دورية أكاديمية
c-MET receptor tyrosine kinase as a molecular target in advanced hepatocellular carcinoma
| العنوان: | c-MET receptor tyrosine kinase as a molecular target in advanced hepatocellular carcinoma |
|---|---|
| المؤلفون: | Granito,Alessandro, Guidetti,Elena, Gramantieri,Laura |
| بيانات النشر: | Dove Press |
| سنة النشر: | 2015 |
| المجموعة: | Dove Medical Press |
| مصطلحات موضوعية: | Journal of Hepatocellular Carcinoma |
| الوصف: | Alessandro Granito,1 Elena Guidetti,1 Laura Gramantieri2,3 1Dipartimento di Scienze Mediche e Chirurgiche Università di Bologna, Bologna, Italy; 2Dipartimento dell'Apparato Digerente, Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy; 3Centro di Ricerca Biomedica Applicata (CRBA), Azienda Ospedaliero-Universitaria Policlinico S Orsola-Malpighi e Università di Bologna, Bologna, Italy Abstract: c-MET is the membrane receptor for hepatocyte growth factor (HGF), also known as scatter factor or tumor cytotoxic factor, a mitogenic growth factor for hepatocytes. HGF is mainly produced by cells of mesenchymal origin and it mainly acts on neighboring epidermal and endothelial cells, regulating epithelial growth and morphogenesis. HGF/MET signaling has been identified among the drivers of tumorigenesis in human cancers. As such, c-MET is a recognized druggable target, and against it, targeted agents are currently under clinical investigation. c-MET overexpression is a common event in a wide range of human malignancies, including gastric, lung, breast, ovary, colon, kidney, thyroid, and liver carcinomas. Despite c-MET overexpression being reported by a large majority of studies, no evidence for a c-MET oncogenic addiction exists in hepatocellular carcinoma (HCC). In particular, c-MET amplification is a rare event, accounting for 4%–5% of cases while no mutation has been identified in c-MET oncogene in HCC. Thus, the selection of patient subgroups more likely to benefit from c-MET inhibition is challenging. Notwithstanding, c-MET overexpression was reported to be associated with increased metastatic potential and poor prognosis in patients with HCC, providing a rationale for its therapeutic inhibition. Here we summarize the role of activated HGF/MET signaling in HCC, its prognostic relevance, and the implications for therapeutic approaches in HCC. Keywords: hepatocellular carcinoma, c-MET, clinical trials |
| نوع الوثيقة: | article in journal/newspaper review |
| وصف الملف: | text/html |
| اللغة: | English |
| العلاقة: | https://www.dovepress.com/c-met-receptor-tyrosine-kinase-as-a-molecular-target-in-advanced-hepat-peer-reviewed-fulltext-article-JHCTest |
| الإتاحة: | https://doi.org/10.2147/JHC.S77038Test https://www.dovepress.com/c-met-receptor-tyrosine-kinase-as-a-molecular-target-in-advanced-hepat-peer-reviewed-fulltext-article-JHCTest |
| حقوق: | info:eu-repo/semantics/openAccess |
| رقم الانضمام: | edsbas.7D833C1C |
| قاعدة البيانات: | BASE |
| الوصف غير متاح. |