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Fang Y.,Life Detection Systems | Zhang C.,Life Detection Systems | Wu T.,Life Detection Systems | Wang Q.,Shaanxi Lifegen Co. | And 2 more authors.
PLoS ONE | Year: 2017

Acquired resistance to cisplatin-based chemotherapy frequently occurs in patients with nonsmall cell lung cancer, and the underlying molecular mechanisms are not well understood. The aim of this study was to investigate whether a distinct gene expression pattern is associated with acquired resistance to cisplatin in human lung adenocarcinoma. Whole-transcriptome sequencing was performed to compare the genome-wide gene expression patterns of the human lung adenocarcinoma A549 cisplatin-resistant cell line A549/DDP with those of its progenitor cell line A549. A total of 1214 differentially expressed genes (DEGs) were identified, 656 of which were upregulated and 558 were downregulated. Functional annotation of the DEGs in the Kyoto Encyclopedia of Genes and Genomes database revealed that most of the identified genes were enriched in the PI3K/AKT, mitogen-activated protein kinase, actin cytoskeleton regulation, and focal adhesion pathways in A549/DDP cells. These results support previous studies demonstrating that the pathways regulating cell proliferation and invasion confer resistance to chemotherapy. Furthermore, the results proved that cell adhesion and cytoskeleton regulation is associated with cisplatin resistance in human lung cancer. Our study provides new promising biomarkers for lung cancer prognosis and potential therapeutic targets for lung cancer treatment. © 2017 Fang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Wang S.,Chengdu Medical College | Chen Y.,PLA Fourth Military Medical University | Qu F.,PLA Fourth Military Medical University | He S.,PLA Fourth Military Medical University | And 5 more authors.
Neuro-Oncology | Year: 2014

Background. Compelling epidemiological evidence indicates that alterations of telomere length are associated with risks of many malignancies in a tumor-specific manner, such as lung cancer, breast cancer, and non-Hodgkin's lymphoma. However, the association between leukocyte telomere length and glioma risk has not been investigated. Methods. Relative telomere length (RTL) of peripheral blood leukocytes from 467 glioma patients and 467 healthy controls, matched by age and sex, was measured using the real-time PCR-based method in a case-control study. An unconditional multivariate logistic regression model was applied to estimate the association between RTL and glioma risk. Results. Glioma patients showed notably longer RTL than controls (median, 0.555 vs 0.444; P >. 04). RTL was negatively correlated with age in both cases (ρ = -0.430; P <. 001) and controls (ρ = -0.388; P <. 001). After adjusting for age, sex, smoking status and family history of cancer, multivariate logistic regression analysis showed that there was a U-shaped association between RTL and glioma risk (P for nonlinearity <.001). Compared with individuals in the second tertile of RTL, the odds ratios (95% CI) for participants in the first and third tertiles were 2.16 (range, 1.52-3.09) and 3.51 (range, 2.45-5.00), respectively. Stratified analysis showed that the association between RTL and glioma risk was not modulated by major host characteristics. Conclusions. Our study demonstrates for the first time that either shorter or longer RTL in peripheral blood leukocytes is associated with increased glioma risk, which warrants further investigation in the future. © 2013 © The Author(s) 2013.

He G.-H.,Kunming General Hospital of Chengdu Military Region | Lu J.,Xi'an Jiaotong University | Shi P.-P.,Kunming General Hospital of Chengdu Military Region | Xia W.,Kunming General Hospital of Chengdu Military Region | And 4 more authors.
Gene | Year: 2013

