Nickel carbonate Hydroxide-based Core-Triple-Shelled nanofibers with ultrahigh specific capacity for flexible hybrid supercapacitors.

Designing novel efficient electrode materials with controlled hierarchical structure and composition for advanced supercapacitors remains a great challenge. Herein, a core-triple-shelled hierarchical GCNF/PANI/NCO nanostructure has been designed and fabricated by sequential growth of the conductive polyaniline (PANI) layers and nickel carbonate hydroxide (Ni2(CO3)(OH)2) nanosheets on the graphene-coated electrospun carbon nanofibers (GCNF) via a facile wet-chemical strategy. Taking full advantage of the free-standing architecture of graphene-coated electrospun carbon nanofibers, high conductivity and flexibility of the PANI layers, and abundant active sites of Ni2(CO3)(OH)2 nanosheets, the optimal GCNF/PANI/NCO (2 h) electrode exhibits a high specific capacitance of 1565F g-1 at 1 A/g and enhanced rate capability, which are higher than those of the GCNF, GCNF/PANI, and GCNF/NCO (2 h) electrodes at the same situation, and also exceeds most of the reported nickel carbonate hydroxide-based electrodes in literature. The superior performance should be mainly ascribed to the collaborative contribution of each component. Moreover, a self-assembled GCNF/PANI/NCO//AC hybrid supercapacitor delivers a high energy density of 35.4 Wh kg-1@750 W kg-1 and a long cycle lifespan. This strategy enables the controllable synthesis of core-triple-shelled hierarchical materials applicable to advanced electrochemical applications.

Heterogeneous cobalt polysulfide leaf-like array/carbon nanofiber composites derived from zeolite imidazole framework for advanced asymmetric supercapacitors.

Developing new electrode materials is one of the keys to improving the energy density of supercapacitors. In this article, a novel cobalt polysulfide/carbon nanofibers (C,N-CoxSy/CNF) film derived from zeolitic imidazolate framework is first prepared by a facile strategy. The composite material with two-dimensional leaf-shaped nanoarray neatly grown on the surface of carbon nanofibers is composed of CoS, CoS2, Co9S8, N-doped carbon nanosheets, and carbon nanofibers. It is found that the composite can not only increase the contact area with the electrolyte but also provide abundant redox-active sites and a Faraday capacitance for the entire electrode. The C,N-CoxSy/CNF composite exhibits excellent electrochemical properties, including a high capacity of up to 1080F g -1 at 1 A g -1 and a good rate capability (80.4 % from 1 A g -1 to 10 A g -1). A C,N-CoxSy/CNF//AC asymmetric supercapacitor device is assembled using C,N-CoxSy/CNF as the positive electrode and activated carbon as the negative electrode, showing high energy density (37.29 Wh kg -1@813.6 W kg -1) and good cycle stability (90.5% of initial specific capacitance at 10 g-1 after 5000 cycles). This C,N-CoxSy/CNF composite material may also be used as a potential electrode for future lithium-ion batteries, zinc-ion batteries, lithium-sulfur batteries, etc.

Brain Metastases Status and Immunotherapy Efficacy in Advanced Lung Cancer: A Systematic Review and Meta-Analysis.

