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Dosimetric comparison of CT-guided iodine-125 seed stereotactic brachytherapy and stereotactic body radiation therapy in the treatment of NSCLC
Li, RR;Zhang, Y;Yuan, Y;Lin, Q;Dai, JJ;Xu, RC;Hu, XD;Han, MY
PLOS ONE 2017年 12卷11期 影响因子:3.057
CELL LUNG-CANCER; EARLY-STAGE; RADIOTHERAPY; IMPLANTS; PROSTATE
This study aimed to assess the dosimetric differences between iodine-125 seed stereotactic brachytherapy (SBT) and stereotactic body radiation therapy (SBRT) in the treatment of non-small cell lung cancer (NSCLC). An SBT plan and an SBRT plan were generated for eleven patients with T1-2 NSCLC. Prescription of the dose and fractionation (fr) for SBRT was 48Gy/4fr. The planning aim for SBT was D90 (dose delivered to 90% of the target volume)>= 120Gy. Student's paired t test was used to compare the dosimetric parameters. The SBT and SBRT plans had comparable PTV D90 (104.73 +/- 2.10Gyvs. 107.64 +/- 2.29Gy), and similar mean volume receiving 100% of the prescription dose (V100%) (91.65% vs. 92.44%, p = 0.410). The mean volume receiving 150% of the prescribed dose (V150%) for SBT was 64.71%, whereas it was 0% for SBRT. Mean heterogeneity index (HI) deviation for SBT vs. SBRT was 0.73 vs. 0.19 (p<0.0001), and the mean conformity index (CI) for SBT vs. SBRT was 0.77 vs. 0.81 (p = 0.031). The mean lung doses (MLD) in SBT were significantly lower than those in SBRT (1.952 +/- 0.713 vs. 5.618 +/- 2.009, p<0.0001). In conclusion, compared with SBRT, SBT can generate a comparable dose within PTV, while the organs at risk (OARs) only receive a very low dose. But the HI and CI in SBT were lower than in SBRT.
Subcellular localization of beta-arrestin1 and its prognostic value in lung adenocarcinoma
Li, XW;Che, KY;Wang, LG;Zhang, TH;Wang, GH;Pang, ZF;Shen, HC;Du, JJ
MEDICINE 2017年 96卷45期
NUCLEAR EXPORT SIGNAL; BETA-ARRESTINS; HIGH EXPRESSION; BREAST-CANCER; UNFAVORABLE PROGNOSIS; PROSTATE-CANCER; POOR-PROGNOSIS; P300; GROWTH; PROGRESSION
-Arrestins play important roles in cancer progression, and the subcellular localization of -arrestin1 has been receiving increasingly more attention. Intriguingly, several studies, including some of our previous work, showed that the effects of -arrestin1 on outcomes of cancer patients were controversial.Specimens were obtained from 133 patients with lung adenocarcinoma. Immunohistochemistry was used to detect the expression of -arrestin1 and p300 in the collected tissues. The Kaplan-Meier analysis and Cox proportional hazards regression were used to examine the relationship between -arrestin1 and patient survival.We found no significant association between -arrestin1 and clinicopathological variables. The Kaplan-Meier plot showed that patients with high expression of -arrestin1 (especially in the nucleus) had a poorer overall survival (OS) and shorter disease-free survival (DFS) (P=.026, P=.015). Additionally, high p300 expression also resulted in worse OS (P=.039). Following the univariate analysis, high expressions of nuclear -arrestin1 and p300 were classed as poor prognostic factors for both OS (P=.016) and DFS (P=.025).The expression of -arrestin1 in the nucleus is associated with increased malignant tendency of lung adenocarcinoma, and the predictive value of -arrestin1 may be optimized by combining information about the expression of p300 acetyltransferase.
