Brägelmann Johannes, Böhm Stefanie, Guthrie Matthew R, Mollaoglu Gurkan, Oliver Trudy G, Sos Martin L
a Molecular Pathology, Institute of Pathology, University of Cologne , Cologne , Germany.
b Department of Translational Genomics , Medical Faculty, University of Cologne , Cologne , Germany.
Cell Cycle. 2017 Aug 18;16(16):1489-1498. doi: 10.1080/15384101.2017.1339849. Epub 2017 Jul 24.
Small cell lung cancer (SCLC) is one of the most deadly cancers and currently lacks effective targeted treatment options. Recent advances in the molecular characterization of SCLC has provided novel insight into the biology of this disease and raises hope for a paradigm shift in the treatment of SCLC. We and others have identified activation of MYC as a driver of susceptibility to Aurora kinase inhibition in SCLC cells and tumors that translates into a therapeutic option for the targeted treatment of MYC-driven SCLC. While MYC shares major features with its paralogs MYCN and MYCL, the sensitivity to Aurora kinase inhibitors is unique for MYC-driven SCLC. In this review, we will compare the distinct molecular features of the 3 MYC family members and address the potential implications for targeted therapy of SCLC.
小细胞肺癌(SCLC)是最致命的癌症之一,目前缺乏有效的靶向治疗方案。小细胞肺癌分子特征的最新进展为该疾病的生物学特性提供了新的见解,并为小细胞肺癌治疗模式的转变带来了希望。我们和其他研究人员已确定MYC的激活是小细胞肺癌细胞和肿瘤对极光激酶抑制敏感性的驱动因素,这转化为针对MYC驱动的小细胞肺癌进行靶向治疗的一种选择。虽然MYC与其旁系同源物MYCN和MYCL具有主要特征,但对极光激酶抑制剂的敏感性是MYC驱动的小细胞肺癌所特有的。在本综述中,我们将比较这3个MYC家族成员的不同分子特征,并探讨其对小细胞肺癌靶向治疗的潜在影响。