王立东
一直从事河南食管癌高发区食管和贲门癌变机制和防治研究。
个性化签名
- 姓名:王立东
- 目前身份:
- 担任导师情况:
- 学位:
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学术头衔:
博士生导师, “973”、“863”首席科学家, 国家杰出青年科学基金获得者
- 职称:-
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学科领域:
肿瘤学
- 研究兴趣:一直从事河南食管癌高发区食管和贲门癌变机制和防治研究。
王立东,男,河南省获嘉县人,1958年8月出生,河南医科大学医学学士、肿瘤病理学硕士、浙江大学医学院肿瘤学博士,美国新泽西Rutgers州立大学博士后。现任郑州大学教授,博士生导师, 河南省高校特聘教授;河南省食管癌重点开放实验室主任;民盟河南省委副主委;第九、十届全国政协委员;美国新泽西Rutgers州立大学,武汉大学客座教授;国家杰出青年科学基金获得者,全国抗癌协会理事;中国抗癌协会食管癌专业委员会常委,中国抗癌协会食管癌病因专业委员会副主任,美国癌症研究协会(AACR)会员;河南省医师协会理事;河南省细胞生物学会副理事长。
1985年至今一直从事河南食管癌高发区食管和贲门癌变机制和防治研究,在食管和贲门癌变早期分子机制研究方面做出了一定的贡献,系统阐明p53-Rb系统在河南食管癌和贲门癌变多阶段演进过程中的变化特征和规律;发现:高发区人群存在O6-烷基鸟嘌呤-DNA烷基转移酶多态变体;提出:p53-Rb系统变化和AGT多态改变是食管癌变和高易感性的重要分子机制;创立了IHSS技术,建立了食管癌前病变细胞增生评价指标和定量分析方法。建立了高危人群筛查和早期诊断的血清学指标和方法。这些研究在一定程度上揭示了食管癌变早期的分子基础,具有重要临床应用价值。已发表中、英文论文和文摘429篇,4部医学专著,其中SCI收录57篇。发表在18种SCI源国际肿瘤相关核心杂志上,其中在“Cancer Research” (IF=7.69)杂志上发表3篇,在“Clin Cancer Res”(IF=5.62)杂志上发表3篇,在“Carcinogenesis”(IF=5.37)杂志上发表8篇。SCI统计(2000-2004),主要论文被“Science” “Cancer Research”等65种国际学术刊物引用900次,单篇论文被引用最高次数为113次(Wang LD, et al, Cancer Research,1993),主要论文还被美国“Surgical Pathology”等5部医学专著所引用,其中一部为美国医学教科书。被国际消化病年鉴(1997)收录全文一篇,该年度消化病年鉴共收录食管癌研究相关文献6篇。18次被国际肿瘤学术会议以及美国、加拿大、法国、荷兰、香港、台湾等地知名大学特邀作有关食管/贲门癌变机制研究专题报告。被美国Evidence-based Oncology杂志特邀撰写专家评论文章(Evidence-based Oncology,2002,4)。获得一项河南省科技进步一等奖,6项美国癌症研究协会和新泽西癌症研究协会等学术性奖励,一项卫生部三等奖,以及河南省教育厅和卫生厅等14项成果奖;获得香港Croucher Foundation基金访问奖。主持国家杰出青年科学基金,国家科技部973等项目、国家自然科学基金重点项目和面上项目、国家教育部重点项目、国家人事部重点项目、美国NCI项目、河南省高校创新人才工程项目、河南省医药卫生创新人才工程项目等科研项目10余项。1995年至今已培养研究生68名(博士23名,硕士45名)。担任《临床实验病理杂志》,《中华肿瘤防治杂志》等6部医学期刊的副主编和编委,被邀请为“Int J Cancer”“Cancer”“Carcinogenesis”“Cancer Epidemiol Biomarkers Prev”等四部杂志评审论文。被国务院授予国家有突出贡献专家称号(政府津贴),被国家人事部选入首批百千万人才工程序列,被河南省政府授予“河南省优秀省管专家”,被河南省政府授予“河南省留学归国人员成就奖”。
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王立东
,-0001,():
-1年11月30日
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王立东, Li Dong Wang, Qi Zhou, Rei Yiong Guo, Ying Xing, Bao Cai Zhang, Qi Ju Li, and Chung S. Yang
Vol.5, 405-406. May 1996,-0001,():
-1年11月30日
The objective of this study was to evaluate the reproducibility of the biopsy sampling procedure in research on esophageal lesions. Biopsies were ta ken from the middle and lower thirds of the esophagus, one from each site, from 25 subjects in a high-incidence area for esophageal cancer in Xinye County of Henan Province, China. The biopsy sampling procedure was repeated on the same subjects 10 days later. When the biopsies were analyzed together and those with worse pathologies were used for diagnosis, 52% of the subjects had the same grade of lesions in the second biopsy examination, 32% had lower-grade lesions, and 16% had higher-grade lesions.