Optimal managements of stage IIIA (N2) non-small cell lung cancer patients: a population-based survival analysis
Pang, ZF;Yang, YF;Ding, N;Huang, CC;Zhang, TH;Ni, Y;Du, JJ;Liu, Q
JOURNAL OF THORACIC DISEASE 2017年 9卷10期 页码:4046-4056
RANDOMIZED CONTROLLED-TRIAL; POSTOPERATIVE RADIOTHERAPY; INDUCTION CHEMOTHERAPY; SURGICAL RESECTION; PREOPERATIVE CHEMOTHERAPY; TNM-CLASSIFICATION; 7TH EDITION; TUMOR SIZE; PHASE-III; SURGERY
Background: This study aimed to investigate the optimal management of stage IIIA (cN2) non-small cell lung cancer (NSCLC) patients and determine potential predictive factors.;-;Methods: We extracted patients diagnosed as NSCLC stage IIIA (cN2) between 2004 and 2011 from Surveillance, Epidemiology, and End Results (SEER) database. Overall survival (OS) and lung cancer-specific survival (LCSS) were compared among patients given different clinical managements by Kaplan-Meier method. Other variables such as age, sex and tumor size were analyzed to explore the factors associated with outcomes.;-;Results: A total of 98,700 IIIA-cN2 NSCLC patients were identified from SEER database. Survival of patients treated with surgery was better than that of patients treated by radiotherapy alone (P<0.001). Radiation prior to surgery significantly improved the survival in comparison with surgery alone (P<0.001). In the subgroups of OS analysis, age > 65 (P=0.902), adenocarcinoma (P=0.279), tumor size =3 cm (P=0.170), well differentiated (P=0.360) patients, preoperative radiotherapy improved survival insignificantly compared with surgery alone.;-;Conclusions: Preoperative radiation with surgery had the most encouraging survival outcomes in stage IIIA-cN2 NSCLC patients compared with radiation or surgery alone. No significant outcome improvement was shown between postoperative radiotherapy (PORT) and surgery alone.
Perfluorodecanoic acid (PFDA) promotes gastric cell proliferation via sPLA2-IIA
Dong, TY;Peng, YP;Zhong, N;Liu, FY;Zhang, HY;Xu, MC;Liu, RT;Han, MY;Tian, XS;Jia, JH;Chang, LK;Guo, LH;Liu, SL
ONCOTARGET 2017年 8卷31期 页码:50911-50920 影响因子:5.008
NORMAL-DECANOIC ACID; PHOSPHOLIPASE A(2) ENZYMES; NEW-YORK-STATE; RAT-LIVER; SECRETORY PHOSPHOLIPASE-A2; PERFLUORINATED COMPOUNDS; PEROXISOME PROLIFERATOR; PERFLUOROOCTANOIC-ACID; PERFLUOROALKYL ACIDS; PPAR-ALPHA
The association of perfluorodecanoicacid (PFDA) with tumor promotion and associated effects is not clear. Given that PDFA is mostly consumed with food and drinking water, we evaluated the effects of PFDA on a gastric cell line. When added to cell cultures, PFDA significantly increased growth rate and colony forming ability compared with control treatment. We found that suppression of cell senescence, but not apoptosis or autophagy was associated with PFDA-induced promotion of cell amount. To determine the molecular mechanism that was involved, DNA microarray assays was used to analyze changes in gene expression in response to PFDA treatment. Data analysis demonstrated that the vascular endothelial growth factor signaling pathway had the lowest p-value, with sPLA2-IIA (pla2g2a) exhibits the most altered expression pattern within the pathway. Moreover, sPLA2-IIA and its transcription factor TCF4, known as a direct target and a binding partner of Wnt/beta-catenin signaling in gastric cells respectively, were the third and second most varied genes globally. Cells transfected with expression plasmids pENTER-tcf4 and pENTER-pla2g2a show reduced cell proliferation by more than 60% and 30% respectively. Knockdown with sPLA2-IIA siRNA provided additional evidence that sPLA2-IIA was a mediator of PFDA-induced cell senescence suppression. The results suggest for the first time that PFDA induced suppression of cell senescence through inhibition of sPLA2-IIA protein expression and might increased the proliferative capacity of an existing tumor.
