Background: Glutathione peroxidase-1 (GPX1) is a member of the GPX family, which considered an enzyme that interacts with oxidative stress. GPX1 differential expression is closely correlated with carcinogenesis and disease progression. In this study, we used bioinformatics analysis to investigate GPX1 expression level and explore the prognostic information in different human cancers. Methods: Expression was analyzed via the Oncomine database and Gene Expression Profiling InteractiveAnalysis tool, and potential prognostic analysis was evaluated using the UALCAN, GEPIA, and DriverDBv3 databases. Then, the UALCAN database was used to find the promoter methylation of GPX1 in defied cancer types. While GPX1 related functional networks were found within the GeneMANIA interactive tool and Cytoscape software. Moreover, Metascape online website was used to analyze Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathways.Results: We found that GPX1 was commonly overexpressed in most human cancers. High expression of GPX1 could lead to poor outcomes in Brain Lower Grade Glioma, while GPX1 over expression was correlated with better prognosis in Kidney renal papillary cell carcinoma (KIPP). High GPX1 expression was marginally associated with poor prognosis in acute myeloid leukemia (AML). Gene regulation network suggested that GPX1 mainly involved in pathways including the glutathione metabolism, ferroptosis, TP53 regulates metabolic genes, reactive oxygen species (ROS) metabolic process, and several other signaling pathways.Conclusions: Our findings revealed that GPX1 showed significant expression differences among cancers and served as a prognostic biomarker for defined cancer types. The data mining effectively revealed useful information about GPX1 expression, prognostic values, and potential functional networks in cancers, thus providing researchers with an available way to further explore the mechanism underlying carcinogenesis of genes of interest in different cancers.
e21666 Background: Previous studies indicated primary resistance to EGFR-TKIs might occur in EGFR co-mutation with other oncogenic alterations, including TP53, KRAS, PIK3CA and so on. However, the optimal therapeutic regimens for EGFR co-mutation other oncogenic alterations were still unknown. This respective observation study aimed to evaluate the efficacy and safety of EGFR-TKIs combined with chemotherapy in this sub-population, in order to offer new treatments in clinical practice. Methods: In this retrospectively study, from March 2017 to November 2019 advanced NSCLC patients with EGFR co-mutation with other oncogenic alterations in Medical Oncology of Respiratory, Affiliated Tumor Hospital of Guangxi Medical University were screened for eligibility. All included patients were administrated with EGFR-TKIs combined with platinum-based chemotherapy or EGFR-TKIs monotherapy. The clinicopathological data of the patients, and the efficacy and safety of treatment were accorded for statistic analysis. The Kaplan-Meier method was used to estimate median PFS and OS. For all analyses, p value < 0.05 was considered statistically significant, and confidence interval use 95% confidence level. The primary outcome was Progression-free survival (PFS), and Overall survival (OS), Disease control rate (DCR) and safety profile were considered to be the secondary endpoints. Results: Total 23 patients were enrolled in this retrospectively study. The median age of the combination and monotherapy group was 58.7± 8.8 and 58.9 ± 13.5years, respectively. The frequency of female patients was 53.8% and 40% in monotherapy and combination group, respectively. The median PFS (mPFS) was 5.03 months (95% CI: 1.16- 8.9) and not reach in combination therapy group (P = 0.004). No significantly different in mOS was observed in two groups (P = 0.244). The DCR was 92.3% and 100% in monotherapy and combination group, respectively. In combination group, the common adverse events of grade 1 or 2 were adverse reactions of the blood system and rash (40%). Treatment-related grade 3 or 4 toxicity appeared in 3 patients and no patients harbored treatment-related above grade 4 side effects. No cases of treatment-related death occurred. Conclusions: EGFR-TKIs combined with chemotherapy was effective in NSLCL patients with EGFR co-mutation with other oncogenic alterations and side-effects were tolerable. The outcomes of this study should be confirmed by prospective clinical trials in future.
e21077 Background: Previous studies indicated primary resistance to EGFR-TKIs might occur in EGFR co-mutation with other oncogenic alterations. However, the optimal therapeutic regimen for advanced NSCLC with EGFR co-mutation was still unknown. This respective observation study aimed to assess the efficacy and safety of the combination therapy with EGFR-TKI and chemotherapy in this sub-population. Methods: In this retrospectively study, from March 2017 to November 2019 advanced NSCLC patients with EGFR mutation detected using next-generation sequencing targeting 59 genes were screened for eligibility. We included patients of EGFR co-mutation with other oncogenic alterations receiving EGFR-TKI monotherapy or TKI plus chemotherapy as first-line therapy. The primary outcome was objective response rate (ORR), progression-free survival (PFS), and overall survival (OS). Disease control rate (DCR) and safety profile were considered to be the secondary endpoints. Results: Total 48 patients were enrolled. Among patients with concomitant mutation, the combination of chemotherapy with TKI was found to prolong mPFS (12.5 vs 7.3 months; HR, 0.38; 95%CI: 0.17-0.81; P = 0.012) compared with TKI monotherapy, with a trend of longer mOS (27.0 vs 22.4 months; HR, 0.40; 95%CI: 0.15-1.05; P = 0.062) and higher ORR (68.4% vs 44.8%, P = 0.113). The DCR were 100% in combination group and 93.1% in monotherapy group (P = 0.99). A proportion of 13.8% patients reported grade≥3 treatment-related adverse events in monotherapy group and 36.8% in combination group. Conclusions: EGFR co-mutation with other oncogenic alterations associated with poor treatment outcome with EGFR-TKI monotherapy. The combination of EGFR-TKI and chemotherapy was effective in this sub-population and side-effects were tolerable. The outcomes of this study should be confirmed by prospective clinical trials in future.
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