Background: Brain metastases (BMs) indicate poor outcomes and are commonly excluded in immunotherapy clinical trials in advanced lung cancer; moreover, the effect of BM status on immunotherapy efficacy is inconsistent and inconclusive. Therefore, we conducted a meta-analysis to assess the influence of BM status on immunotherapy efficacy in advanced lung cancer. Methods: Electronic databases and all major conference proceedings were searched without language restrictions according to the Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines. We extracted randomized clinical trials on lung cancer immunotherapy that had available overall survival (OS) and/or progression-free survival (PFS) data based on the BM status. All analyses were performed using random effects models. Results: Fourteen randomized clinical trials with 9,089 patients were identified. Immunotherapy conferred a survival advantage to BM patients [OS-hazard ratio (HR), 0.72; 95% confidence interval (CI), 0.58-0.90; P = 0.004; and PFS-HR, 0.68; 95% CI, 0.52-0.87, P = 0.003]. Non-BM patients could also derive a survival benefit from immunotherapy (OS-HR, 0.76; 95% CI, 0.71-0.80; P <0.001; and PFS-HR, 0.68; 95% CI, 0.56-0.82, P <0.001). The pooled ratios of OS-HRs and PFS-HRs reported in BM patients versus non-BM patients were 0.96 (95% CI, 0.78-1.18; P = 0.72) and 0.97 (95% CI, 0.79-1.20; P = 0.78), respectively, indicating no statistically significant difference between them. Subsequent sensitivity analyses did not alter the results. Subgroup analyses according to tumor type, line of therapy, immunotherapy type, study design, and representation of BM patients reconfirmed these findings. Conclusion: We demonstrated that BM status did not significantly influence the immunotherapy efficacy in lung cancer, suggesting that both BM and non-BM patients could obtain comparable benefits. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, identifier (CRD42020207446).

CDCA2 protects against oxidative stress by promoting BRCA1-NRF2 signaling in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) patients mostly suffer from poor survival outcomes. It is necessary to identify effective therapeutic targets to improve prognosis for HCC patients. Here, we report a new factor, CDCA2, in promoting HCC development. CDCA2 amplification is an independent risk factor for the recurrence and survival of HCC patients, which is positively correlated with elevated level of alpha-fetoprotein (AFP), high histological grade, large tumor size, advanced TNM stage, and poor prognosis for HCC patients. In HCC cells, CDCA2 promotes cell growth and inhibits apoptosis. Mechanistically, CDCA2's transcription is activated through the binding of E2F2/E2F8 with its promoter. CDCA2 depletion contributes to the suppression of cell proliferation and induction of apoptosis due to reactive oxygen species (ROS)-mediated stress, which can be reversed by antioxidants N-acetyl cysteine (NAC) and glutathione (GSH). Interestingly, we found that CDCA2 triggers the BRCA1-NRF2 cascade, which elevates antioxidant response and attenuates ROS levels. In response to oxidative stress, CDCA2 promotes BRCA1's chromatin relocalization to NRF2, activating NRF2-driven downstream signaling (HO-1, TXNRD1, and NQO1), which then protects HCC cells against oxidative damage. In conclusion, our results reveal that CDCA2 is a prognostic biomarker for HCC patients, and present the E2F2/E2F8-CDCA2-BRCA1-NRF2-ROS signaling axis that have implications for HCC therapeutics.

Development of high performance alpha-Co(OH)2/reduced graphene oxide microfilm for flexible in-sandwich and planar micro-supercapacitors.

Herein, a series of alpha-Co(OH)2/reduced graphene oxide (rGO) microfilms and film-based nanodevices were developed via a new scalable technique. Due to the unique hexagonal nanoplates of ultrathin alpha-Co(OH)2 and the intrinsically conductive nature of rGO sheets, such thin films not only can improve the conductivity of alpha-Co(OH)2 and prevent the re-stacking of alpha-Co(OH)2 and rGO sheets but also short the transport routes of electrons and ions between the electrode and the electrolyte. The optimized alpha-Co(OH)2/rGO flexible electrode presents high specific capacitance (273.86 mF/cm2 at 0.1 mA/cm2), advanced rate capability, and excellent coulombic efficiency. Simultaneously, in-sandwich symmetric and asymmetric supercapacitors assembled with polyvinyl alcohol-KOH gel as the solid-state electrolyte achieved high areal and volumetric specific capacitances. Furthermore, a self-assembled planar alpha-Co(OH)2/rGO micro-supercapacitor (MSC) delivers high specific area capacitance (130F/cm2 at 0.5 mA/cm2) and excellent energy density (20 mWh/cm3@56 mW/cm3), which are superior to most of the recently reported carbon-based and metal hydroxides/oxides/sulfides-based planar MSCs. Also, our planar MSC shows excellent cycling performance, good flexibility, and mechanical stability. This work promotes the syntheses of other two-dimensional metal hydroxides/rGO composite film for high-performance flexible micro-electronics.

