High KIT and PDGFRA are associated with shorter patients survival in gastroenteropancreatic neuroendocrine tumors, but mutations are a rare event

Knösel, Thomas; Chen, Yuan; Altendorf-Hofmann, A.; Danielczok, Christine; Freesmeyer, Martin; Settmacher, Utz; Wurst, Christine; Schulz, Stefan; Yang, Lin; Petersen, Iver

doi:10.1007/s00432-011-1107-9

Cited by 23 publications

(16 citation statements)

References 20 publications

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“…7,8,15,16 In contrast, Ki67 has been investigated extensively in both functioning and nonfunctioning PNETs for its prognostic value. The current series is the only report that attempts to correlate the prognostic values of Ki67 in comparison with 4 other markers strictly in nonfunctioning PNETs.…”

Section: Discussionmentioning

confidence: 92%

Comparison of tumor markers for predicting outcomes after resection of nonfunctioning pancreatic neuroendocrine tumors

Cherenfant

Talamonti

Hall

et al. 2014

Surgery

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Section: Discussionmentioning

confidence: 92%

Comparison of tumor markers for predicting outcomes after resection of nonfunctioning pancreatic neuroendocrine tumors

Cherenfant

Talamonti

Hall

et al. 2014

Surgery

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“…All entities described above were removed endoscopically or surgically, and were fixed in formalin and embedded in paraffin (FFPE). The GEP-NET collective represented a subgroup from a recently published series [18]. The grading for the tumor samples was defined according to the WHO classification of tumors of the digestive system [19].…”

Section: Methodsmentioning

confidence: 99%

GNAS1 mutation analysis in gastrointestinal tumors

Walther

Chen³

et al. 2014

Folia Histochem Cytobiol.

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GNAS1 codes for a part of the a-stimulatory subunit (Gsa) of the G protein. Mutation of GNAS1 has been frequently found in myxoid soft tissues, however, in gastrointestinal tumors, little is known about the mutation status of GNAS1. The aim of the study was to analyze the occurrence of GNAS1 mutations in different gastrointestinal, gastroenteropancreatic neuroendocrine tumors (GEP-NETs) and colorectal tumors. Mutation status of GNAS1 exon 8 was analyzed in one hundred thirty-five formalin-fixed, paraffin-embedded (FFPE) gastrointestinal tumor samples including 45 tubular-villous adenomas, 11 tubular adenomas, 6 villous adenomas, 10 hyperplastic gastric polyps, 31 GEP-NETs and 32 colorectal adenocarcinomas by using polymerase chain reaction (PCR) and direct sequencing. Five GNAS1 mutations were found in 2 tubular-villous adenomas, 2 villous adenomas and 1 colorectal adenocarcinoma. No mutations were detected in the tubular adenomas, the hyperplastic gastric polyps or GEP-NETs. GNAS1 mutation is not a frequent molecular event in GEP-NETs or hyperplastic gastric polyps. The study confirms the presence of GNAS1 mutations in colon tumors with villous differentiation. (Folia Histochemica et Cytobiologica 2014, Vol. 52, No. 2, 90-95)

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“…Although CK20 expression in PNENs has been reported in up to 33% of cases [95], it was not observed in the present study. The published data also vary widely -only 5% of gastroenteropancreatic tumours expressed CK20 in Knosel et al [96] study.…”

Section: Cytokeratinsmentioning

confidence: 97%

Original paper Morphological and immunohistochemical profile of pancreatic neuroendocrine neoplasms

Simtniece¹,

Vanags²,

Štrumfa³

et al. 2015

pjp

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The study represents a comprehensive retrospective morphological and immunohistochemical profiling of pancreatic neuroendocrine neoplasms (PNENs) in order to reveal the associations between morphological and molecular parameters. The local tumour spread (T), presence of metastases in regional lymph nodes (N) and distant organs (M), tumour grade (G) and resection line status (R) by pathology findings (pTNMGR), mitotic activity, perineural, vascular and lymphatic invasion were assessed in 16 surgically resected PNENs. By immunohistochemistry, expression of Ki-67, p53, p27, p21, cyclin D1, Bcl-2, E-cadherin, CD44, vimentin, cyclooxygenase 2 (COX-2), microvascular density, and cytokeratin (CK) spectrum, along with neuroendocrine, intestinal and squamous markers were detected. Descriptive statistics, Chi-square test, Spearman's rank correlation, Mann-Whitney and Kruskal-Wallis methods were applied; p < 0.05 was considered significant. Ki-67, CK19, p63, vimentin and COX-2 were significantly up-regulated in PNENs in comparison to benign pancreatic islets. A complex network of morphological and molecular associations was identified. Ki-67 correlated with PNEN size (p = 0.022), the World Health Organization 2004 and 2010 classification grades (p = 0.021 and p = 0.002), stage (p = 0.028) and mitotic count (p = 0.007) but among molecular markers -with CK19 (p = 0.033) and vimentin (p = 0.045). CK19 was significantly up-regulated in PNENs, having higher pT (p = 0.018), pR (p = 0.025), vascular (p = 0.020), perineural (p = 0.026) and lymphatic invasion (p = 0.043). In conclusion, proliferation activity (by Ki-67), E-cadherin, vimentin and CK19 are important molecular characteristics of PNENs due to significant associations with morphological tumour characteristics, pTNMGR and invasive growth.

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High KIT and PDGFRA are associated with shorter patients survival in gastroenteropancreatic neuroendocrine tumors, but mutations are a rare event

Abstract: High expression of KIT and PDGFRA was significantly correlated with shorter patients survival and could serve as prognostic marker. Mutations of the KIT gene might open new avenues for tyrosine kinase inhibitor therapy in a subset of patients with advanced pancreatic neuroendocrine tumors.

Cited by 23 publications

References 20 publications

Comparison of tumor markers for predicting outcomes after resection of nonfunctioning pancreatic neuroendocrine tumors

Comparison of tumor markers for predicting outcomes after resection of nonfunctioning pancreatic neuroendocrine tumors

GNAS1 mutation analysis in gastrointestinal tumors

Original paper Morphological and immunohistochemical profile of pancreatic neuroendocrine neoplasms

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