Atsumi Jun, Shimizu Kimihiro, Ohtaki Yoichi, Kaira Kyoichi, Kakegawa Seiichi, Nagashima Toshiteru, Enokida Yasuaki, Nakazawa Seshiru, Obayashi Kai, Takase Yoshiaki, Kawashima Osamu, Kamiyoshihara Mitsuhiro, Sugano Masayuki, Ibe Takashi, Igai Hitoshi, Takeyoshi Izumi
, , , , , , , , , , and , Gunma University Graduate School of Medicine, Maebashi, Gunma; and , National Hospital Organization Nishi-Gunma Hospital, Shibukawa, Gunma; and , , and , Maebashi Red Cross Hospital, Maebashi, Gunma, Japan.
J Glob Oncol. 2015 Dec 23;2(1):15-25. doi: 10.1200/JGO.2015.000638. eCollection 2016 Feb.
A deletion polymorphism of the gene has been reported to be a prognostic factor for patients with non-small-cell lung cancer (NSCLC) treated with epidermal growth factor receptor-tyrosine kinase inhibitors in the Asian population. We investigated the impact of the deletion polymorphism on survival among patients with completely resected NSCLC.
The polymorphism was detected by polymerase chain reaction analysis. We measured overall survival (OS) and recurrence-free survival rates in 411 patients and postrecurrence survival (PRS) in 94 patients who experienced recurrence and received additional anticancer therapy.
The deletion polymorphism was detected in 61 patients (14.8%). OS rates were significantly lower for patients with the deletion polymorphism than for those with the wild-type sequence. On multivariable analysis, the deletion polymorphism was identified as an independent prognostic factor for OS (hazard ratio, 1.98; 95% CI, 1.17 to 3.36; = .011). Among the 94 patients who experienced recurrence and were treated with anticancer therapy, patients with the deletion polymorphism showed significantly poorer PRS than those with the wild-type sequence (median, 9.8 months 26.9 months, respectively; < .001). Multivariable analysis revealed that the deletion polymorphism was an independent predictor of PRS (hazard ratio, 3.36; 95% CI, 1.75 to 6.47; < .001). This trend remained apparent in subgroup analyses stratified by status, histology, and therapeutic modality.
The deletion polymorphism is a novel indicator of shortened PRS among patients with recurrent NSCLC treated with anticancer therapy in the Asian population.
据报道,在亚洲人群中,某基因的缺失多态性是接受表皮生长因子受体酪氨酸激酶抑制剂治疗的非小细胞肺癌(NSCLC)患者的一个预后因素。我们研究了该缺失多态性对完全切除的NSCLC患者生存的影响。
通过聚合酶链反应分析检测该多态性。我们测量了411例患者的总生存期(OS)和无复发生存率,以及94例复发并接受额外抗癌治疗患者的复发后生存期(PRS)。
61例患者(14.8%)检测到该缺失多态性。具有该缺失多态性的患者的OS率显著低于野生型序列患者。多变量分析显示,该缺失多态性被确定为OS的独立预后因素(风险比,1.98;95%可信区间,1.17至3.36;P = 0.011)。在94例复发并接受抗癌治疗的患者中,具有该缺失多态性的患者的PRS明显比野生型序列患者差(中位数分别为9.8个月对26.9个月;P < 0.001)。多变量分析显示,该缺失多态性是PRS的独立预测因素(风险比,3.36;95%可信区间,1.75至6.47;P < 0.001)。在按分期、组织学和治疗方式分层的亚组分析中,这一趋势仍然明显。
在亚洲人群中,该缺失多态性是接受抗癌治疗的复发性NSCLC患者PRS缩短的一个新指标。