Purpose As a third-generation EGFR TKI has been taken orally, Osimertinib effectively inhibits mutant EGFR, including T790M EGFR resistance mutations. Here, we examined real-world efficacy and tolerability of Osimertinib among Chinese patients with advanced EGFR T790M-mutant NSCLC. Patients and Methods A total of 106 advanced NSCLC patients who were taking Osimertinib following disease progression after EGFR-TKIs or other treatments were retrospectively recruited in this study. The PFS and OS after Osimertinib treatment were analyzed as the primary endpoints. Results Osimertinib was used as a second line and ≥3rd line treatment in 22.6% and 77.4% of the patients, respectively. DCR and ORR were 93.4% and 57.5%, respectively. Median PFS was 12.4 12 (95% CI, 10.5–13.5) months. The PFS was 11 (8.0, 14.0) and 12 (10.3,13.7) months ( p = 0.373), in patients with and without CNS metastasis, respectively. PFS in 2nd and ≥3rd line treatment was 11 (9.0, 13.0) and 12.4 12 (8.9, 15.1) months ( p = 0.799), respectively. In patients with EGFR exon 19 deletion and exon 21 L858 mutation, the median PFS was 11 (9.2, 12.8) and 12 (9.2, 14.8) months, respectively ( p = 0.833). Median PFS in the monotherapy group and combined anti-angiogenesis group was 11 (9.9,12.1) and 14 (11.2,16.8) months, respectively. Median OS after Osimertinib initiation was 27 (19.6, 34.4) months: 15 (6.9, 23.1) and 27 (22, 32) months in patients with and without CNS metastasis (p=0.027), 27 (20.3,33.7) months and (undefined) as second line or ≥3rd line of treatment ( p = 0.421), respectively. In patients with exon 19 deletion, the median OS was not reached, and in patients with exon 21 L858 mutations, the median OS was 23 (19.1,29.9) months (p=0.027). Median OS in the monotherapy group was 27 (21.7,32.3) months, and in combined anti-angiogenesis group was not reached (p=0.68). Conclusion Osimertinib can effectively treat advanced NSCLC with T790M mutations independently of previous treatment lines.
Related studies have reported that cystatin C (Cys C), uric acid (UA) and lactate dehydrogenase (LDH) affect tumor growth and invasion; however, the correlation between them and the prognosis of patients with small-cell lung cancer (SCLC) remains unclear. The present study aimed to investigate the effects of serum Cys C, UA and LDH concentrations on the prognosis of patients with SCLC prior to initial treatment, in order to identify potential targets for determining the clinical outcome of patients with SCLC. A total of 205 patients with SCLC were enrolled in the present study, and the clinical and laboratory data were obtained from the medical records. The receiver operating characteristic curve was used to determine the optimal cutoff values of Cys C, UA and LDH, while the Kaplan-Meier method was used for survival analysis. The Cox proportional hazard model was used for univariate and multivariate analyses to identify independent prognostic factors. The optimal cutoff values for Cys C, UA and LDH were 0.775 mg/l, 296.45 µmol/l and 198.5 U/l, respectively. The survival curves demonstrated that progression-free survival (PFS) and overall survival (OS) time were shorter in patients with high levels of Cys C, UA and LDH prior to chemotherapy. Univariate and multivariate analyses indicated that LDH concentration prior to chemotherapy may be an independent prognostic factor for both PFS and OS in patients with SCLC, while Cys C concentration may be an independent prognostic factor for PFS in patients with SCLC. The concentrations of Cys C, UA and LDH prior to chemotherapy were associated with prognosis of patients with SCLC. PFS and OS time were shorter, and the prognosis was poor in patients with elevated serum levels of Cys C, UA and LDH. Taken together, the results of the present study suggest that high concentrations of LDH and Cys C prior to chemotherapy may indicate rapid disease progression, thus it is important to focus on the progression and recurrence of the disease. High LDH concentration may also indicate a shorter survival time.
In recent years, the incidence of lung cancer has been increasing, and lung cancer has become the leading cause of cancer-related death. Non-small cell lung cancer (NSCLC) accounts for 85% of all lung cancers. Platinum-containing chemotherapy is the first-line treatment for advanced patients. For patients with epidermal growth factor receptor ( EGFR ) mutation, EGFR-tyrosine kinase inhibitor (EGFR-TKI) is the best treatment choice. In studies, these patients have initially shown excellent response to EGFR-TKI treatment. However, the median progression-free survival (PFS) of NSCLC patients treated with EGFR-TKI is only 10–12 months, so the problem of drug resistance in treatment needs to be urgently solved. Clinical studies have shown that metformin and EGFR-TKI have synergistic effects in the treatment of NSCLC patients. Additionally, patients who are diagnosed with type 2 diabetes mellitus, with EGFR mutation have shown synergistic effects. This combination therapy can lead to longer PFS and overall survival (OS). This article reviews the synergistic effect of metformin and EGFR-TKI in the treatment of NSCLC.
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