Histologic characteristics of insulinomas and gastrinomas

Woodtli, W; Hedinger, Chr.

doi:10.1007/bf00428053

Cited by 18 publications

(4 citation statements)

References 41 publications

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“…In our series, gastrin was identified in at least 1 tumor in 6 of the 8 patients with ZES and in 1 patient with hypoglycemia who had no evidence of ulcer disease or diarrhea. This finding is in accord with reports of others who studied gastrinomas by the immunoperoxidase method [21][22][23][24][25]. In a study by Solcia et al [24], gastrin was found by immuno-peroxidase techniques or by extraction in 25 of 36 pancreatic tumors from ZES patients.…”

Section: Immunohistochemical Findingssupporting

confidence: 90%

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MEN I pancreas: A histological and immunohistochemical study

et al. 1984

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The spectrum and extent of islet cell histopathological findings in patients with multiple endocrine neoplasia, type I (MEN I) syndrome has never been clearly defined. Although some patients have discreet tumors causing clinically evident syndromes, others may have no symptoms until metastatic islet cell carcinoma is apparent. Whether diffuse islet cell disease occurs in all patients with grossly apparent tumors is not known. This study is an attempt to define both the functional and anatomical extent of islet cell disease and its relationship with the clinical course of patients with MEN I syndrome.The resected specimens of pancreas from 14 patients with MEN I syndrome were evaluated for hyperplasia, nesidioblastosis, multiple tumors, and evidence of malignancy. In 12 cases, specimens consisted of distal pancreas and, in 2 cases, the entire pancreas was available. Multiple sections were taken from each specimen. Immunoperoxidase staining was done for gastrin, pancreatic polypeptide, glucagon, serotonin, VIP, somatostatin, and neuron-specific enolase in sections of 24 tumors from 10 patients. Five of the 10 patients with Zollinger-Ellison syndrome underwent total gastrectomy and 3 others underwent only pancreatic procedures to control their acid hypersecretion.The following is concluded. All MEN I patients with pancreatic neoplasms have diffuse islet cell involvement consisting of nesidioblastosis, micro-and macronodular hyperplasia. Some tumors produce multiple hormones and these patients are at risk to develop new tumors, but complete excision of grossly apparent tumors may result in

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Section: Immunohistochemical Findingssupporting

confidence: 90%

“…Creutzfeldt et al [21] reported similar findings in 20 of 2! ZES tumors as did Woodtli and Hedinger [25] in 7 of 9 patients. Failure to identify gastrin is most likely explained by inappropriate fixation and processing of tumor tissue or sampling deficiencies when multiple tumors are present [23].…”

Section: Immunohistochemical Findingsmentioning

confidence: 67%

MEN I pancreas: A histological and immunohistochemical study

et al. 1984

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“…These au-thors subdivided two groups of neoplasms, one with trabecular architecture showing equal, polarized insulin immunofluorescence in all tumour cells and the other with a solid or medullary structure with unevenly distributed immunofluorescent cells scattered among unreactive cells. Immunofluorescent analysis of three cases in group A consistently revealed a trabecular pattern according to Woodtli and Hedinger [26], whereas the four cases in group B showed a purely or predominantly solid pattern. Immunofluorescent analysis of three cases in group A consistently revealed a trabecular pattern according to Woodtli and Hedinger [26], whereas the four cases in group B showed a purely or predominantly solid pattern.…”

Section: Discussionmentioning

confidence: 77%

“…A relation between the histological structure of insulinomas and their pattern of insulin immunostaining was originally proposed by Woodtli and Hedinger [26] using polyclonal antiserum raised in the guinea pig. These au-thors subdivided two groups of neoplasms, one with trabecular architecture showing equal, polarized insulin immunofluorescence in all tumour cells and the other with a solid or medullary structure with unevenly distributed immunofluorescent cells scattered among unreactive cells.…”

Section: Discussionmentioning

confidence: 99%

Functioning human insulinomas

et al. 1998

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Sixty-seven insulinomas were investigated by immunohistochemistry using site-directed antibodies against insulin, proinsulin, chromogranin A, HISL-19, and four proteins directly or indirectly involved in the proteolytic processing of proinsulin: the prohormone convertases PC2 and PC3, carboxypeptidase H (CPH) and 7B2. Results were expressed in a six-grade score according to the frequency of immunoreactive tumour cells. Insulin was expressed by all tumours, appearing in either a diffuse or a polarized pattern and being detected in more than 30% of tumour cells in all cases but three. Proinsulin was also expressed in all tumours, with more than 50% of tumour cells immunoreactive in all cases but 5. It was consistently localized in the Golgi apparatus. In about half the cases, moreover, it also showed diffuse cytoplasmic staining, usually with a very sparse distribution. Trabecular and solid insulinomas did not present specific, homogeneous patterns of insulin immunostaining. However, insulin immunoreactivity was much more abundant in trabecular than in solid neoplasms, being present in virtually all tumour cells (score 6) in 50% and 8% of cases, respectively. Virtually all insulinomas expressed PC2, PC3, CPH and 7B2, usually in 30-100% of tumour cells, with a frequency significantly related to that of insulin. However, detection of PC2 and 7B2 was slightly less frequent than that of PC3 and CPH. In consecutive sections these proteins were found to be mostly co-localized with insulin and chromogranin A but not with proinsulin. They were heavily expressed in all 10 tumours with more than 10% of cells showing cytoplasmic proinsulin immunoreactivity, indicating that the leakage of proinsulin from the Golgi compartment is not associated with faulty expression of converting enzymes and possibly reflects a saturated processing capacity. HISL-19 immunoreactivity was found in both Golgi apparatus and insulin stores, indicating that the relevant antigen is different from all other proteins investigated. These results do not support a defect in expression or localization of proinsulin-processing enzymes in most insulinomas.

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Pseudoneoplastic proliferation of endocrine cells in pancreatic fibrosis

Bartow

Mukai

Rosaí

1981

Cancer

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Twenty cases of florid pancreatic endocrine neoformation and hyperplasia in a background of pancreatic fibrosis were culled from a review of 70 cases of pancreatic fibrosis, atrophy, chronic inflammation, and duct obstruction and 29 cases of pancreatic islet cell hyperplasia and neoplasia. Three of these cases had morphologic features suggestive of neoplasia. The phenomenon of endocrine tissue proliferation in a setting of exocrine tissue destruction and fibrosis, especially that secondary to major exocrine duct obstruction is reviewed. The criteria for diagnosis of endocrine neoplasia vs. hyperplasia and the attendant biologic continuum, including applicability of immunohistochemical studies, are discussed.

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Histologic characteristics of insulinomas and gastrinomas

Cited by 18 publications

References 41 publications

MEN I pancreas: A histological and immunohistochemical study

MEN I pancreas: A histological and immunohistochemical study

Functioning human insulinomas

Pseudoneoplastic proliferation of endocrine cells in pancreatic fibrosis

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