Association of menopausal status with COVID-19 outcomes: a propensity score matching analysis.

BACKGROUND: Despite the growing number of studies on the coronavirus disease-19 (COVID-19), little is known about the association of menopausal status with COVID-19 outcomes. MATERIALS AND METHODS: In this retrospective study, we included 336 COVID-19 inpatients between February 15, 2020 and April 30, 2020 at the Taikang Tongji Hospital (Wuhan), China. Electronic medical records including patient demographics, laboratory results, and chest computed tomography (CT) images were reviewed. RESULTS: In total, 300 patients with complete clinical outcomes were included for analysis. The mean age was 65.3 years, and most patients were women (n = 167, 55.7%). Over 50% of patients presented with comorbidities, with hypertension (63.5%) being the most common comorbidity. After propensity score matching, results showed that men had significantly higher odds than premenopausal women for developing severe disease type (23.7% vs. 0%, OR 17.12, 95% CI 1.00-293.60; p = 0.003) and bilateral lung infiltration (86.1% vs. 64.7%, OR 3.39, 95% CI 1.08-10.64; p = 0.04), but not for mortality (2.0% vs. 0%, OR 0.88, 95% CI 0.04-19.12, p = 1.00). However, non-significant difference was observed among men and postmenopausal women in the percentage of severe disease type (32.7% vs. 41.7%, OR 0.68, 95% CI 0.37-1.24, p = 0.21), bilateral lung infiltration (86.1% vs. 91.7%, OR 0.56, 95% CI 0.22-1.47, p = 0.24), and mortality (2.0% vs. 6.0%, OR 0.32, 95% CI 0.06-1.69, p = 0.25). CONCLUSIONS: Men had higher disease severity than premenopausal women, while the differences disappeared between postmenopausal women and men. These findings support aggressive treatment for the poor prognosis of postmenopausal women in clinical practice.

Safety and efficacy of aprepitant as mono and combination therapy for the prevention of emetogenic chemotherapy-induced nausea and vomiting: post-marketing surveillance in China.

BACKGROUND: The goal of this study was to evaluate aprepitant usage in the context of routine clinical practice with dose/regimens at the discretion of prescribers for chemotherapy-induced nausea and vomiting (CINV) treatments. METHODS: In this single arm, multicenter prospective study 1,000 patients with solid malignancies were enrolled across 21 centers in China. The primary endpoint was the rate of adverse events (AEs), including drug related AEs and serious AEs (SAEs). Secondary efficacy endpoints included the proportion of patients achieving complete response (CR; no vomiting, no nausea, and no use of rescue medication) within 120 h after highly emetogenic chemotherapy, the rates of no nausea and no vomiting, as well as quality of life (QoL). Multivariable logistic regression analysis was carried out to determine factors associated with the overall (0-120 h), acute (0-24 h) and delayed (25-120 h) CR. RESULTS: Of the 1,000 highly emetogenic chemotherapy treated patients enrolled in the study ≥1 AE, ≥1 drug related AE, ≥1 SAE and drug related SAE rates in 998 patients were 45.9%, 2.5%, 4.0% and 0.1%, respectively. Approximately half of the patients (455/990, 46.0%) received aprepitant as part of a 3-drug anti-CINV regimen consistent with prescribing guidelines. The overall CR (0 to 120 h) for anti-emetic drug use was 41.0%, with an acute CR of 66.0% and a delayed CR of 46.5%. The rates of no vomiting and no nausea after solely aprepitant anti-emetic therapy from 0 to 120 h were 70.9% and 43.0%, for dual anti-emetic therapy 86.9% and 64.6%, and for triple therapy 86.4% and 69.5%, respectively. Multivariate regression analysis revealed that triple anti-emetic therapy (P=0.038), male gender (P<0.001) and a history of chemotherapy (P=0.016) were significantly associated with the overall acute CR. CONCLUSIONS: Especially as a combination treatment, aprepitant is safe and efficient for preventing CINV in patients receiving highly emetogenic chemotherapy.

