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KRAS as a druggable target in NSCLC: Rising like a phoenix after decades of development failures.
Cancer Treatment Reviews ( IF 11.8 ) Pub Date : 2020-02-07 , DOI: 10.1016/j.ctrv.2020.101978
Alex Friedlaender 1 , Alexander Drilon 2 , Glen J Weiss 3 , Giuseppe L Banna 4 , Alfredo Addeo 1
Affiliation  

Cancers of nearly all lineages harbor alterations that deregulate mitogen-activated protein kinase signaling, a crucial signaling pathway for tumor formation and maintenance. Of these, KRAS mutations are the most frequent gain-of-function alterations found in patients with cancer. In particular they represents the most common molecular alteration detected in non-small cell lung cancer (NSCLC) accounting for up to 25% of all oncogenic mutations. They were identified decades ago and prior efforts to target these proteins have been unsuccessful. KRAS mutation profiles (i.e. frequency of specific codon substitutions) in smokers and never-smokers are distinct and not all KRAS alterations are driver mutations. KRAS has evolved from a mutation with possible predictive value to a therapeutic target with great promise. Here, we will discuss the biology of KRAS in lung cancer and its clinical implications in oncology today and in the foreseeable future.

中文翻译:

KRAS作为NSCLC的可治疗目标:经过数十年的开发失败,像凤凰一样崛起。

几乎所有谱系的癌症都有改变,这些改变使有丝分裂原激活的蛋白激酶信号转导失调,这是肿瘤形成和维持的关键信号转导途径。其中,KRAS突变是在癌症患者中发现的最常见的功能获得性改变。特别地,它们代表了在非小细胞肺癌(NSCLC)中检测到的最常见的分子改变,占所有致癌突变的25%。几十年前就已鉴定出它们,并且先前针对这些蛋白的努力还没有成功。吸烟者和从不吸烟者的KRAS突变特征(即特定密码子替换的频率)是截然不同的,并非所有KRAS改变都是驱动突变。KRAS已从具有可能的预测价值的突变演变为具有广阔前景的治疗靶标。这里,
更新日期:2020-02-07
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