Molecular Oncology Laboratory, Genetic Engineering and Biotechnology Institute, TUBITAK Marmara Research Center, Kocaeli, Turkey.
Laboratory and Veterinary Health Program, Department of Veterinary Medicine, Artova Vocational School, Tokat Gaziosmanpaşa University, Tokat, Turkey.
Mol Biol Rep. 2021 Apr;48(4):3813-3825. doi: 10.1007/s11033-021-06314-z. Epub 2021 Apr 15.
Lung cancer is the leading cancer type of death rate. The lung adenocarcinoma subtype is responsible for almost half of the total lung cancer deaths. Despite the improvements in cancer treatment in recent years, lung adenocarcinoma patients' overall survival rate remains poor. Immunetherapy and chemotherapy are two of the most widely used options for the treatment of cancer. Although many cancer types initially respond to these treatments, the development of resistance is inevitable. The rapid development of drug resistance mainly characterizes lung adenocarcinoma. Despite being the subject of many studies in recent years, the resistance initiation and progression mechanism is still unclear. In this review, we have examined the role of the primary DNA repair pathways (non-homologous end joining (NHEJ) pathway, homologous-recombinant repair (HR) pathway, base excision repair (BER) pathway, and nucleotide excision repair (NER) pathway and transactivation mechanisms of tumor protein 53 (TP53) in drug resistance development. This review suggests that mentioned pathways have essential roles in developing the resistance against chemotherapy and immunotherapy in lung adenocarcinoma patients.
肺癌是死亡率最高的癌症类型。肺腺癌亚型占总肺癌死亡人数的近一半。尽管近年来癌症治疗有所改善，但肺腺癌患者的总体生存率仍然较差。免疫疗法和化疗是癌症治疗中最广泛使用的两种选择。尽管许多癌症类型最初对这些治疗有反应，但耐药性的发展是不可避免的。耐药性的快速发展主要是肺腺癌的特征。尽管近年来已经进行了许多研究，但耐药性的起始和进展机制仍不清楚。在这篇综述中，我们研究了主要的 DNA 修复途径（非同源末端连接 (NHEJ) 途径、同源重组修复 (HR) 途径、碱基切除修复 (BER) 途径和核苷酸切除修复 (NER) 途径）和肿瘤蛋白 53 (TP53) 的转激活机制在肺癌患者对化疗和免疫治疗的耐药性发展中的作用。这篇综述表明，上述途径在肺腺癌患者对化疗和免疫治疗产生耐药性方面起着重要作用。
