Glucagonomas: Ultrastructure and immunocytochemistry

Warner, Thomas F.; Block, Margaret; Hafez, G. Reza; Mack, Eberhard; Lloyd, Ricardo V.; Bloom, Stephen R.

doi:10.1002/1097-0142(19830315)51:6<1091::aid-cncr2820510620>3.0.co;2-g

Cited by 20 publications

(3 citation statements)

References 45 publications

(2 reference statements)

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“…At present, there is no plausible explanation for the association between pancreatic polypeptide expression and VEGF-C expression, apart from the observation that glucagonomas frequently co-express pancreatic polypeptide. 35 Although there is ample experimental evidence of an association between VEGF-C expression and lymphangiogenesis, 36 -40 this relationship is less conspicuous in human tumors. A correlation between VEGF-C expression and high LVD was recently reported in a small series of oral squamous cell carcinomas 41 but has been shown to be absent in melanomas 3,4 and in squamous cell carcinomas of the head and neck.…”

Section: Discussionmentioning

confidence: 99%

Expression of Lymphangiogenic Factors and Evidence of Intratumoral Lymphangiogenesis in Pancreatic Endocrine Tumors

Sipos

Klapper

Kruse

et al. 2004

The American Journal of Pathology

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Lymphangiogenesis is thought to promote the progression of malignant tumors. Because the lymphangiogenic factors vascular endothelial factor (VEGF)-C and -D are expressed in endocrine cells, we investigated their expression in pancreatic endocrine tumors (PETs) and correlated these data and intratumoral lymph vessel density (iLVD) with clinicopathological features. Lymph vessels were identified with anti-podoplanin antiserum and with podoplanin/proliferating cell nuclear antigen double labeling. PETs (n ‫؍‬ 104) were investigated by immunohistochemical staining for VEGF, basic fibroblast growth factor, and VEGF-C expression. VEGF-C and VEGF-D mRNA were quantified by real-time reverse transcriptase-polymerase chain reaction. PETs showed higher iLVD than normal pancreata, but iLVD did not discriminate between benign and malignant PETs. In PETs proliferating lymph vessels were identified. High iLVD was associated with lymph vessel invasion and it was more frequent in angioinvasive/metastatic tumors than in grossly invasive tumors. The biological behavior of pancreatic endocrine tumors (PET) is difficult to predict on the basis of histological criteria. In the absence of clear signs of malignancy, such as invasion of adjacent organs, angioinvasion, or metastasis, the prognosis remains uncertain. Because most human carcinomas metastasize via lymphatic invasion, lymph node metastasis is a key prognostic factor for the clinical outcome. By which mechanism tumor cells spread through the lymph vessels is unknown. One proposed mechanism is the induction of new lymph vessels by tumor or inflammatory cells, facilitating lymphangioinvasion. Intratumoral lymph vessels have been detected in head and neck squamous cell carcinomas 1,2 and in cutaneous melanomas. 3,4 In squamous cell carcinomas intratumoral lymph vessel density (iLVD) has been shown to correlate with lymph node metastasis, whereas the results for melanomas are inconsistent. Beasley and colleagues 1 and Straume and colleagues 3 showed that intratumoral lymphatic endothelial cells were capable of proliferation, suggesting de novo lymphangiogenesis. No evidence of intratumoral lymph vessels was found in ovarian, 5 liver, 6 breast, 7,8 or cervical carcinomas. 9

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Section: Discussionmentioning

confidence: 99%

Expression of Lymphangiogenic Factors and Evidence of Intratumoral Lymphangiogenesis in Pancreatic Endocrine Tumors

