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| 1 | Survival difference between EGFR Del19 and L858R mutant advanced non-small cell lung cancer patients receiving gefitinib:a propensity score matching analysis显示文摘Objective: Although superior clinical benefits of epidermal growth factor receptor(EGFR) tyrosine kinase inhibitors(TKIs) in the treatment of advanced non-small-cell lung cancer(NSCLC) had been reported,the survival difference between exon 19 deletion(Del19) and exon 21 Leu858 Arg substitution(L858 R) remains controversial.The purpose of this study is to investigate the differences in progression-free survival(PFS) and overall survival(OS) between different EGFR mutant subtypes among advanced NSCLC patients receiving gefitinib.Methods: There were 204 advanced NSCLC patients with EGFR mutations treated with gefitinib were enrolled in this retrospective cohort study.Patients were divided into the EGFR Del19 group and the L858 R mutated group according to their mutant subtype.Propensity score matching(PSM) was conducted by using a nearest-neighbor algorithm(1:1) to adjust for demographical and clinical covariates.Survival curves were constructed with the Kaplan-Meier method and compared by using the log-rank test.Results: The PFS in Del19 group was similar to that in the L858 R group [before PSM 8.6 vs.7.2 months,P=0.072; after PSM 7.3 vs.7.2 months,P=0.155].No differences were detected in OS between the L858 R and the Del19 group(before PSM 17.8 vs.13.1 months,P=0.253; after PSM 16.9 vs.13.1 months,P=0.339).The Del19 group was significantly younger compared with the L858 R mutation group in age(P=0.015).Conclusions: No significant difference was found in the PFS or OS between the Del19 and L858 R mutant NSCLC patients receiving gefitinib.The age gap might contribute to the survival differences between Del19 and L858 R groups.PSM is of important value to the elimination of potential bias. | Minglei Zhuo Qiwen Zheng Jun Zhao Meina Wu Tongtong An Yuyan Wang Jianjie Li Shuhang Wang Jia Zhong Xue Yang Hanxiao Chen Bo Jia Zhi Dong Emei Gao JingjingWang Ziping Wang | 2017 | Chinese Journal of Cancer Research2017,29,6: | 4 |
| 2 | A phase I study of nimotuzumab plus docetaxel in chemotherapy- refractory/resistant patients with advanced non-small-cell lung cancer显示文摘Background: To determine the safety and therapeutic efficacy of nimotuzumab(h-R3) combined with docetaxel in advanced non-small-cell lung cancer(NSCLC) patients who have failed to respond to prior first-line chemotherapy.Methods: In this single-center, open-label, dose-escalating phase I trial, patients with epidermal growth factor receptor(EGFR)-expressing stage IV NSCLC were treated with nimotuzumab plus docetaxel according to a dose escalation schedule. The safety and efficacy of the combination treatment were observed and analyzed.Results: There were 12 patients with EGFR-expressing stage IV NSCLC enrolled. The dose of nimotuzumab was escalated from 200 to 600 mg/week. The longest administration of study drug was 40 weeks at the 600 mg/week dose level. Grade III–IV toxicities included neutropenia and fatigue, and other toxicities included rash. Dose-limiting toxicity occurred with Grade 3 fatigue at the 200 mg dose level of nimotuzumab and Grade 4 neutropenia with pneumonia at the 600 mg dose level of nimotuzumab. No objective responses were observed, and stable disease was observed in eight patients(66.7%). The median progression-free survival(PFS) was 4.4 months in all patients, 1.3 months in patients with the EGFR mutation, and 4.4 months in those with wild type EGFR(EGFR WT). The median survival time(MST) was 21.1 months in all patients, 21.1 months in patients with EGFR mutation, and 26.4 months in patients with EGFR WT.Conclusions: Nimotuzumab and docetaxel combination therapy was found to be well tolerated and efficacious. Further study of nimotuzumab is warranted in advanced NSCLC patients. | Jun Zhao Minglei Zhuo Zhijie Wang Jianchun Duan Yuyan Wang Shuhang Wang Tongtong An Meina Wu Jie Wang | 2016 | Chinese Journal of Cancer Research2016,28,1: | 3 |
