• Complex
  • Title
  • Author
  • Keyword
  • Abstract
  • Scholars
Search
High Impact Results & Cited Count Trend for Year Keyword Cloud and Partner Relationship

Query:

学者姓名:侯鹏

Refining:

Type

Submit Unfold

Co-Author

Submit Unfold

Language

Submit

Clean All

Export Sort by:
Default
  • Default
  • Title
  • Year
  • WOS Cited Count
  • Impact factor
  • Ascending
  • Descending
< Page ,Total 5 >
miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway Scopus PubMed SCIE
期刊论文 | 2019 , 215 (2) , 243-250 | Pathology Research and Practice | IF: 2.05
WoS CC Cited Count: 3 SCOPUS Cited Count: 4
Abstract&Keyword Cite

Abstract :

© 2018 Background: Previous studies indicated that miR-218 was deregulated in gastric cancer patients and correlated with tumor invasion and prognosis. The aim of this study was to clarify the effect of miR-218 on the malignant behavior of gastric cancer and its role in regulating Bmi-1/Akt signaling pathway. Materials and methods: We used miR-218 mimic to transfect gastric cancer cell lines AGS and SGC-7901, and the overexpression efficiency was validated using qRT-PCR assay. MTT assay and Transwell chamber system were performed to detect the effect of miR-218 on cell proliferation, invasion and migration on gastric cancer. Western blot and qRT-PCR assay was used to test the role of miR-218 in regulating Bmi-1/Akt signaling pathway. Results: As shown in our research, ectopic expression of miR-218 in gastric cancer cells inhibits the proliferation, invasion and migration of gastric cancer cells. In addition, miR-218 re-expression inhibits the expression of Bmi-1 and its downstream target p-Akt473, as well as MMPs and EMT process. Conclusions: miR-218 inhibits the proliferation, invasion and migration of gastric cancer cells through modulating EMT process and the expression of MMPs via Bmi-1/Akt signaling pathway.

Keyword :

Akt Bmi-1 EMT Gastric cancer miR-218 MMPs

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Wu, Yongxing , Tian, Sijia , Chen, Yijun et al. miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway [J]. | Pathology Research and Practice , 2019 , 215 (2) : 243-250 .
MLA Wu, Yongxing et al. "miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway" . | Pathology Research and Practice 215 . 2 (2019) : 243-250 .
APA Wu, Yongxing , Tian, Sijia , Chen, Yijun , Ji, Meiju , Qu, Yiping , Hou, Peng . miR-218 inhibits gastric tumorigenesis through regulating Bmi-1/Akt signaling pathway . | Pathology Research and Practice , 2019 , 215 (2) , 243-250 .
Export to NoteExpress RIS BibTex
甲状腺癌中CYP1A1和CYP1B1基因启动子区甲基化分析 CSCD PKU
期刊论文 | 2018 , (8) , 667-673 | 中华内分泌代谢杂志
Abstract&Keyword Cite

Abstract :

目的 研究甲状腺癌中药物代谢基因CYP1A1、CYP1B1启动子区异常甲基化及其与临床病理特征之间的关系.方法 取201例甲状腺癌及23例正常甲状腺石蜡包埋组织基因组DNA,采用甲基化特异性PCR(MSP)检测上述基因启动子区甲基化状态,对比甲状腺乳头状癌(PTC)及正常对照中CYP1A1、CYP1B1基因甲基化的发生率.在体外实验中利用甲基化转移酶抑制剂5-氮-2′-脱氧胞苷(5-Aza-dC)处理5种甲状腺癌细胞系,用实时定量PCR(RT-PCR)方法检测5-Aza-dC处理前后CYP1A1、CYP1B1基因的表达变化.用logistic回归方法分析CYP1A1、CYP1B1基因的异常甲基化与临床特点之间的相关性.结果 在各种病理类型的甲状腺癌中均存在CYP1A1、CYP1B1基因甲基化的情况;在PTC中CYP1A1基因启动子区甲基化水平高于对照组,CYP1B1基因启动子区甲基化水平低于对照组;CYP1A1基因在PTC中的表达低于对照组(P<0.01),CYP1B1基因在PTC中的表达高于对照组(P<0.01);利用5-Aza-dC处理甲状腺癌细胞系后可使CYP1A1基因的表达水平在K1及C643细胞系中较对照分别升高6.92及8.30倍;CYP1B1基因在K1细胞中表达较对照升高7.62倍;CYP1B1基因启动子区甲基化与淋巴结转移呈负相关.结论 在PTC中基因启动子区甲基化调控CYP1A1及CYP1B1基因的表达,CYP1B1启动子区异常甲基化与PTC的淋巴结转移有关.