Epidermal growth factor receptor gene mutations in non-small-cell lung cancer cells are associated with increased radiosensitivity in vitro.

INTRODUCTION: There is still lack of specific biomarkers in predicting the radiosensitivity of non-small cell lung cancer (NSCLC) patients in clinic. Previous studies have shown that the EGFR gene status may correlate with radiosensitivity of NSCLC. However, the underlying mechanisms remain unknown. The aim of this study was to further investigate the correlation between EGFR mutation status and the NSCLC cell radiosensitivity and to explore the possible cellular mechanism. METHODS: Eight NSCLC cell lines with different EGFR gene status were irradiated by linear accelerator, and the radiosensitivity between the cell lines was compared by cell colony formation assay and cell proliferation assay. Cell cycle and apoptosis were analysed by flow cytometry. Radiosensitivity-related protein expression was detected by Western blotting. RESULTS: In the present study, we found that NSCLC cell lines with the epidermal growth factor receptor (EGFR) gene mutations were more sensitive to X-ray irradiation than those with wild-type EGFR (P<0.05). No difference in radiosensitivity was observed between NSCLC cells with EGFR exon19 deletion (Del 19) mutation and exon 21 point mutation at position 858 (L858R) with or without T790M mutation (P<0.05), as well as between NSCLC cells with EGFR mutation and those with acquired EGFR-tyrosine kinase inhibitors (TKIs) resistance. Mechanistically, EGFR mutations promoted NSCLC cell apoptosis in response to X-ray irradiation through the upregulation of proapoptotic protein Bax and downregulation of anti-apoptotic proteins such as Bcl-2 and DNA-dependent protein kinase catalytic subunit. In addition, phosphorylated histone (γ-H2AX) foci assay showed that EGFR mutations sustained irradiation-induced DNA damage. CONCLUSION: Taken together, our study demonstrates that EGFR mutations are closely associated with the increased sensitivity of NSCLC cell lines to X-ray irradiation and that EGFR mutation status is a potentially useful indicator to evaluate the effectiveness of radiotherapy in the treatment of NSCLC.

Predictive value of excision repair cross-complementation group 1 protein in locoregionally advanced nasopharyngeal carcinomas receiving cisplatin-based concurrent chemoradiotherapy.

OBJECTIVE: To investigate the ability of excision repair cross-complementation group 1 (ERCC1) protein to predict cisplatin-based concurrent chemoradiotherapy (CCRT) response in locoregionally advanced nasopharyngeal carcinoma (NPC). MATERIALS AND METHODS: The clinical data of 205 patients with locoregionally advanced NPC, who received cisplatin-based CCRT, were analyzed retrospectively. Immunohistochemical analysis was used to assess the ERCC1 expression in nasopharyngeal tumor tissues. Receiver operating characteristic (ROC) curve analysis, univariate and multivariate Cox proportional hazards analyses were performed to evaluate the association between ERCC1 expression and failure-free survival (FFS), overall survival (OS), locoregional-FFS (L-FFS), and distant-FFS (D-FFS). RESULTS: Our results revealed that although the overall response rate in patients with high-ERCC1 expression (97.3%) and those with low-ERCC1 expression (100.0%) were not statistically different, but treatment-sensitive group displayed significantly lower ERCC1 expression in comparison to the treatment-resistant group (P = 0.001). The Kaplan-Meier plots revealed that the low-ERCC1 expression was significantly associated with better L-FFS, FFS, and OS of locally advanced NPC patients receiving cisplatin-based CCRT. Both univariate and multivariate analysis demonstrated that the ERCC1 expression, tumor node metastasis stage and performance status were independent predictors of OS and FFS. CONCLUSION: ERCC1 expression may be a useful predictive marker in patients with locoregionally advanced NPC, who are receiving cisplatin-based CCRT.

Predictive value of excision repair cross- complementation group 1 expression in locoregionally advanced nasopharyngeal carcinoma receiving cisplatin-based concurrent chemoradiotherapy.