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王立东, Stephanie T.Shi, Guang-Yu Yang, Li-Dong Wang, Zhihong Xue, Bo Feng, Wei Ding, Eric Poe Xing and Chung S.Yang
Carcinogenesis vol.20 no.4 pp.591-597, 1999,-0001,():
-1年11月30日
In order to characterize p53 alterations in esophageal cancer and to study their roles in carcinogenesis, we performed gene mutation and immunohistochemical analysis on 43 surgically resected human esophageal specimens, which contain squamous cell carcinoma (SCC) and adjacent non-cancerous lesions, from a high-incidence area of Linzhou in Henan, China. A newly developed immunohisto-selective sequencing (IHSS) method was used to enrich the p53 immunostain-positive cells for mutation analysis. p53 gene mutations were detected in 30 out of 43 (70%) SCC cases. Among 29 SCC cases that were stained positive for p53 protein, 25 (86%) were found to contain p53 mutations. In five cases of SCC with homogeneous p53 staining, the same mutation was observed in samples taken from four different positions of each tumor. In a well differentiated cancer nest, p53 mutation was detected in only the peripheral p53-positive cells. In tumor areas with heterogeneous p53 staining, either the area stained positive for p53 had an additional mutation to the negatively stained area or both areas lacked any detectable p53 mutation. In the p53-positive non-cancerous lesions adjacent to cancer, p53 mutations were detected in seven out of 16 (47%) samples with basal cell hyperplasia (BCH), eight out of 12 (67%) samples with dysplasia (DYS), and six out of seven (86%) samples with carcinoma in situ (CIS). All mutations found in lesions with DYS and CIS were the same as those in the nearby SCC. In seven cases of BCH containing mutations, only three had the same mutations as the nearby SCC. The results suggest that p53 mutation is an early event in esophageal carcinogenesis occurring in most of the DYS and CIS lesions, and cells with such mutations will progress to carcinoma, whereas the role of p53 mutations in BCH is less clear.
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王立东, Li Dong Wang*, Qi Zhou*, Chang Wei Feng*, Bin Liu*, Yi Jun QI*, Yan Run Zhang*, Shan Shan Cao*, Zong Min Fan*, Yun Zhou*, Chang S Yang*, Jun Ping Wei*, and Shu Zheng*
Vol. 29: Supplement 1, February, 2002,-0001,():
-1年11月30日
dies with calcium and decaffeinated green tea (DGT). Each group included 200 subjects (100 sub-jects for treatment, and 100 subjects of placebo). In calcium group, each subject received and oral supplementation of 1, 200mg of calcium daily for 11 months. In DGT group, each subject received 5mg of DGT daily for 12 months. In placebo group, each subject received placebo pill for 11 months (calciurn group) and 12 month (DGT group). At the entry and end trial, esophagecal biopsy specimens were taken at the middle and the lower thirds of the esophagus and from macroscopic iesions, if only, of each subject. Resulet: DGT trail did not show apparent difference between the treatment and placebo group in alleviatin the esophageal precancerous lesions and abnormal cell proliferation. For the calcium intervention study, after 11 years'follow-up. 10 subjects had developed into can-cers in the calcium group (10%, 8 EC and 2GCA), and 8 subjects developed into EC in the placebo group (8%). All these patients were diagnosed at very early stage of cancer (symptom-free). Of the 578 subjects, 25 (18 males and 7 females) had developed into EC (n=23, 43%) and gastric cardia cancer (GCA, n=2, 0.3%), during the 11 years'follow-up. The mean time of cancer development (from entry of the follow-up strdy to the detection) was 5.0±2.9 years (males) and 4.7±3.2 years (females). Of the 25 patients with EC and GCA, 11 were from the 387 followed subject with "normal" histomorphology of biopsy at the entry of the follow-up study (3%, 11/387), 2 were from the subjects with basal cell hyperpla-sia, grade 1 (BCH1, 2%, 2/94), 7 from the subjects with BCH grade Ⅱ (BCHⅡ, 10%, 7/72), and 5 from BCH Ⅲ and dysplasia (20%, 5/25). Conclusions: DGT trail was not shown to have beneficial effects in alleviation esophageal precancerous was not shown to have beneficial effects in alleviating esophageal precancerous le-sions and abnormal cell proliferation patterns. Calcium supplementation did not produce apparent long-term effects on EC. BCH Ⅱ could be considered as precan-cerous lesions of EC. The quantitative histopathological analysis in terms of num-ber of proliferating basal cell layers is importance in determining the high-risk subjects for EC and evaluating the intervention results. Follow-up studies with repeated endoscopic biopsies are the powerful strategy for early detection and mortality control of EC and GAC in the high incidence area.
