摘要
成纤维细胞生长因子家族(FGFs)及其受体(FGFRs)在许多生物过程中调节重要作用,影响细胞增殖、迁移、分化及存活。FGF/FGFR癌症信号通路的反常得到了更好的理解而且负责这一途径的激活的主要分子机制是基因突变基因突变、基因融合和基因扩增。基于DNA和RNA的技术已被用来检测这些异常,尤其在FGFR1,FGFR2和FGFR3和为了检测他们而发展的测试,但没有检测技术已被证明是理想的分子诊断。有趣的是,分子生物学知识的丰富支持和辅助针对这一途径的最重要的组成部分的治疗药物的开发。多选择性酪氨酸激酶抑制剂(TKI)以及单克隆抗体抗FGFR正在临床前试验和临床研究。在这篇文章中,我们回顾了这些方面对实体肿瘤相关基因改变的途径,特别强调和分子诊断检测患者的受体酪氨酸激酶抑制剂治疗的潜在能力。
关键词: FGF受体,基因突变,基因扩增,基因融合,荧光原位杂交。
Current Molecular Medicine
Title:Fibroblast Growth Factor Receptors: From the Oncogenic Pathway to Targeted Therapy.
Volume: 16 Issue: 1
Author(s): S. Saichaemchan, W. Ariyawutyakorn and M. Varella-Garcia
Affiliation:
关键词: FGF受体,基因突变,基因扩增,基因融合,荧光原位杂交。
摘要: The family of fibroblast growth factor (FGFs) and their receptors (FGFRs) regulates vital roles in many biological processes affecting cell proliferation, migration, differentiation and survival. Deregulation of the FGF/FGFR signaling pathway in cancers has been better understood and the main molecular mechanisms responsible for the activation of this pathway are gene mutations, gene fusions and gene amplification. DNA and RNA-based technologies have been used to detect these abnormalities, especially in FGFR1, FGFR2 and FGFR3 and tests have been developed for their detection, but no assay has been proved ideal for molecular diagnosis. Interestingly, the increase in the molecular biology knowledge has supported and assisted the development of therapeutic drugs targeting the most important components of this pathway. Multi- and selective tyrosine kinase inhibitors (TKIs) as well as monoclonal antibodies anti-FGFR are under investigation in preclinical and clinical trials. In this article, we reviewed those aspects with special emphasis on the pathway genomic alterations related to solid tumors, and the molecular diagnostic assays potentially able to stratify patients for the treatment with FGFR TKIs.
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S. Saichaemchan, W. Ariyawutyakorn and M. Varella-Garcia , Fibroblast Growth Factor Receptors: From the Oncogenic Pathway to Targeted Therapy., Current Molecular Medicine 2016; 16 (1) . https://dx.doi.org/10.2174/1566524016666151222144231
DOI https://dx.doi.org/10.2174/1566524016666151222144231 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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