EGFR and HER2 FISH status were not associated with KRAS mutation. Frequency of EGFR FISH+ status was higher and its predictive power for TKI sensitivity was lower in this Japanese cohort than in Western NSCLC cohorts. These findings support differences in the mechanisms of EGFR pathway activation ...
PRL in breast cancer cells via PRLR/JAK2 can also induce phosphorylation of ERBB2/HER2, which in turn activates the downstream RAS/MEK/ERK pathway required for ERα phosphorylation. EGFR, independent of PRL/PRLR, can activate STAT5 indirectly via c-SRC and drive the expression of target genes...
人EGFR 2(HER2)基因扩增发生在约3-5%的RAS野生型肿瘤中,也是抗EGFR治疗的原发和/或继发耐药机制[51, 52]。就这方面而言,HER2抑制剂对于HER2扩增的mCRC患者是一个非常有前景的治疗方案[53-57]。作为亚克隆改变的MET基因扩增也发生在小部...
EGFR(Epidermal Growth Factor Receptor)是上皮生长因子(EGF)细胞增殖和信号传导的受体。EGFR属于受体磷酸激酶(Receptor Tyrosine Kinases, RTK)HER 家族的四个成员之一,该家族包括EGFR (ErbB-1),HER2/ (E…
两处极大的不同就是这位成功的战友有着KRAS+、EGFR+、HER2+ 的免疫组化的表达区别并且一直没有放弃靶向轮换,而另一位完全放弃靶向方案,同样是肺腺癌基因全阴,因免疫和肿瘤的微环境的大不同而最后的PD1抑制剂应用结果却如此大不同,令人唏嘘。 也想到两位EGFR基因...
目的:探讨Iressa对非小细胞肺癌患者EGFR,HER2表达水平的影响.方法:选择在我院胸外科接受治疗的非小细胞肺癌患者68名,符合IRESSA国际慈善研究(EAP)条件,每日固定时间口服Iressa 250mmg,每日一次,每4周为一个疗程,直到疾病进展或出现不可耐受的副反应.治疗前后,测定血清和肿瘤组织中的EGFR,HER2的含量.结果:治疗结束后,...
EGFR(Epidermal Growth Factor Receptor)是上皮生长因子(EGF)细胞增殖和信号传导的受体。EGFR属于受体磷酸激酶(Receptor Tyrosine Kinases, RTK)HER 家族的四个成员之一,该家族包括EGFR (ErbB-1),HER2/ (ErbB-2),Her3(ErbB-3) 和Her4(ErbB-4)。研究表明,EGFR突变或过表达会引发肿瘤[1-2]。
The Prognostic Role of Ephrin \\{A2\\} and Endothelial Growth Factor Receptor Pathway Mediators in Patients With Advanced Colorectal Cancer Treated With Ce... 2 (IGFBP2), insulin growth factor receptor 1 (IGF1R), cMET, EphA2, human epidermal growth factor receptor 2 (HER2), HER3, and \...
EGFR/HER2 SIGNALING REGULATES UROKINASE SECRETION AND CELL INVASION IN HIGHLY INVASIVE PROSTATE CANCER CELLS. Claudio Festuccia1, Adriano Angelucci1, Giovanni Luca Gravina2, Paola Muzi1, Danilo Millimaggi1, Carlo Vicentini2 and Mauro Bologna1,3. Departments of Experimental Medicine1, Surgery2 and Ba...
The Hippo pathway is frequently dysregulated in cancer, leading to the unrestrained activity of its downstream targets, YAP/TAZ, and aberrant tumor growth. However, the precise mechanisms leading to YAP/TAZ activation in most cancers is still poorly unde