Keyword :

CYP1A1 DNA甲基化 CYP1B1 聚合酶链反应 甲状腺癌

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 张利红 , 石静 , 郝文庆 et al. 甲状腺癌中CYP1A1和CYP1B1基因启动子区甲基化分析 [J]. | 中华内分泌代谢杂志 , 2018 , (8) : 667-673 .
MLA 张利红 et al. "甲状腺癌中CYP1A1和CYP1B1基因启动子区甲基化分析" . | 中华内分泌代谢杂志 8 (2018) : 667-673 .
APA 张利红 , 石静 , 郝文庆 , 田竹芳 , 祭美菊 , 侯鹏 et al. 甲状腺癌中CYP1A1和CYP1B1基因启动子区甲基化分析 . | 中华内分泌代谢杂志 , 2018 , (8) , 667-673 .
Export to NoteExpress RIS BibTex
Long telomere length predicts poor clinical outcome in esophageal cancer patients SCIE PubMed Scopus
期刊论文 | 2017 , 213 (2) , 113-118 | PATHOLOGY RESEARCH AND PRACTICE | IF: 1.466
WoS CC Cited Count: 6 SCOPUS Cited Count: 5
Abstract&Keyword Cite

Abstract :

Background: Abnormal telomere length is widely reported in various human cancers, and it is considered to be an important hallmark of cancer. However, there is remarkably little consensus on the value of telomere length in the prognostic evaluation of esophageal cancers. Here, we attempted to determine the association of variable telomere length with clinical outcome of esophageal cancer patients. Materials and methods: Using real-time quantitative PCR, we examined relative telomere lengths (RTL) in a cohort of esophageal cancer and normal esophageal tissues, and statistically investigated the association between RTL and clinical outcomes of esophageal cancer patients. Results: The majority of esophageal cancers in this study had longer RTLs as compared to adjacent non tumor tissues. Enhanced tumor RTL was associated with smoking habit, poor differentiation, advanced tumor stage, lymph node metastasis and cancer related death. In particular, a close relationship between longer RTL and poor survival was fully demonstrated by using cox regression and Kaplan-Maier survival curves. Conclusions: We found frequent telomere elongation in esophageal cancer tissues, and demonstrated longer RTL may be an independent poor prognostic factor for esophageal cancer patients. (C) 2016 Elsevier GmbH. All rights reserved.

Keyword :

Clinical outcome Esophageal cancer Relative telomere length Biomarker

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Lv, Yanyan , Zhang, Yong , Li, Xinru et al. Long telomere length predicts poor clinical outcome in esophageal cancer patients [J]. | PATHOLOGY RESEARCH AND PRACTICE , 2017 , 213 (2) : 113-118 .
MLA Lv, Yanyan et al. "Long telomere length predicts poor clinical outcome in esophageal cancer patients" . | PATHOLOGY RESEARCH AND PRACTICE 213 . 2 (2017) : 113-118 .
APA Lv, Yanyan , Zhang, Yong , Li, Xinru , Ren, Xiaojuan , Wang, Meichen , Tian, Sijia et al. Long telomere length predicts poor clinical outcome in esophageal cancer patients . | PATHOLOGY RESEARCH AND PRACTICE , 2017 , 213 (2) , 113-118 .
Export to NoteExpress RIS BibTex
Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study SCIE PubMed Scopus
期刊论文 | 2016 , 46 (6) , 542-547 | XENOBIOTICA | IF: 1.932
WoS CC Cited Count: 2 SCOPUS Cited Count: 2
Abstract&Keyword Cite

