Department of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Institute of Digestive Disease, State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, China.
Cells. 2019 Jun 25;8(6):637. doi: 10.3390/cells8060637.
Gastric cancer (GC) is one of the most wide-spread malignancies in the world. The oncogenic role of signaling of fibroblast growing factors (FGFs) and their receptors (FGFRs) in gastric tumorigenesis has been gradually elucidated by recent studies. The expression pattern and clinical correlations of FGF and FGFR family members have been comprehensively delineated. Among them, FGF18 and FGFR2 demonstrate the most prominent driving role in gastric tumorigenesis with gene amplification or somatic mutations and serve as prognostic biomarkers. FGF-FGFR promotes tumor progression by crosstalking with multiple oncogenic pathways and this provides a rational therapeutic strategy by co-targeting the crosstalks to achieve synergistic effects. In this review, we comprehensively summarize the pathogenic mechanisms of FGF-FGFR signaling in gastric adenocarcinoma together with the current targeted strategies in aberrant FGF-FGFR activated GC cases.
胃癌(GC)是世界上最广泛传播的恶性肿瘤之一。最近的研究逐渐阐明了成纤维细胞生长因子(FGFs)及其受体(FGFRs)信号在胃肿瘤发生中的致癌作用。已经全面描绘了 FGF 和 FGFR 家族成员的表达模式和临床相关性。其中,FGF18 和 FGFR2 由于基因扩增或体细胞突变而在胃肿瘤发生中表现出最突出的驱动作用,并作为预后生物标志物。FGF-FGFR 通过与多种致癌途径的串扰促进肿瘤进展,这为通过共同靶向串扰来实现协同作用提供了合理的治疗策略。在这篇综述中,我们全面总结了 FGF-FGFR 信号在胃腺癌中的发病机制,以及异常 FGF-FGFR 激活 GC 病例中的当前靶向策略。