BACKGROUND: Cisplatin-based concurrent chemoradiotherapy is recommended for nasopharyngeal carcinoma (NPC) at advanced stages. Excision repair cross-complementation group 1 (ERCC1) plays an important function in the repair of DNA damage that is a critical process of chemo- and radiotherapy. OBJECTIVE: This study aimed to investigate the clinical significance of ERCC1 expression in NPC treated with cisplatin-based concurrent chemoradiotherapy in locoregionally advanced NPC. METHODS: The expression level of ERCC1 and its association with clinicopathological characteristics in 205 locoregionally advanced NPC patients receiving cisplatin-based concurrent chemoradiotherapy were analyzed retrospectively. RESULTS: The correlation analysis revealed that the treatment-sensitive patients displayed dramatically lower ERCC1 expression than treatment-resistant cases did. Furthermore, the Kaplan-Meier plots revealed lower ERCC1 expression was significantly associated with better survival. Multivariate analysis further showed that the ERCC1 expression was an independent predictor of NPC patients' survival. CONCLUSIONS: ERCC1 expression might be a useful predictive marker in patients with locoregionally advanced NPC receiving cisplatin-based concurrent chemoradiotherapy.

Sensitivity to chemotherapeutics of NSCLC cells with acquired resistance to EGFR-TKIs is mediated by T790M mutation or epithelial-mesenchymal transition.

Chemotherapy is one of the methods to treat patients with non-small cell lung cancer (NSCLC) developing resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), such as gefitinib. Previous studies revealed that the sensitivity to chemotherapy may depend on different cellular mechanisms of acquired EGFR-TKIs resistance. Thus, the present study aimed to investigate the sensitivity of distinct gefitinib-resistant NSCLC cell lines to chemotherapy in order to help select effective treatment regimens for patients with EGFR-TKI resistance. In the present study, we established two gefitinib-resistant cell lines (PC-9/ZD and PC-9/GR) with the human lung adenocarcinoma cell line PC-9 (carrying the delE746-A750 mutation in the EGFR gene). PC-9/ZD cell line expressed the T790M mutation, while PC-9/GR presented the phenotypes of epithelial to mesenchymal transition (EMT). PC-9/ZD cells were more sensitive to paclitaxel and docetaxel than PC-9 cells and knockdown of T790M decreased this sensitivity. In addition, PC-9/GR cells were less sensitive to chemotherapeutic drugs tested, including cisplatin, gemcitabine, pemetrexed, paclitaxel and docetaxel, compared to PC-9 and PC-9/ZD cells. CDH1 transfection reversed the EMT and restored the sensitivity to chemotherapy in PC-9/GR cells. Furthermore, PC-9 cells became resistant to chemotherapy after TGF-ß1-induced EMT. The EMT in NSCLC cells significantly increased cancer stem cell (CSC) properties and tumorgenicity. Collectively, the present study revealed that gefitinib-resistant NSCLC cells carrying the T790M mutation were sensitive to taxane chemotherapy, indicating that T790M is a useful biomarker for the selection of chemotherapy. EMT in NSCLC cells confers resistance to chemotherapy, which may be associated with enhanced CSC properties.

Implication of epithelial-mesenchymal transition in IGF1R-induced resistance to EGFR-TKIs in advanced non-small cell lung cancer.

The underlying mechanisms for acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) in about 30%-40% of non-small cell lung cancer (NSCLC) patients remain elusive. Recent studies have suggested that activation of epithelial-mesenchymal transition (EMT) and type 1 insulin-like growth factor receptor (IGF1R) is associated with acquired EGFR-TKIs resistance in NSCLC. Our study aims to further explore the mechanism of EMT and IGF1R in acquired EGFR-TKIs resistance in NSCLC cell lines with mutant (PC-9) or wild-type EGFR (H460). Compared to parental cells, EGFR-TKIs-resistant PC-9/GR and H460/ER cells displayed an EMT phenotype and showed overexpression of IGF1R. SiIGF1R in PC-9/GR and H460/ER cells reversed EMT-related morphologies and reversed their resistance to EGFR-TKIs. Exogenous IGF-1 alone induced EMT in EGFR-TKIs-naïve PC-9 and H460 cells and increased their resistance against EGFR-TKIs. Inducing EMT by TGF-ß1 in PC-9 and H460 cells decreased their sensitivity to EGFR-TKIs, whereas reversing EMT by E-cadherin overexpression in PC-9/GR and H460/ER cells restored their sensitivity to EGFR-TKIs. These data suggest that IGF1R plays an important role in acquired drug resistance against EGFR-TKIs by inducing EMT. Targeting IGF1R and EMT may be a potential therapeutic strategy for advanced NSCLC with acquired EGFR-TKIs resistance.