Abstract :

1. CYP1A2 is a highly polymorphic gene and CYP1A2 enzyme results in broad inter-individual variability in response to certain pharmacotherapies, while little is known about the genetic variation of CYP1A2 in Uyghur Chinese population. The aim of the present study was to screen Uyghur volunteers for CYP1A2 genetic polymorphisms. 2. We used DNA sequencing to investigate promoter, exons, introns, and 3' UTR of the CYP1A2 gene in 96 unrelated healthy Uyghur individuals. We also used SIFT (Sorting Intolerant From Tolerant) and PolyPhen-2 (Polymorphism Phenotyping v2) to predict the protein function of the novel non-synonymous mutation in CYP1A2 coding regions. 3. We identified 20 different CYP1A2 polymorphisms in the Uyghur Chinese population, including two novel variants (119A > G and 2410G > A). Variant 119A > G was predicted to be probably damaging on protein function by PolyPhen-2, by contrast, 2410G > A was identified as benign. The allele frequencies of CYP1A2*1A, *1B, *1F, *1G, *1J, *1M, *4, and *9 were 23.4%, 53.1%, 3.7%, 2.6%, 2.6%, 13.5%, 0.5%, and 0.5%, respectively. The frequency of *1F, a putative high inducibility allele, was higher in our sample population compared with that in the Caucasian population (p < 0.05). The most common genotype combinations were *1A/*1B (46.9%) and *1B/*1M (27.1%). 4. Our results provide basic information on CYP1A2 polymorphisms in Uyghur individuals and suggest that the enzymatic activities of CYP1A2 may differ among the diverse ethnic populations of the world.

Keyword :

CYP1A2 Uyghur populations ethnic groups genetic polymorphism

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Geng, Tingting , Zhang, Xi Yang , Wang, Li et al. Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study [J]. | XENOBIOTICA , 2016 , 46 (6) : 542-547 .
MLA Geng, Tingting et al. "Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study" . | XENOBIOTICA 46 . 6 (2016) : 542-547 .
APA Geng, Tingting , Zhang, Xi Yang , Wang, Li , Wang, Huijuan , Shi, Xugang , Kang, Longli et al. Genetic polymorphism analysis of the drug-metabolizing enzyme CYP1A2 in a Uyghur Chinese population: a pilot study . | XENOBIOTICA , 2016 , 46 (6) , 542-547 .
Export to NoteExpress RIS BibTex
TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas SCIE PubMed Scopus
期刊论文 | 2016 , 7 (8) , 8712-8725 | ONCOTARGET | IF: 5.168
WoS CC Cited Count: 42 SCOPUS Cited Count: 45
Abstract&Keyword Cite

Abstract :

Increasing evidences have implicated somatic gain-of-function mutations at the telomerase reverse transcriptase (TERT) promoter as one of the major mechanisms that promote transcriptional activation of TERT and subsequently maintain telomere length in human cancers including glioma. To investigate the prognostic value of these mutations and telomere length, individually and their coexistence, in gliomas, we analyzed two somatic mutations C228T and C250T in the TERT promoter, relative telomere length (RTL), IDH1 mutation and MGMT methylation in 389 glioma patients, and explored their associations with patient characteristics and clinical outcomes. Our data showed that C228T and C250T mutations were found in 17.0% (66 of 389) and 11.8% (46 of 389) of gliomas, respectively, and these two mutations were mutually exclusive in this cancer. Moreover, they were significantly associated with WHO grade. We also found that the RTL was significant longer in gliomas than in meningiomas and normal brain tissues (Median, 0.89 vs. 0.44 and 0.50; P < 0.001), and demonstrated that the RTL was strongly correlated with tumor recurrence. Importantly, TERT promoter mutations or long RTL caused a significantly poorer survival than TERT wild-type or short RTL. Coexisting TERT promoter mutations and long RTL were more commonly associated with poor patient survival than they were individually. Notably, the patients with TERT promoter mutations particularly C228T or long RTL were resistant to radiotherapy. Collectively, TERT promoter mutations and long RTL are not only prognostic factors for poor clinical outcomes, but also the predictors of radiotherapy resistance in gliomas.

