FGFR1 扩增突变体的信号传导
中文名称
通路描述
据报道，FGFR1 扩增或激活存在于肺癌 (Weiss, 2001; Marek, 2009; Dutt, 2011)、乳腺癌 (Reis-Filho, 2006; Turner, 2010)、口腔鳞状细胞癌 (Freier, 2007)、食管鳞状细胞癌 (Ishizuka, 2002)、卵巢癌 (Gorringe, 2007)、膀胱癌 (Simon, 2001)、前列腺癌 (Edwards, 2003; Acevedo, 2007) 和肉瘤 (Missiaglia, 2009)。与 FGFR2 扩增不同，FGFR1 扩增不与额外的点突变相关，且不影响受体的内在激酶活性。过表达的 FGFR1 似乎以配体独立的方式在基线水平上信号传导，但也能够被外源配体刺激。下游激活可能是由于异常的旁分泌或自分泌刺激的结果 (综述 Turner and Gross, 2010; Greulich and Pollock, 2011)。FGFR1 扩增尚未确凿地证明是所有上述癌症类型中的致癌驱动因素，8p11 区域的其他基因也可能是某些情况下的候选基因 (Bass, 2009; Bernard-Pierrot, 2008; Ray, 2004)。
英文描述
Signaling by FGFR1 amplification mutants Amplification or activation of FGFR1 has been reported in lung cancer (Weiss, 2001; Marek, 2009; Dutt, 2011), breast cancer (Reis-Filho, 2006; Turner, 2010), oral squamous carcinoma (Freier, 2007), esophageal squamous cell carcinomas (Ishizuka, 2002), ovarian cancer (Gorringe, 2007), bladder cancer (Simon, 2001), prostate cancer (Edwards, 2003; Acevedo, 2007) and rhabodomyosarcoma (Missiaglia, 2009). Unlike the case for FGFR2 amplifications, FGFR1 amplifications are not associated with additional point mutations and affect signaling without altering the intrinsic kinase activity of the receptor. Overexpressed FGFR1 appears to signal at a basal level in a ligand-independent fashion, but is also able to be stimulated by exogenous ligand. Downstream activation may be the result of aberrant paracrine or autocrine stimulation (reviewed in Turner and Gross, 2010; Greulich and Pollock, 2011). FGFR1 amplification has not been conclusively demonstrated to be the causative oncogenic agent in all of the cancer types mentioned above, and other genes in the 8p11 region may also be candidates in some cases (Bass, 2009; Bernard-Pierrot, 2008; Ray, 2004).
所含基因
0 个基因