Esophageal precancerous lesion, follow-up, intervention, green tea, calciun
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王立东
,-0001,():
-1年11月30日
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王立东, Eric Poe Xing, Guang-Yu Yang, Li-Dong Wang, Stephanie Tao Shi, and Chung S. Yang
Vol.5, 1231-1240, May 1999,-0001,():
-1年11月30日
To understand the alterations of Rb tumor suppressor gene and the relationship between defects in the Rb and p53 pathways in human esophageal carcinogenesis, we examined the loss of heterozygosity (LOH) of the Rb gene and immunohistochemical staining of pRb protein in 56 esophageal squamous cell carcinoma specimens and related the results to the p53 gene alterations. Using four introgenic polymorphic markers as probes, we observed LOH of the Rb gene in 30 of the 55 informative tumor samples. Immunohistochemical analysis revealed different patterns of pRb expression among the tumor samples. In the 56 cases, 16 displayed extensive pRb staining comparable to that of the adjacent normal epithelia, whereas 33 showed either significantly decreased or no pRb staining and 7 had a focal staining pattern reflecting heterogeneous cancer nests in the tumor with respect to Rb status. In the tumor samples containing Rb LOH, 90% showed low or no pRb expression, whereas in samples without Rb LOH, only 20% had altered pRb expression. There was a strong association between LOH of the Rb gene and alteration of pRb expression in our samples (P<0.0001), suggesting LOH is a main event leading to Rb inactivation. We found that Rb LOH was more frequent in tumors with p53 mutations (P<0.05), which occurred in 31 of the 49 cases analyzed. When the status of Rb and p53 alterations was evaluated by the combined results of immunohistochemical and genetic analyses, we found that alteration of Rb and p53 had an even stronger association in our esophageal squamous cell carcinoma samples (P=0.0015). Among the 51 cases in which both the Rb and p53 status were determined, 31 contained alterations in both genes, and only 5 and 6 cases were altered in only Rb and only p53, respectively. Our results suggest that defects in the Rb and p53 pathways and their potential synergistic effect in deregulating cell cycle and apoptosis are major mechanisms for esophageal carcinogenesis.
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王立东
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王立东, L. Dong Wang, , W. Bin Yue, Y. Zhou, C. Wei Feng, B. Liu, Q. Zhou, Y. Ying Jia, S. Zheng, S. Shan Gao, X. Ji Xie, Z. Min Fan, H. Min Niou, Z. Hao Zhuang, C. S. Yang, Y. Min Bai, Y. Jun Qi
,-0001,():
-1年11月30日
The objective of this study was to characterize the histologic changes from endoscopic screening for early esophageal cancer (EC) on subjects at high-incidence area (HIA) and low-incidence area (LIA) in Henan, China, and to further compare the changes in p53 and proliferating cell nuclear antigen (PCNA) in the multistage of human esophageal carcinogenesis from these two populations. The detection rate of basal cell hyperplasia (BCH) and dysplasia (DYS) was higher in the subjects from HIA than in those from LIA. Out of the 1568 symptom-free subjects examined at HIA, 10 (0.6%) cases with early squamous cell carcinoma (SCC) were identified. Immunoreactivity of p53 and PCNA was observed in cell nuclei of esophageal biopsies and surgically resected esophageal cancer specimens both in HIA and LIA. With the lesions progressed from normal epithelium to BCH to DYS to SCC, the positive-immunostaining cells expanded from basal layer to superficial layer, and the number of positive cells/mm2 for p53 and PCNA increased, and was significantly higher in HIA than in LIA among the similar morphological lesions (P<0.01). The number of p53 positive cells/mm2 in SCC from HIA was almost fivefold higher than SCC from LIA (P<0.01). The remarkable difference was also observed between HIA and LIA in DYS and BCH. The present results indicate that p53 protein accumulation is an important early biomarker for identifying high-risk subjects for EC.
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