Previous investigations indicated that histamine receptor H4 (HRH4) played important roles in many aspects of breast cancer pathogenesis, and that the polymorphisms of HRH4 gene may result in expression and functional changes of HRH4 proteins. However, the relationship between polymorphisms of HRH4 and breast cancer risk and malignant degree is unclear. In the present study, we conducted a case-control investigation among 185 Chinese Han breast cancer patients and 199 ethnicity-matched health controls. Four tag-SNPs (i.e. rs623590, rs16940762, rs11662595 and rs1421125) of HRH4 were genotyped and association analysis was performed. Odds ratios (ORs) with 95% confidence intervals (CI) were used to assess the association. We found that the T allele of rs623590 had a decreased risk of breast cancer (adjusted OR, 0.667; 95% CI, 0.486-0.913; P= 0.012) while the A allele of rs1421125 had an increased risk (adjusted OR, 1.653; 95% CI, 1.139-2.397; P= 0.008). Further haplotype analysis showed that the CAA haplotype of rs623590-rs11662595-rs1421125 was more frequent among patients with breast cancer (adjusted OR, 1.856; 95% CI, 1.236-2.787; P= 0.003). Additionally, polymorphisms of rs623590 and rs11662595 were also correlated with clinical stages, lymph node involvement, and HER2 status. These findings indicated that the variants of rs623590, rs11662595 and rs1421125 genotypes of HRH4 gene were significantly associated with the risk and malignant degree of breast cancer in Chinese Han populations, which may provide us novel insight into the pathogenesis of breast cancer although further studies with larger participants worldwide are still needed for conclusion validation. © 2013 Elsevier B.V.

Zhou F.,Tangdu Hospital | He X.,Tangdu Hospital | Liu H.,PLA Fourth Military Medical University | Zhu Y.,Yale University | And 7 more authors.
Cancer | Year: 2012

Background: Previous studies have demonstrated that circadian genes play a role in the development and progression of many cancers. This study aims to assess the effects of single nucleotide polymorphisms (SNPs) in circadian genes on recurrence and survival of colorectal cancer (CRC) patients. Methods: Nine functional SNPs in 3 genes (CLOCK, NPAS2, and BMAL1) on the circadian positive feedback loop were selected and genotyped using the Sequenom iPLEX genotyping system in a cohort of 411 resected Chinese CRC patients. Multivariate Cox proportional hazards model and Kaplan-Meier curve were used for the prognosis analysis. Results: The authors identified 2 SNPs in the CLOCK gene to be significantly associated with CRC overall survival. SNP rs3749474 exhibited a significant association with survival of CRC patients in the additive model (hazard ratio [HR], 0.55; 95% confidence interval [CI], 0.37-0.81; P =.003). In addition, patients carrying the heterozygous variant of rs1801260 had significantly increased overall survival compared with those carrying homozygous wild-type genotype (HR, 0.31; 95% CI, 0.11-0.88; P =.03). Findings from functional assay provided further biological support for these significant associations. Stratified analysis found no modifying effect of chemotherapy on the prognostic significance of both SNPs. Moreover, we observed cumulative effects of these 2 SNPs on CRC overall survival (P for trend =.01). Compared with patients carrying no unfavorable genotypes, those carrying 2 unfavorable genotypes had a 2.92-fold increased risk of death (P =.03). Conclusions: The results suggest for the first time that CLOCK gene polymorphisms may serve as an independent prognostic marker for CRC patients. © 2011 American Cancer Society.

Li S.,PLA Fourth Military Medical University | Jin T.,Life Detection Systems | Zhang J.,Life Detection Systems | Lou H.,Guangzhou First Municipal Peoples Hospital | And 4 more authors.
Cancer Epidemiology | Year: 2012

Introduction: Glioma is one of the most aggressive human tumors; however, little is known about its genetic risk factors. The role of heredity is likely to be explained by combinations of common low-risk variants. Previous studies have indicated that more than 100 single nucleotide polymorphisms (SNPs) are associated with the risk of glioma. Methods: To further investigate how and to what extent these SNPs contribute to glioma susceptibility in a Chinese population, we analyzed 43 SNPs of 226 glioma patients and 254 normal people in order to evaluate the associations between SNPs and the risk of glioma. Results: Overall, we found three protective alleles for glioma in patients: the allele " G" of rs1801275 in the IL4R gene by allele model (odds ratio [OR], 0.71; 95% confidence interval [CI], 0.50-0.99; P= 0.04) and dominant model (OR, 0.67; 95% CI, 0.46-0.99; P= 0.04) analysis respectively, the allele " T" of rs17748 in the TREH gene by recessive model (OR, 0.48; 95% CI, 0.23-1.01; P= 0.05) analysis, and the allele " G" of rs6470745 in CCDC26 gene by recessive model (OR, 0.48; 95% CI, 0.26-0.89; P= 0.02) analysis. Conclusion: This study provides evidence for three glioma susceptibility genes - TREH, IL4R and CCDC26 - in a Chinese population; this may shed light on molecular markers of glioma susceptibility and could therefore be used as a diagnostic and prognostic marker for glioma patients in clinical study. © 2012 Elsevier Ltd.