| 3 | Clinical outcomes of atezolizumab in combination with etoposide/platinum for treatment of extensive-stage small-cell lung cancer:A real-world,multicenter,retrospective,controlled study in China显示文摘Objective:Atezolizumab along with chemotherapy has prolonged the survival of patients with extensive-stage small-cell lung cancer(ES-SCLC)worldwide,although real-world(RW)data are lacking in China.This study was designed to evaluate the efficacy and clinical outcomes of atezolizumab plus etoposide/platinum(EP).Methods:Data obtained in this retrospective study were captured from six oncology units of five medical facilities from January 2019 to April 2022.For first-line treatments,atezolizumab combined with EP vs.EP alone,we primarily evaluated progression-free survival(PFS);other efficacy indicators,including overall survival(OS),objective response rate(ORR),and patterns of SCLC progression and adverse events(AEs)were assessed.Results:The primary analysis included data from 225 patients,of whom 133 received EP along with atezolizumab(atezolizumab group)and 92 received EP alone(EP group).The PFS duration of the atezolizumab group[7.10 months;95%confidence interval(95%CI),6.53-9.00]exceeded that of the EP group(6.50 months;95%CI,4.83-7.53).Overall,the hazard ratio(HR)was 0.69(95%CI,0.49-0.97)(P=0.029);particularly,the HR was 0.54(95%CI,0.36-0.80)among patients undergoing≥4 chemotherapy cycles and 0.33(95%CI,0.20-0.56)among individuals with atezolizumab maintenance.The ORR and disease-control rate(DCR)were similar between the two groups.Because of incomplete OS data,the median OS was not determined for either group.Bone marrow suppression was the most common AE detected(58.6%)in the atezolizumab group.Immune-related AEs occurred in 19 patients in the atezolizumab group(14.3%),with only one case of grade 3 encephalitis.Conclusions:This RW study in China demonstrated improved clinical outcomes of atezolizumab along with EP for ES-SCLC,particularly in the chemosensitive population.These results align with the results of the IMpower133 study,although the impact of this treatment modality on OS warrants additional follow-up studies. | Hanxiao Chen Xiangjuan Ma Jie Liu Yu Yang Yong Fang Liping Wang Jian Fang Jun Zhao Minglei Zhuo | 2022 | Chinese Journal of Cancer Research2022,34,4: | 1 |
| 4 | Influence of Chemotherapy on EGFR Mutation Status Among Patients With Non–Small-Cell Lung Cancer显示文摘 | Hua Bai Zhijie Wang Keneng Chen Jun Zhao J. Jack Lee Shuhang Wang Qinghua Zhou Minglei Zhuo Li Mao Tongtong An Jianchun Duan Lu Yang Meina Wu Zhen Liang Yuyan Wang Xiaozheng Kang Jie Wang | 2012 | Journal of Clinical Oncology2012,,25: | 1 |
| 5 | PLSCR1 promotes apoptosis and clearance of retinal ganglion cells in glaucoma pathogenesis显示文摘Glaucoma is the leading cause of irreversible blindness worldwide.In the pathogen-esis of glaucoma,activated microglia can lead to retinal ganglion cells(RGCs)apoptosis and death,however,the molecular mechanisms remain largely unknown.We demonstrate that phospholipid scramblase 1(PLSCR1)is a key regulator promoting RGCs apoptosis and their clearance by microglia.As evidenced in retinal progenitor cells and RGCs of the acute ocular hypertension(AOH)mouse model,overexpressed PLSCR1 induced its translocation from the nucleus to the cytoplasm and cytomembrane,as well as elevated phosphatidylserine exposure and reactive oxygen species generation with subsequent RGCs apoptosis and death.These damages were effectively attenuated by PLSCR1 inhibition.In the AOH model,PLSCR1 led to an increase in M1 type microglia activation and retinal neuroinflammation.Upregulation of PLSCR1 resulted in strongly elevated phagocytosis of apoptotic RGCs by activated microglia.Taken together,our study provides important insights linking activated microglia to RGCs death in the glaucoma pathogenesis and other RGC-related neurodegenerative diseases. | Jingyi Luo Qing Lian Deliang Zhu Minglei Zhao Tingfang Mei Bizhi Shang Zeqiu Yang Chujun Liu Wenchang Xu Lan Zhou Keling Wu Xinqi Liu Yuhua Lai Fuxiang Mao Weihua Li Chengguo Zuo Kang Zhang Mingkai Lin Yehong Zhuo Yizhi Liu Lin Lu Ling Zhao | 2023 | Genes & Diseases2023,10,4: | 0 |