Oncogene expression in gastroenteropancreatic neuroendocrine tumors

Wang, Da-Gong; Johnston, C.F.; Buchanan, K. D.

doi:10.1002/(sici)1097-0142(19970815)80:4<668::aid-cncr4>3.3.co;2-1

Cited by 17 publications

(18 citation statements)

References 6 publications

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“…Wang et al, demonstrated HER-3 expression in 6 of 98 (6%) malignant GEP NETs (22). Our study identified HER-3 positivity in 6% of GEP NETs (3 of 52 cases) and 50% (3 of 6 cases) of paragangliomas.…”

Section: ------------------------------------------------------------supporting

confidence: 61%

“…The reasons for this difference in staining are unclear and may be related to the age of the slides or the scoring system used to interpret the slides. Other studies have also demonstrated variable expression of HER-2 in NETs using immunohistochemical and PCR techniques (21,22,29). The negative expression of HER-2 immunohistochemistry in this study could be due to a number of reasons; possibly related to low levels of receptor expression in these specimens which were below the threshold of detection by immunohistochemistry.…”

Section: ------------------------------------------------------------mentioning

confidence: 42%

“…Previous studies have demonstrated the expression of EGFR in NETs (13,20). We have previously demonstrated high EGFR expression in NETs (13 (21)(22)(23)(24). Expression of all four members of the HER family has not been studied in NETs.…”

Section: Introductionmentioning

confidence: 94%

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Expression of the HER-1-4 family of receptor tyrosine kinases in neuroendocrine tumours

Srirajaskanthan

Shah²,

Watkins³

et al. 2010

Oncol Rep

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Section: ------------------------------------------------------------supporting

confidence: 61%

Section: ------------------------------------------------------------mentioning

confidence: 42%

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Expression of the HER-1-4 family of receptor tyrosine kinases in neuroendocrine tumours

Srirajaskanthan

Shah²,

Watkins³

et al. 2010

Oncol Rep

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“…20,21 In addition, they frequently express c-Myc, 22 a TGFb1 pathway antagonist. This information as well as data that TGFb1 suppresses neuroendocrine cell proliferation 23 has led us to hypothesize that neoplastic EC cells are characterized by down-regulation or loss of the TGFb1-mediated cytostatic program.…”

mentioning

confidence: 99%

Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1

Kidd

Modlin

Pfragner

et al. 2007

Cancer

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Objective To examine whether and to what extent the intracellular trafficking features of HLA–B*2705, which is associated with the development of spondylarthritis (SpA), differ from those of HLA–B*2709 and HLA–B*0702, which are not associated with SpA. Methods HeLa cells were transfected with complementary DNA encoding for HLA–B proteins fused to Renilla luciferase or yellow fluorescent protein. The subcellular distribution of properly folded and unfolded/misfolded HLA–B proteins was examined by flow cytometry and confocal microscopy of cells labeled with ME1 and HC‐10 antibodies, respectively. HLA–B/HLA–B interactions were monitored in endoplasmic reticulum (ER)– and plasma membrane–enriched subcellular fractions, by bioluminescence resonance energy transfer (BRET). Results All 3 HLA–B alleles displayed a similar distribution pattern (properly folded heavy chain at the cell surface, unfolded/misfolded proteins only in the cytoplasm). By means of BRET, we provided evidence that both HLA–B*2705 and HLA–B*2709 formed more oligomers in the ER and the plasma membrane than did HLA–B*0702. The propensity of HLA–B*2705 to form oligomers in the ER was partly attributable to residue Cys67 of the molecule. For all 3 alleles, increased expression of HLA–B proteins was associated with intracytoplasmic accumulation of unfolded/misfolded proteins and intracellular vesicles, probably corresponding to expanded ER–Golgi intermediate compartments, in which these proteins accumulated together with the stress sensor BiP. Conclusion Our results suggest that the difference in disease susceptibility conferred by HLA–B*2705 and HLA–B*2709 cannot be explained by their different propensity to form dimers or misfolded proteins, thus presumably implicating other, still unknown factors.

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“…Previous studies have shown that forced Bcl-2 expression suppresses apoptosis of PC12 cells [15,16] and it has been speculated that the observed expression of Bcl-2 in oxyntic endocrine cells may promote cytosurvival during their maturation and downward migration from isthmal/neck-localised stem cells [8]. Numerous studies have documented Bcl-2 expression in neuroendocrine tumours such as phaeochromocytomas [18], thymic neuroendocrine tumours [19], and gastroenteropancreatic neuroendocrine tumours [20]. Investigations into the function of this oncoprotein in the pathology of neuroendocrine tumour development are, however, sparse and whether in this setting its actions differ from the apoptosis-inhibitory role it plays in more common cancers remains to be established.…”

Section: Resultsmentioning

confidence: 99%

An investigation into the role of Bcl-2 in neuroendocrine differentiation

Cadden

Johnston

Connolly

et al. 2005

Biochemical and Biophysical Research Communications

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Introduction: In addition to its role in apoptosis suppression, Bcl-2 has been reported to be co-expressed with neuroendocrine markers in several tissues, leading to speculation that this oncoprotein may promote neuroendocrine differentiation.Aim: This study investigated whether Bcl-2 modulated neuroendocrine biopeptide expression. Methods: Levels of chromogranin A, neurone specific enolase, protein gene peptide 9.5, pancreatic polypeptide, and the chromogranin-derived peptides, intervening peptide and vasostatin-1 were examined by immunocytochemistry in rat phaeochromocytoma (PC12) cell lines genetically engineered to over-express Bcl-2 and their mock-transfected controls. Intensity of fluorescence was graded using a semi-quantitative scale from (À) indicating negative expression to (+++) indicating intense positivity.Results: Mann-Whitney U analysis indicated that no significant differences in expression existed between control and Bcl2 overexpressing cell lines for any of the six peptides examined.Conclusions: The results of this study do not support the hypothesis that Bcl-2 promotes the acquisition of a neuroendocrine phenotype.

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Oncogene expression in gastroenteropancreatic neuroendocrine tumors

Abstract: histopathologic signs of malignancy. No etiologic factors are proven to be associated with them, and their exact ontogeny and carcinogenesis remain unknown.

Cited by 17 publications

References 6 publications

Expression of the HER-1-4 family of receptor tyrosine kinases in neuroendocrine tumours

Expression of the HER-1-4 family of receptor tyrosine kinases in neuroendocrine tumours

Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1

An investigation into the role of Bcl-2 in neuroendocrine differentiation

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