Keyword :

TERT promoter mutations poor survival radiotherapy resistance glioma relative telomere length

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Gao, Ke , Li, Gang , Qu, Yiping et al. TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas [J]. | ONCOTARGET , 2016 , 7 (8) : 8712-8725 .
MLA Gao, Ke et al. "TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas" . | ONCOTARGET 7 . 8 (2016) : 8712-8725 .
APA Gao, Ke , Li, Gang , Qu, Yiping , Wang, Maode , Cui, Bo , Ji, Meiju et al. TERT promoter mutations and long telomere length predict poor survival and radiotherapy resistance in gliomas . | ONCOTARGET , 2016 , 7 (8) , 8712-8725 .
Export to NoteExpress RIS BibTex
专业学位与学术型研究生转化医学教学模式的初探
期刊论文 | 2015 , (6) , 985-987 | 西北医学教育
Abstract&Keyword Cite

Abstract :

当前,我国医学研究生培养模式存在一些缺陷:学术型研究生的培养着重科研训练,不能充分了解临床工作的需求,不能提出具有前瞻性的应用基础研究课题;专业学位研究生主要以培养临床能力为主,但多缺乏必要的科研能力训练,缺乏科研思维,无法提出操作性强的科学问题,因而培养模式需要改革.本文提出在研究生教育中融入转化医学的理念和思维,旨在打破基础医学及临床医学之间的固有屏障,弥补基础科学研究与临床应用实践之间的鸿沟.实践证实该培养模式对培养全面型医学人才具有重要意义.

Keyword :

转化医学 学术型研究生 专业学位研究生

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 赵真真 , 黄葶 , 崔巍 et al. 专业学位与学术型研究生转化医学教学模式的初探 [J]. | 西北医学教育 , 2015 , (6) : 985-987 .
MLA 赵真真 et al. "专业学位与学术型研究生转化医学教学模式的初探" . | 西北医学教育 6 (2015) : 985-987 .
APA 赵真真 , 黄葶 , 崔巍 , 侯鹏 , 施秉银 . 专业学位与学术型研究生转化医学教学模式的初探 . | 西北医学教育 , 2015 , (6) , 985-987 .
Export to NoteExpress RIS BibTex
专业学位与学术型研究生转化医学教学模式的初探
期刊论文 | 2015 , (6) | 西北医学教育
Abstract&Keyword Cite

Abstract :

当前,我国医学研究生培养模式存在一些缺陷:学术型研究生的培养着重科研训练,不能充分了解临床工作的需求,不能提出具有前瞻性的应用基础研究课题;专业学位研究生主要以培养临床能力为主,但多缺乏必要的科研能力训练,缺乏科研思维,无法提出操作性强的科学问题,因而培养模式需要改革。本文提出在研究生教育中融入转化医学的理念和思维,旨在打破基础医学及临床医学之间的固有屏障,弥补基础科学研究与临床应用实践之间的鸿沟。实践证实该培养模式对培养全面型医学人才具有重要意义。

Keyword :