Gao W.,Life Detection Systems
Chinese Journal of Organic Chemistry | Year: 2010

Naturally occurring terpenes constitute the largest group of natural products with complicated and variable structures and a great number of important biological activities. 2-Methyl-7D-erythreitol 4-phosphate (MEP) pathway is a newly found and established biosynthetic route for terpenoids and all the enzymes involved in this pathway can be used as targets for the screening of new antibiotics. Progress in chemical and enzymatic preparation of the key intermediates in MEP pathway, namely 1-deoxy-D-xylulose 5-phosphate and 2-methyk-D-erythreitol 4-phosphate is reviewed with the emphasis on the synthesis of these two compounds with isotope labels.

Methods and systems for monitoring the well-being of a target are disclosed. In a method embodiment, data representing a signal is received by a computer system. The signal may be generated at least in part by one or more sensors in response to the detection of a change in an electrical field, electric potential, capacitance, and/or dielectric constant of a target spaced apart from the one or more sensors. The method may further include identifying, using the computer system and based at least in part on the data electronically received by the computer system, a recurring pattern in the received data. The method may also include determining, using the computer system and based at least in part on the received data, whether a deviation from the recurring pattern transgresses a threshold. The deviation may comprise a subset of the data electronically received by the computer system.

Life Detection Systems | Date: 2014-06-29

Integrated circuits and software for use in monitoring, reporting and sending alerts regarding a person, animal or objects physical conditions, for use in detecting, recording, measuring, receiving, transmitting and displaying distances, location, activity and movement and biological function data about a person, animal or object and for use in monitoring and sending alerts regarding the activity of persons, animals and objects.

Li G.,PLA Fourth Military Medical University | Zhang Z.,PLA Fourth Military Medical University | Tu Y.,PLA Fourth Military Medical University | Jin T.,Life Detection Systems | And 4 more authors.
Diagnostic Pathology | Year: 2013

MicroRNA-372 (miR-372) acts as either an oncogenic miRNA or an anti-oncomiR in various human malignancies. However, its roles in gliomas have not been elucidated. To address this problem, we here detected miR-372 expression in human gliomas and non-neoplastic brain tissues by real-time quantitative RT-PCR assay. The association of miR-372 expression with clinicopathological factors or prognosis of glioma patients was also statistically analyzed. As the results, miR-372 expression levels were significantly upregulated in glioma tissues compared to the corresponding non-neoplastic brain tissues (P<0.001). In addition, the high miR-372 expression was significantly associated with the advanced pathological grade (P=0.008) and the low Karnofsky performance score (KPS) of glioma patients (P=0.01). Moreover, the overall survival of patients with high miR-372 expression was dramatically shorter than those with low miR-372 expression (P<0.001). Furthermore, multivariate Cox regression analysis indicated that miR-372 expression was an independent prognostic factor for glioma patients (P=0.008). More importantly, subgroup analyses according to tumor pathological grade revealed that the cumulative overall survival of glioma patients with advanced pathological grades was significantly worse for high miR-372 expression group than for low miR-372 expression group (P<0.001), but no significant difference was found for patients with low pathological grades (P=0.08). Taken together, these data offer the convincing evidence for the first time that miR-372 may act as an oncogenic miRNA in gliomas and represent a potential regulator of aggressive development and a candidate prognostic marker for this malignancy, especially for advanced tumors with high pathological grades.Virtual slides: The virtual slide(s) for this article can be found here: © 2013 Li et al.; licensee BioMed Central Ltd.

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