Alteration of stomach microbiota compositions in the progression of gastritis induces nitric oxide in gastric cell
Dong, TY;Feng, Q;Lu, FY;Chang, LK;Zhou, XY;Han, MY;Tian, XS;Zhong, N;Liu, SL
EXPERIMENTAL AND THERAPEUTIC MEDICINE 2017年 13卷6期 页码:2793-2800
HELICOBACTER-PYLORI; COLORECTAL-CANCER; SYNTHASE; CARCINOGENESIS; EXPRESSION; LESIONS; GROWTH; CHINA; P53
Atrophic gastritis is considered to be an antecedent to intestinal metaplasia and gastric cancer. A previous study identified that Helicobacter pylori was absent at the severe atrophic gastritis stage, and alterations in the gastric microbial composition resembled those in gastric cancer. To explore the role of the bacteria absence of H. pylori in gastric carcinogenesis, in the current study, we compared the microbiota of clinically collected H. pylori-free gastric fluids from 30 patients with non-atrophic gastritis (N) and 22 patients with severe atrophic gastritis (S). We estimated the bacterial loads in the N and S groups by colony counting in culture agar as well as by measuring the concentration of the extracted DNA. The results showed a significant increase in bacterial load in patients with atrophic gastritis in comparison to non-atrophic gastritis. Then, we analyzed the microbial communities of the gastric fluids from all 52 patients using high-throughput sequencing of 16S rRNA amplicons. The Chao 1, Shannon and Simpson diversity indexes demonstrated that the bacterial richness and diversity were not significantly different between the N and S groups. Moreover, principal component analysis illustrated that the microbiomes from the S group were more scattered. Microbiota composition analysis showed that the entire dataset was clustered into 27 phyla, 61 classes, 106 orders, 177 families, 292 genera and 121 species. At the genus level, only the abundance of Prevotella was significantly different between the N and S groups. Further analysis showed that all the higher taxonomic categories were significantly different between the N and S groups. To assess the effects of the metabolic products of Prevotella spp. on gastric cell physiology, we treated the human gastric epithelial cell line AGS with acetic acid and monitored nitric oxide (NO) production. The results showed that acetic acid at low concentrations (0.5 and 5 mu M) significantly inhibited AGS cells to secrete NO compared to phosphate buffer saline-treated control cells. These results suggest that the microbiota in non-atrophic gastritis may influence gastric epithelial cell physiology.
Diagnostic and prognostic value of blood samples for KRAS mutation identification in lung cancer: a meta-analysis
Shen, HC;Che, KY;Cong, L;Dong, W;Zhang, TH;Liu, Q;Du, JJ
ONCOTARGET 2017年 8卷22期 页码:36812-36823 影响因子:5.008
CIRCULATING TUMOR DNA; GROWTH-FACTOR RECEPTOR; K-RAS MUTATIONS; CELL-FREE DNA; SIGNALING PATHWAY; ONCOLOGY-GROUP; EGFR-TKIS; PHASE-III; CHEMOTHERAPY; THERAPY
Circulating tumor DNA (ctDNA) and tumor cells (CTC) are novel approaches for identifying genomic alterations. Thus, we designed a meta-analysis to evaluate the diagnostic value and prognostic significance of a KRAS proto-oncogene, GTPase (KRAS) mutation for lung cancer patients. All included articles were from PubMed, EMBASE, Web of Science and Cochrane Library. Twelve articles that described 1,131 patients were reviewed. True positives (TP), false positives (FP), true negatives (TN), and false negatives (FN) were used to calculate pooled sensitivity, specificity, the positive likelihood ratio (PLR), the negative likelihood ratio (NLR), a diagnostic odds ratio (DOR), the area under the curve (AUC) and corresponding 95% confidence intervals (95% CI). PLR is calculated as sensitivity/(1-specificity) and NLR is (1sensitivity)/specificity. DOR is a measured of diagnostic effectiveness (PLR/NLR). A survival analysis subgroup was also designed to evaluate prognostic significance. Pooled sensitivity, specificity, PLR, NLR, DOR and AUC were 0.79 (95% CI, 0.63-0.89), 0.93 (95% CI, 0.89-0.96), 12.13 (92% CI, 7.11-20.67), 0.22 (95% CI, 0.12-0.41), 54.82 (95% CI, 23.11-130.09), and 0.95 (95% CI, 0.93-0.96), respectively. KRAS mutation and wild-type hazard ratios for overall survival and progression-free survival were 1.37 (95% CI, 1.08-1.66), 1.46 (95% CI, 1.15-1.77) in blood samples, and 1.16 (95% CI, 1.03-1.28), 1.28 (95% CI, 1.09-1.46) in tumor tissue.
