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Genotype Driven Therapy for Non-Small Cell Lung Cancer: Resistance, Pan Inhibitors and Immunotherapy.
Current Medicinal Chemistry ( IF 4.1 ) Pub Date : 2020-08-31 , DOI: 10.2174/0929867326666190222183219
Sitanshu S Singh 1 , Achyut Dahal 1 , Leeza Shrestha 1 , Seetharama D Jois 1
Affiliation  

Eighty-five percent of patients with lung cancer present with Non-small Cell Lung Cancer (NSCLC). Targeted therapy approaches are promising treatments for lung cancer. However, despite the development of targeted therapies using Tyrosine Kinase Inhibitors (TKI) as well as monoclonal antibodies, the five-year relative survival rate for lung cancer patients is still only 18%, and patients inevitably become resistant to therapy. Mutations in Kirsten Ras Sarcoma viral homolog (KRAS) and epidermal growth factor receptor (EGFR) are the two most common genetic events in lung adenocarcinoma; they account for 25% and 20% of cases, respectively. Anaplastic Lymphoma Kinase (ALK) is a transmembrane receptor tyrosine kinase, and ALK rearrangements are responsible for 3-7% of NSCLC, predominantly of the adenocarcinoma subtype, and occur in a mutually exclusive manner with KRAS and EGFR mutations. Among drug-resistant NSCLC patients, nearly half exhibit the T790M mutation in exon 20 of EGFR. This review focuses on some basic aspects of molecules involved in NSCLC, the development of resistance to treatments in NSCLC, and advances in lung cancer therapy in the past ten years. Some recent developments such as PD-1-PD-L1 checkpoint-based immunotherapy for NSCLC are also covered.



中文翻译:

非小细胞肺癌的基因型驱动疗法:耐药性,泛抑制剂和免疫疗法。

百分之八十五的肺癌患者患有非小细胞肺癌(NSCLC)。靶向治疗方法是有希望的肺癌治疗方法。然而,尽管开发了使用酪氨酸激酶抑制剂(TKI)和单克隆抗体的靶向疗法,肺癌患者的五年相对存活率仍仅为18%,患者不可避免地变得对治疗产生抗药性。Kirsten Ras肉瘤病毒同源物(KRAS)和表皮生长因子受体(EGFR)的突变是肺腺癌中两个最常见的遗传事件。他们分别占案件的25%和20%。间变性淋巴瘤激酶(ALK)是一种跨膜受体酪氨酸激酶,ALK重排可导致NSCLC的3-7%(主要是腺癌亚型),并以相互排斥的方式与KRAS和EGFR突变发生。在耐药的NSCLC患者中,近一半的人在EGFR外显子20处出现T790M突变。这篇综述着重于NSCLC中涉及的分子的一些基本方面,NSCLC中对治疗的耐药性的发展以及过去十年中肺癌治疗的进展。还涵盖了一些近期的进展,例如针对NSCLC的基于PD-1-PD-L1检查点的免疫疗法。

更新日期:2020-09-25
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