Ou Sai-Hong Ignatius, Zhu Viola W
Chao Family Comprehensive Cancer Center, Department of Medicine, Division of Hematology and Oncology, University of California Irvine School of Medicine, Orange, California.
JTO Clin Res Rep. 2020 Mar 30;1(2):100037. doi: 10.1016/j.jtocrr.2020.100037. eCollection 2020 Jun.
Since the discovery of fusion-positive () NSCLC around late 2011 to early 2012, clinical trials of multikinase inhibitors and highly potent and selective RET tyrosine kinase inhibitors have indicated that fusion is an actionable oncogenic driver in NSCLC. There seems to be a differential response to multikinase inhibitors depending on the fusion partner ( versus non-); thus, knowledge of the fusion partners in NSCLC is important. To date, we identified 48 unique fusion partners in from published literature and congress proceedings. Two of the novel fusion partners ( and ) were identified in fusions that emerged as resistant to EGFR tyrosine kinase inhibitors. In addition, multiple intergenic rearrangements were identified.
自2011年末至2012年初发现融合阳性（）非小细胞肺癌（NSCLC）以来，多激酶抑制剂以及高效且选择性RET酪氨酸激酶抑制剂的临床试验表明，融合是NSCLC中一种可作用的致癌驱动因素。根据融合伴侣（与非融合伴侣）的不同，对多激酶抑制剂似乎存在不同反应；因此，了解NSCLC中融合伴侣的情况很重要。迄今为止，我们从已发表的文献和会议记录中确定了48个独特的融合伴侣。在对表皮生长因子受体（EGFR）酪氨酸激酶抑制剂产生耐药性的融合中，发现了两个新的融合伴侣（和）。此外，还发现了多个基因间重排。