Sequence-dependent antiproliferative effects of gefitinib and docetaxel on non-small cell lung cancer (NSCLC) cells and the possible mechanism.

PURPOSE: Recent clinical trials showed that the sequential combination of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) and chemotherapy could prolong the PFS and/or OS of advanced non-small cell lung cancer (NSCLC) patients with EGFR mutation. The aim of present study was to assess the optimal combination sequence and to explore its possible mechanism. METHODS: PC-9 cells and A549 cells, the lung adenocarcinoma cells with mutant and wide-type EGFR respectively, were treated with docetaxel/gefitinib alone or in different combination schedules. The EGFR and K-ras gene status was determined by qPCR-HRM technique. Cell proliferation was detected by MTT assay. The expression and phosphorylation of EGFR, ERK, Akt and IGF-1R were detected by western blot. Cell cycle distribution was observed by flow cytometry. RESULTS: Only sequential administration of docetaxel followed by gefitinib (D → G) induced significant synergistic effect in both cell lines (Combination Index<0.9). The reverse sequence (G → D) resulted in an antagonistic interaction in both cell lines (CI>1.1), whereas the concurrent administration (D+G) showed additive (0.9

Metastatic nasopharyngeal carcinoma outcomes in patients on cisplatin with nolatrexed or 5-fluorouracil.

BACKGROUND: Nasopharyngeal carcinoma (NPC) is one of the most common malignant tumors in southern China. In this study, we compared the clinical efficacy and toxicity of cisplatin with nolatrexed (LP) or 5-fluorouracil (FP) for NPC. PATIENTS AND METHODS: 33 patients with metastatic NPC were randomized to the LP and FP regimens. The LP regimen consisted of continuous intravenous infusions of 740 mg/m(2) nolatrexed on days 1-5 and 25 mg/m(2) intravenous cisplatin on days 2-4. The FP regimen consisted of continuous intravenous infusions of 600 mg/m(2) 5-fluorouracil on days 1-5 and 25 mg/m(2) intravenous cisplatin on days 2-4. Cycles were repeated every 3 weeks until disease progression or completion of a total of 6 courses. RESULTS: There were no significant differences in the response rates (RR), disease control rates (DCR), times to progression (TTP), and median survival times (MST) between the regimens. The toxicities of the two regimens were mostly grade I/II, but the stomatitis incidence in the patients on the LP regimen was significantly lower than that on the FP regimen. CONCLUSIONS: The efficacy of the LP regimen was similar to that of the FP regimen. The LP regimen had lower toxicity.

Estrogen decreases anoikis of ovarian cancer cell line Caov-3 through reducing release of Bit1.

Few studies have referred to the implication of anoikis processes following hormonal treatment. No data are available on the influence of estrogen in ovarian cancer anoikis. To gain insights into the effects and mechanism of estrogen in ovarian cancer cells, we have carried out studies on the anoikis of ovarian cancer cells treated with estrogen and on the pathways involved. We observed an anti-anoikis role of E2 in suspended Caov-3 cells, and this was mainly due to the decreasing of Bit1 level in cytosol. We also found that estrogen receptor α (ERα) was the main mediator involved in this process. To study the signaling pathways well, phosphatidylinositol 3-kinase (PI3K)/AKT were further investigated. Results demonstrated that the decreasing of the Bit1 level in cytosol mediated by E2 binding to ERα was mainly through PI3K/AKT pathways. Overall, these findings disclose a new perspective for estrogen on ovarian cancer therapy.

