دورية أكاديمية
The HGF Receptor c-Met Is Overexpressed in Esophageal Adenocarcinoma
| العنوان: | The HGF Receptor c-Met Is Overexpressed in Esophageal Adenocarcinoma |
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| المؤلفون: | Luis J. Herrera, Talal El-Hefnawy, Pierre E. Queiroz de Oliveira, Siva Raja, Sydney Finkelstein, William Gooding, James D. Luketich, Tony E. Godfrey, Steven J. Hughes |
| المصدر: | Neoplasia: An International Journal for Oncology Research, Vol 7, Iss 1, Pp 75-84 (2005) |
| بيانات النشر: | Elsevier, 2005. |
| سنة النشر: | 2005 |
| المجموعة: | LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
| مصطلحات موضوعية: | c-Met, HGF, Barrett's esophagus, COX-2, CD95, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282 |
| الوصف: | The hepatocyte growth factor (HGF) receptor, Met, has established oncogenic properties; however, its expression and function in esophageal adenocarcinoma (EA) remain poorly understood. We aimed to determine the expression and potential alterations in Met expression in EA. Met expression was investigated in surgical specimens of EA, Barrett's esophagus (BE), and normal esophagus (NE) using immunohistochemistry (IHC) and quantitative reverse transcriptase polymerase chain reaction. Met expression, phosphorylation, and the effect of COX-2 inhibition on expression were examined in EA cell lines. IHC demonstrated intense Met immunoreactivity in all (100%) EA and dysplastic BE specimens. In contrast, minimal immunostaining was observed in BE without dysplasia or NE specimens. Met mRNA and protein levels were increased in three EA cell lines, and Met protein was phosphorylated in the absence of serum. Sequence analysis found the kinase domain of c-met to be wild type in all three EA cell lines. HGF mRNA expression was identified in two EA cell lines. In COX-2-overexpressing cells, COX-2 inhibition decreased Met expression. Met is consistently overexpressed in EA surgical specimens and in three EA cell lines. Met dysregulation occurs early in Barrett's dysplasia to adenocarcinoma sequence. Future study of Met inhibition as a potential biologic therapy for EA is warranted. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1476-5586 1522-8002 |
| Relation: | http://www.sciencedirect.com/science/article/pii/S1476558605801010; https://doaj.org/toc/1476-5586; https://doaj.org/toc/1522-8002 |
| DOI: | 10.1593/neo.04367 |
| URL الوصول: | https://doaj.org/article/62f2a9b206ff4b889356c4a737f10944 |
| رقم الأكسشن: | edsdoj.62f2a9b206ff4b889356c4a737f10944 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 14765586 15228002 |
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| DOI: | 10.1593/neo.04367 |