PDF(Pubmed)
Abstract：
UNASSIGNED: The c-met proto-oncogene (MET) serves as a significant primary oncogenic driver in non-small cell lung cancer (NSCLC) and has the potential to fuse with other genes, such as KIF5B, although it occurs infrequently. Only a limited number of reported cases have examined the clinical efficacy of crizotinib in patients with KIF5B-MET gene fusion, with no known data regarding acquired resistance to crizotinib and its potential mechanisms. In this report, we present the clinical progression of a female patient diagnosed with NSCLC and harboring a KIF5B-MET gene fusion.
UNASSIGNED: The patient initially exhibited partial response to first-line crizotinib treatment, albeit for a short duration and with limited efficacy. Subsequent disease progression revealed the emergence of a secondary MET mutation, specifically MET Y1230H, leading to acquired resistance to crizotinib.
UNASSIGNED: The reporting of this case is imperative for informing clinical practice, given the uncommon occurrence of NSCLC with MET fusion, displaying responsiveness to MET tyrosine kinase inhibitor therapy, as well as the emergence of the secondary Y1230H alteration as a potential resistance mechanism.
UNASSIGNED: The patient initially exhibited partial response to first-line crizotinib treatment, albeit for a short duration and with limited efficacy. Subsequent disease progression revealed the emergence of a secondary MET mutation, specifically MET Y1230H, leading to acquired resistance to crizotinib.
UNASSIGNED: The reporting of this case is imperative for informing clinical practice, given the uncommon occurrence of NSCLC with MET fusion, displaying responsiveness to MET tyrosine kinase inhibitor therapy, as well as the emergence of the secondary Y1230H alteration as a potential resistance mechanism.
摘要：
■c-met原癌基因（MET）在非小细胞肺癌（NSCLC）中充当重要的原发性致癌驱动因子，并有可能与其他基因融合，比如KIF5B，虽然它很少发生。只有少数报道的病例检查了克唑替尼在KIF5B-MET基因融合患者中的临床疗效。没有关于克唑替尼获得性耐药及其潜在机制的已知数据。在这份报告中,我们介绍了1例诊断为NSCLC并携带KIF5B-MET基因融合的女性患者的临床进展.
■患者最初对克唑替尼一线治疗表现出部分反应，尽管持续时间短，疗效有限。随后的疾病进展揭示了继发性MET突变的出现，特别是METY1230H，导致获得性克唑替尼耐药。
■此病例的报告对于告知临床实践是必要的，鉴于MET融合的非小细胞肺癌的罕见发生，显示对MET酪氨酸激酶抑制剂治疗的反应性，以及次级Y1230H改变的出现作为潜在的抗性机制。
■患者最初对克唑替尼一线治疗表现出部分反应，尽管持续时间短，疗效有限。随后的疾病进展揭示了继发性MET突变的出现，特别是METY1230H，导致获得性克唑替尼耐药。
■此病例的报告对于告知临床实践是必要的，鉴于MET融合的非小细胞肺癌的罕见发生，显示对MET酪氨酸激酶抑制剂治疗的反应性，以及次级Y1230H改变的出现作为潜在的抗性机制。