The role of epithelial-mesenchymal transition and IGF-1R expression in prediction of gefitinib activity as the second-line treatment for advanced nonsmall-cell lung cancer.

OBJECTIVE: Except for EGFR gene mutation, there is still lack of predictive factors for gefitinib activity as the second-line treatments for advanced NSCLC with wild-type (WT) EGFR or patients with mutant EGFR but showed poor response. Our purpose was to assess the predictive value of epithelial-mesenchymal transition (EMT) and IGF-1R for gefitinib efficacy as the second-line treatment for NSCLC. METHODS: 53 advanced NSCLC patients who accepted gefitinib as the second-line treatment were enrolled in this study. Expression of E-cadherin, vimentin, and IGF-1R was determined by immunohistochemistry. EGFR gene mutation was determined by liquidchip technique. RESULTS: The positive rate of EMT, IGF-1R, and EGFR gene mutation was 54.7%, 58.5%, and 39.6%, respectively. EMT (-) was positively correlated with EGFR gene mutation (p = .034) and EMT (+) was associated with IGF-1R (+) (p = .000). EMT (-) was associated with a significantly higher objective response rate (ORR) for all the 53 patients (41.7% vs. 6.9%, p = .024) and showed a higher ORR tendency than EMT (+) in EGFR mutation patients (50.0% vs. 28.6%) and WT EGFR patients (20.0% vs. 4.5%) (p > .05). EMT (-) showed a significant longer median survival time (MST) than EMT (+) for all 53 patients (8 months vs. 4 months) and WT EGFR patients (6 months vs. 3 months) (p < .05). IGF-1R (-) showed a higher ORR tendency than IGF-1R (+) in EGFR mutation patients (54% vs. 30%) and WT EGFR patients (18.2% vs. 4.8%) (p > .05). CONCLUSION: EMT is correlated with efficacy of gefitinib as the second-line treatment for NSCLC, and combined detection of EMT and IGF-1R may be used as new predictors besides EGFR mutation, especially for patients with WT EGFR.

[Analysis of responses and prognostic factors in different chemotherapy regimens for metastatic nasopharyngeal carcinoma: a report of 171 cases].

OBJECTIVE: The aim of this study was to compare the results of different combined chemotherapy regimens and to find the best regimen for metastatic nasopharyngeal carcinoma (NPC), and determine its prognostic factors. METHODS: The clinical data of 171 patients with pathologically proven metastatic NPC were retrospectively analyzed. Of them, 26 were treated with best support care (BSC group), 92 with platinum-based regimen of two drugs (FP group: 5-Fu and cisplatin; TP group: paclitaxel and cisplatin; DP group: docetaxel and cisplatin), and 53 with platinum-based regimen of three-drugs (TFP group: FP plus paclitaxel, DFP group: FP plus doxtale). RESULTS: The response rate (RR) in the three-drug regimens was significantly higher than that in the two-drug regimen (84.9% vs. 52.2%, P = 0.000), however, grade III approximately IV myelosuppression in the three-drug regimen group was also significantly higher than that in the two-drug regimen (58.5% vs. 27.2%, P = 0.000). Among the groups treated with platinum-based combination regimens of either two drugs or three drugs, no significant differences were observed in RR (P = 0.967, P = 0.400) or median survival time (MST) (P = 0.278, P = 0.413). The MST and one-year survival rate were 4.0 months, 13.2 months and 15.0 months, 24.0%, 64.1% and 70.3% in the BSC group, two-drug group and three-drug group, respectively. The MST in the chemotherapy group was significantly longer than that in BSC group (P = 0.000). Cox multivariate regression analysis showed that Karnovsky performance scores, time to progression or chemotherapy cycles were independent prognostic factors (P < 0.05). CONCLUSION: Chemotherapy can improve the survival of metastatic NPC. Platinum-based combination regimen with two drugs is still the standard treatment. The combination regimens with three drugs can increase the RR, but no survival benefit can be achieved for its high toxicity.