Update of IGF-1 receptor inhibitor (ganitumab, dalotuzumab, cixutumumab, teprotumumab and figitumumab) effects on cancer therapy
Qu, X;Wu, ZA;Dong, W;Zhang, TH;Wang, LG;Pang, ZF;Ma, W;Du, JJ
ONCOTARGET 2017年 8卷17期 页码:29501-29518 影响因子:5.008
METASTATIC COLORECTAL-CANCER; CELL LUNG-CANCER; GROWTH-FACTOR RECEPTOR; PLACEBO-CONTROLLED PHASE-2; FACTOR-I RECEPTOR; OPEN-LABEL; MONOCLONAL-ANTIBODIES; PANCREATIC-CANCER; DOUBLE-BLIND; III TRIAL
Background: Prognostic studies of insulin-like growth factor-1 receptor( IGF-1R) inhibitors in cancer therapy had promising results in infratests, which exhibited that IGF-1R signalling was crucial in cancer cells growth. However, the conclusion of later clinical trials revealed a dim future for IGF-1R inhibitors to treat cancer. We conducted this analysis to figure out how IGF-1R inhibitors acted in clinical cancer therapy. Material and Methods: We searched up-to-date studies about the single agent of IGF-1R inhibitors or combination with other therapies in solid tumor. Five IGF-1R anti-agents were involved. The primary endpoint was progression- free survival (PFS). The secondary endpoint was overall survival (OS). Result: 17studies were enrolled. The results was not significant in overall survival (I-2= 37.1%, P= 0.080, HR=1.08, 95% CI= 0.97-1.21) and in progression- free survival (I-2= 0.0%, P= 0.637, HR= 1.05, 95% CI= 0.98-1.12). OS for dalotuzumab, breast cancer, colorectal cancer, and PFS for prostate cancer even indicated harmful effects. Conclusion: So far, anti-IGF-1R mono-antibodies did not make significant differences in solid tumor prognosis. On the contrary, pessimistic effects were shown in the dalotuzumab, breast cancer, colorectal cancer and prostate cancer subgroups. Further studies of IGF-1R anti-agents were needed, but unwarranted in unselected patients by predictive biomarkers.
Perfluorodecanoic acid stimulates NLRP3 inflammasome assembly in gastric cells
Zhou, XY;Dong, TY;Fan, ZY;Peng, YP;Zhou, RB;Wang, XQ;Song, N;Han, MY;Fan, BB;Jia, JH;Liu, SL
SCIENTIFIC REPORTS 2017年 7卷
ALPHA-DEPENDENT APOPTOSIS; KAPPA-B ACTIVATION; NEW-YORK-STATE; PERFLUOROOCTANESULFONATE PFOS; PERFLUORINATED COMPOUNDS; SERUM CONCENTRATIONS; BLOOD-DONORS; CANCER; EXPOSURE; INHIBITOR
Perfluorodecanoic acid (PFDA), a perfluorinated carboxylic acid, presents in the environment and accumulates in human blood and organs, but its association with tumor promotion are not clear. Given that inflammation plays a significant role in the development of gastric malignancies, we evaluated the effects of PFDA on activation of the inflammasome and inflammation regulation in the gastric cell line AGS. When added to cell cultures, PFDA significantly stimulated IL-1 beta and IL18 secretion and their mRNA levels compared with control cells. By RT-PCR and western-blot we found that up-regulation of NLRP3 were associated with promotion of IL-1 beta and IL-18 production. Then expression variation of cIAP1/ 2, c-Rel and p52 were analyzed, the results demonstrated raised mRNA expression in all the tested genes concomitant with enhanced inflammasome activity after exposure to PFDA. Assays with cIAP2 siRNA and NF kappa B reporter provided additional evidence that these genes were involved in PFDA-induced inflammasome assembly. Furthermore, increased secretion of IL-1 beta and IL-18 were detected in stomach of PFDA-treated mice, disorganized alignment of epithelial cells and inflammatory cell infiltration were also observed in the stomach tissues upon PFDA treatment. This study reports for the first time that PFDA regulates inflammasome assembly in human cells and mice tissues.