转化医学 学术型研究生 专业学位研究生

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 赵真真 , 黄葶 , 崔巍 et al. 专业学位与学术型研究生转化医学教学模式的初探 [J]. | 西北医学教育 , 2015 , (6) .
MLA 赵真真 et al. "专业学位与学术型研究生转化医学教学模式的初探" . | 西北医学教育 6 (2015) .
APA 赵真真 , 黄葶 , 崔巍 , 侯鹏 , 施秉银 . 专业学位与学术型研究生转化医学教学模式的初探 . | 西北医学教育 , 2015 , (6) .
Export to NoteExpress RIS BibTex
A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter EI SCIE
期刊论文 | 2015 , 11 (6) , 1016-1026 | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY | IF: 3.929
WoS CC Cited Count: 6
Abstract&Keyword Cite

Abstract :

5-Methylcytosine (5mC) can be converted to 5-hydroxymethylcytosine (5hmC) in mammalian DNA by the ten-eleven translocation (TET) enzymes. Traditional bisulfite-based DNA methylation analysis techniques have been widely used in the detection of 5mC. However, they can not discriminate 5hmC from 5mC, leading to overestimate 5mC levels. We here introduce a strategy, combination of selective oxidation and bisulfite pyrosequencing (BS-Pyroseq), for quantification of both 5mC and 5hmC at CpG sites within the promoters of CDH1, DAPK, RAR ss and RUNX3 genes in a panel of cell lines and clinical samples. As expected, oxidative bisulfite pyrosequencing (oxBS-Pyroseq) assay decreased overall or site-specific methylation levels of three of these genes in most cell lines as compared with BS-Pyroseq assay. Similarly, decreased overall or site-specific methylation levels of DAPK, RAR ss and RUNX3 genes in laryngeal, gastric and thyroid cancer and their matched normal tissues, respectively, were also found by a comparison between these two techniques, particularly in cancerous tissues. In addition, by using this combined strategy and hydroxymethylcytosine DNA immunoprecipitation (hMeDIP) assay, we demonstrated that TET1 up-regulated DAPK expression through promoter demethylation. Collectively, this strategy is easy to establish and accurately discriminates and quantifies 5mC and 5hmC at CpG sites within selected gene promoters.

Keyword :

5-Methylcytosine (5mC) Gene Promoter Bisulfite Pyrosequencing Selective Oxidation 5-Hydroxymethylcytosine (5hmC)

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Qu, Yiping , Yang, Qi , Sui, Fang et al. A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter [J]. | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY , 2015 , 11 (6) : 1016-1026 .
MLA Qu, Yiping et al. "A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter" . | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY 11 . 6 (2015) : 1016-1026 .
APA Qu, Yiping , Yang, Qi , Sui, Fang , Lu, Rong , Dang, Siwen , Ji, Meiju et al. A Strategy for Accurate Quantification of 5-Methylcytosine and 5-Hydroxymethylcytosine at CpG Sites Within Gene Promoter . | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY , 2015 , 11 (6) , 1016-1026 .
Export to NoteExpress RIS BibTex
Frequent amplification of AIB1, a critical oncogene modulating major signaling pathways, is associated with poor survival in gastric cancer SCIE
期刊论文 | 2015 , 6 (16) , 14344-14359 | ONCOTARGET | IF: 5.008
WoS CC Cited Count: 24
Abstract&Keyword Cite

Abstract :

Amplified in breast cancer 1 (AIB1) is a member of p160 steroid receptor coactivator (SRC) family that mediates the transcriptional activities of nuclear receptors and other transcription factors. It acts as a major oncogene in diverse cancers, whereas biological function of AIB1 in gastric cancer remains largely unclear. This study was designed to explore the role of AIB1 in gastric tumorigenesis and its potential as a useful prognostic marker and therapeutic target in this cancer. Our data demonstrated that AIB1 was significantly up-regulated in gastric cancer tissues as compared with control subjects. Moreover, AIB1 amplification was found in 47 of 133 (35.3%) gastric cancer cases, but not in control subjects. AIB1 amplification was positively associated with its protein expression, and was significantly correlated with poor patient survival. AIB1 knockdown in gastric cancer cells dramatically inhibited cell proliferation, invasiveness and tumorigenic potential in nude mice, and induced cell cycle arrest and apoptosis. Mechanically, AIB1 promotes gastric cancer cell proliferation, survival and invasiveness through modulating major signaling pathways such as ErbB and Wnt/beta-catenin pathways. Collectively, these findings suggest that AIB1 plays an important role in the pathogenesis of gastric cancer and represents a potential prognostic marker and therapeutic target for this cancer.