[The retrospective analysis of different therapies on 150 elderly patients with advanced non-small cell lung cancer.].

BACKGROUND: There is still no standard regiment for the treatment of advanced elderly patients with non-small cell lung cancer (NSCLC). The aim of this study is to explore the best method for the advanced elderly NSCLC patients by analyzing the efficacy and toxicity of cisplatin combined chemotherapy, docetaxel chemotherapy and the best support care (BSC). METHODS: One hundred and fifty elderly NSCLC patients (>=65 years) with different treatments from March 2003 to March 2007 in our hospital were retrospectively analyzed. RESULTS: The objective response rate (ORR) was 41.2% in cisplatin combined chemotherapy, which was significantly higher than 20.0% in docetaxel chemotherapy (P <0.05). Median survival time (MST) was 10.7 months, 9.2 months and 6.3 months, and one year survival rate was 39.7%, 36.7% and 17.3%, respectively in cisplatin combined chemotherapy, docetaxel chemotherapy and the best support care. MST was significantly longer (P <0.05) and one year survival rate was significantly higher (P <0.05) in the patients with chemotherapy than that with best support care. There was no significant difference of MST and one year survival between cisplatin combined chemotherapy and docetaxel chemotherapy (P >0.05). Grade 3-4 toxicity was more serious in cisplatin combined group than that in docetaxel group (P <0.05). CONCLUSIONS: Chemotherapy can prolong the survival time in elderly NSCLC patients. Even though the ORR is higher in cisplatin combined chemotherapy than that in docetaxel chemotherapy, there was no significant difference of MST and one year survival between cisplatin combined chemotherapy and docetaxel chemotherapy (P >0.05), which may due to the more serious toxicity. Docetaxel chemotherapy should be one of the standard regiment for the elderly NSCLC patients.

[Clinical investigation of IRESSA in the treatment of patients with advanced refractory non-small cell lung cancer].

BACKGROUND: Chemotherapy is a main method for patients with advanced non-small cell lung cancer (NSCLC). NSCLC is usually a drug-resistant neoplasm. Innate or acquired drug-resis-tance contributes to the chief cause for bad effect in the treatment of patients with NSCLC. To search for a new anti-cancer drug becomes a goal of clinical oncologists. The aim of the present study is to evaluate the curative effect and side reactions of IRESSA in the treatment of patients with advanced refractory NSCLC. METHODS: The curative investigation was carried out after 100-day oral IRESSA by a dosage of 250mg/d in patients with advanced refractory NSCLC. The patients had ever experienced at least one regimen of chemotherapy. RESULTS: Totally 33 patients enrolled in this study and all were stage IV. There were 25 males and 8 females. All enrolled patients except one patient who died of severe adverse side reaction completed treatment by IRESSA. Thirty-two cases were evaluated. Complete response was obtained in 1 patient (3.1%). Partial response was seen in 11 patients (34.4%). The overall effective rate was 37.5% (12/32). The disease-control rate was 65.6% (21/32). Time to progression was 5.7 months. Overall survival time was 3.3 to 25.9 months (median survival time was 9.6 months). One-year survival rate was 28.1% (9/32). Two-year survival rate was 6.3% (2/32). The longest survivor lived for 25.9 months. The curative effect was correlated with the pathological type, in sequence of alveolar cell carcinoma, adenocarcinoma and squamous cell carcinoma. Almost all the adverse reactions were acceptable. The main adverse reactions included rash, itching of skin, arthralgia, diarrhea, anorexia, nausea, vomiting, dizziness, headache, chest distress and abdominal pain. No patients showed abnormal in liver or kidney function. No electrocardiogram abnormality was found. One patient who had chronic pulmonary fibrosis before died of respiratory failure due to severe interstitial pneumonia. CONCLUSIONS: IRESSA takes better effect on the advanced drug-resistant patients with NSCLC. So IRESSA may be accepted as third line in the treatment of advanced NSCLC and as first line in the treatment of patients with bad constitution who have no opportinities for operation, irradiation therapy or chemotherapy.