Sipos

Klapper

Kruse

et al. 2004

The American Journal of Pathology

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“…Although the secretory response of plasma glucagon has been investigated in patients with suspected glucagonoma, the diagnostic value of provocation tests has been inconclusive (Stacpoole et al, 1981a;1981b;Fujita et al, 1986). Although pancreatic islet tumours constitute an integral component of the multiple endocrine neoplasia type 1 (MEN 1), the association of glucagonoma syndrome in MEN 1 is rare (Warner et al, 1983;Stacpoole et al, 1981a;Klöppel & Heitz, 1988). Skogseid et al (1987) reported that MEN 1 patients with even no pancreatic endocrine tumours had significantly higher mean basal levels of plasma glucagon.…”

Section: Discussionmentioning

confidence: 99%

Cystic glucagonoma with loss of heterozygosity on chromosome 11 in multiple endocrine neoplasia type 1

Sarui

Yoshimoto

Okumura³

et al. 1997

Clinical Endocrinology

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A 52-year-old man with a past history of a pituitary adenoma and hyperparathyroidism due to a parathyroid adenoma was admitted because of a solitary tumour of the pancreas revealed by ultrasonography. His family history was unremarkable. Plasma glucagon levels were slightly elevated (280 ng/l, normal range, 40-180 ng/l) with decreased plasma amino acid levels. Plasma glucagon levels disclosed an exaggerated response during an arginine infusion test and paradoxical elevation during a 75 g oral glucose tolerance test. Endoscopic ultrasonography revealed a monolocular cystic mass of about 3 cm in diameter in the body of the pancreas. A pancreatic tumour was diagnosed before surgery as a cystic glucagonoma. Intra-operative ultrasonography showed one cystic mass in the body of pancreas and two other solid tumours, about 1 cm and 0.5 cm in diameter, in the tail of the pancreas. Histologically, all three tumours showed neoplastic epithelial cells with round nuclei forming cords and/or a ribbon-like arrangement. They showed positive staining for Grimelius' silver stain and immunopositive cells for glucagon. Genetic analysis of the main cystic tumour revealed loss of heterozygosity (LOH) on chromosome 11. After the operation, the responses of plasma glucagon to arginine infusion and oral glucose became normal. Here we describe the usefulness of these provocation tests for early diagnosis and post-operative follow-up in a rare cystic glucagonoma associated with multiple endocrine neoplasia type 1 (MEN 1) which had LOH on chromosome 11.

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“…31 The gastrinomas in these patients reside predominantly in the proximal part of the duodenum, are usually smaller than 1 cm in diameter, and show multicentricity (see section on gastrinomas above). The occurrence of WDHA syndrome, 2,147 glucagonoma syndrome, 179,180 or acromegaly due to a tumor-secreting growth-hormone-releasing factor 156,157 is very rare in the setting of MEN1.…”

Section: Pancreatic Endocrine Tumors In Multiple Endocrine Syndrome Tmentioning

confidence: 99%

Pancreatic Endocrine Tumors

ppel¹,

Anlauf

2006

Pathology Case Reviews

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The endocrine tumors of the pancreas are composed of cells with a neuroendocrine phenotype. Well-differentiated tumors, welldifferentiated carcinomas, poorly differentiated carcinomas, functioning (insulinomas, gastrinomas, glucagonomas, etc.) and nonfunctioning tumors are identified. In order to predict their clinical behavior, pancreatic endocrine tumors are classified on the basis of their clinicopathological features including size; local invasion; angioinvasion; proliferative activity; histological differentiation; and metastases into benign, uncertain malignant potential, low-grade malignant, and high-grade malignant neoplasms. A small percentage of tumors are associated with the inherited syndromes of multiple endocrine neoplasia type 1 and von Hippel-Lindau.

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Glucagonomas: Ultrastructure and immunocytochemistry

Cited by 20 publications

References 45 publications

Expression of Lymphangiogenic Factors and Evidence of Intratumoral Lymphangiogenesis in Pancreatic Endocrine Tumors

Expression of Lymphangiogenic Factors and Evidence of Intratumoral Lymphangiogenesis in Pancreatic Endocrine Tumors

Cystic glucagonoma with loss of heterozygosity on chromosome 11 in multiple endocrine neoplasia type 1

Pancreatic Endocrine Tumors

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