Prognostic effects of preoperative obstructive pneumonitis or atelectasis and comparison with tumor size in non-small cell lung cancer
Pang, ZF;Ding, N;Dong, W;Ni, Y;Zhang, TH;Qu, X;Du, JJ;Liu, Q
JOURNAL OF THORACIC DISEASE 2017年 9卷3期 页码:768-778
LYMPHOCYTE RATIO; INFLAMMATION; MACROPHAGES; STATISTICS; SURVIVAL
Background: In the eighth TNM staging system proposal, lung cancer with part or complete obstructive pneumonitis/atelectasis was classified to T2 category, and dividing lines of T category were changed. We conducted this study to search prognostic effect of preoperative obstructive pneumonitis/atelectasis and its comparison with tumor size.;-;Methods: We collected clinical characteristics, preoperative hematological indicators, follow-up information of 1,313 lung cancer patients. Chi-square test was used to search relationship between obstruction pneumonitis/atelectasis and other factors. Kaplan-Meier (K-M) curves and cox regression methods were used for survival analysis.;-;Results: Preoperative obstructive pneumonitis/atelectasis indicated shorter OS (HR: 1.308; 95% CI: 1.058-1.619) and RFS (HR: 1.276; 95% CI: 1.032-1.579) as an independent factor. In comparison with tumor size, we found patients with obstructive pneumonitis/atelectasis and T1 size tumor had similar prognosis to those with T2 size but without obstructive pneumonitis/atelectasis, and OS, RFS of patients with obstructive pneumonitis/atelectasis and T2 size were significantly shorter than those with T2 tumor size but without obstructive pneumonitis/atelectasis, while similar to patients with T3 tumor size but without obstructive pneumonitis/atelectasis according to division by the eighth edition. We also found obstructive pneumonitis/atelectasis was significantly related to higher neutrophil (P<0.001), platelet (P<0.001), monocyte (P<0.001), NLR (P<0.001), PLR (P=0.002), ESR (P<0.001) and lower LMR (P<0.001).;-;Conclusions: Preoperative obstructive pneumonitis/atelectasis predicted poor survival independently in non-small cell lung cancer (NSCLC). And we suggested which T staging group the patients with obstructive pneumonitis/atelectasis would be divided to should depend on tumor size in the eighth TNM staging system.
ARRB1 enhances the chemosensitivity of lung cancer through the mediation of DNA damage response
Shen, HC;Wang, LG;Zhang, JG;Dong, W;Zhang, TH;Ni, Y;Cao, HX;Wang, K;Li, Y;Wang, YB;Du, JJ
ONCOLOGY REPORTS 2017年 37卷2期 页码:761-767
FLOW-CYTOMETRY; BETA-ARRESTINS; CELL; CARCINOMA; APOPTOSIS; BETA-ARRESTIN-1; EXPRESSION; PROGNOSIS; THERAPY; ASSAY
ARRB1 (also known as beta-arresting) serves as a multifunctional adaptor contributing to the regulation of signaling pathways. ARRB1 may be involved in DNA damage accumulation; however the underlying mechanism involved is unclear. In the present study, non-small cell lung cancer (NSCLC) cell lines (H520 and SK-MES-1) were transfected with ARRB1 plasmids or small interfering ribonucleic acid (siRNA) and received treatment with DNA-damaging agents (cisplatin and etoposide). A mouse xenograft model was used to assess the impact of ARRB1 on the efficacy of cisplatin in vivo. A total of 30 surgically resected NSCLC patients were recruited for the present study and qRT-PCR was performed to determine the mRNA levels in cancer tissues compared with para-carcinoma tissues. Our data showed that DNA damage was abrogated in the ARRB1-knockdown cells and enhanced in the ARRB1-overexpressing cells. ATR and Chk1 were more activated in the ARRB1-overexpressing cells compared to the ARRB1-knockdown cells, followed by increased H2AX phosphorylation. DNA damage and apoptosis were increased in the ARRB1-overexpressing cells treated with cisplatin. These data provided strong evidence that ARRB1 contributes to the response of NSCLC to DNA-damaging agents and is essential for DNA damage response (DDR). ARRB1 may enhance the efficacy of DNA-damaging agents in NSCLC.
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