Keyword :

gastric cancer poor prognosis signaling pathways genomic amplification AIB1

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Shi, Jing , Liu, Wei , Sui, Fang et al. Frequent amplification of AIB1, a critical oncogene modulating major signaling pathways, is associated with poor survival in gastric cancer [J]. | ONCOTARGET , 2015 , 6 (16) : 14344-14359 .
MLA Shi, Jing et al. "Frequent amplification of AIB1, a critical oncogene modulating major signaling pathways, is associated with poor survival in gastric cancer" . | ONCOTARGET 6 . 16 (2015) : 14344-14359 .
APA Shi, Jing , Liu, Wei , Sui, Fang , Lu, Rong , He, Qingyuan , Yang, Qi et al. Frequent amplification of AIB1, a critical oncogene modulating major signaling pathways, is associated with poor survival in gastric cancer . | ONCOTARGET , 2015 , 6 (16) , 14344-14359 .
Export to NoteExpress RIS BibTex
Hypermethylation in gastric cancer SCIE PubMed Scopus
期刊论文 | 2015 , 448 , 124-132 | CLINICA CHIMICA ACTA | IF: 2.799
WoS CC Cited Count: 20 SCOPUS Cited Count: 20
Abstract&Keyword Cite

Abstract :

Although gastric cancer (GC) is highly prevalent in China and is a leading cause of cancer-related death, major advances in early diagnostic and effective therapeutic strategies have not been made. GC patients are usually diagnosed at an advanced stage and the prognosis is still poor. Over the years, many efforts have been done on exploring the pathology of GC. In particular, genome-wide analysis tools have been widely used in the detection of genetic and epigenetic alterations in GC. For example, many tumor suppressor genes have been found to be aberrantly hypermethylated in GCs, and some even in gastric precancerous lesions, suggesting a role of this molecular event in early gastric tumorigenesis. In addition, accumulating evidences have demonstrated that some hypermethylated genes can be used as potential biomarkers for detection and diagnosis of GC in biopsy specimens and non-invasive body fluids. These exciting advances provide unprecedented opportunities for the development of molecular-based novel diagnostic, prognostic, and therapeutic strategies for GC. Here, we reviewed recent findings on the promoter hypermethylation of tumor suppressor genes in GC and aimed to provide better understanding of the contribution of this epigenetic event to gastric tumorigenesis. (C) 2015 Elsevier B.V. All rights reserved.

Keyword :

Clinical utility Gastric cancer Epigenetics Biomarkers Gene methylation

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Li, Yujun , Liang, Junrong , Hou, Peng . Hypermethylation in gastric cancer [J]. | CLINICA CHIMICA ACTA , 2015 , 448 : 124-132 .
MLA Li, Yujun et al. "Hypermethylation in gastric cancer" . | CLINICA CHIMICA ACTA 448 (2015) : 124-132 .
APA Li, Yujun , Liang, Junrong , Hou, Peng . Hypermethylation in gastric cancer . | CLINICA CHIMICA ACTA , 2015 , 448 , 124-132 .
Export to NoteExpress RIS BibTex
10| 20| 50 per page
< Page ,Total 5 >

Export

Results:

Selected

to

Format:
FAQ| About| Online/Total:949/98213050
Address:XI'AN JIAOTONG UNIVERSITY LIBRARY(No.28, Xianning West Road, Xi'an, Shaanxi Post Code:710049) Contact Us:029-82667865
Copyright:XI'AN JIAOTONG UNIVERSITY LIBRARY Technical Support:Beijing Aegean Software Co., Ltd.