedgehog by parietal cells and increased expression of the transcriptional activators of intestinal and pancreatic differentiation, namely CDX2 and PDX1, seem to be crucial for the development of gastric atrophy and for intestinal, endocrine and pancreatic transdifferentiation processes. Altered expression of these morphogenic factors is partly caused by changes in the gastric milieu. Further studies concerning the normal and pathological morphogenesis of the gastric mucosa and related tissues might give new insight into the pathogenesis of gastric atrophy and metaplasia.

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Morphological, molecular, and prognostic aspects of gastric endocrine tumors

Cited by 43 publications

References 70 publications

Diagnosis and treatment of gastric neuroendocrine tumours

Diagnosis and treatment of gastric neuroendocrine tumours

Up-regulation of the hypoxia-inducible factor–1 transcriptional pathway in colorectal carcinomas

Immunological and morphogenic basis of gastric mucosa atrophy and metaplasia

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