王和
妇产科
个性化签名
- 姓名:王和
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学术头衔:
博士生导师
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学科领域:
妇产科学
- 研究兴趣:妇产科
王和, 教授,博士生导师。现任四川大学华西第二医院副院长、四川省产前诊断中心主任。兼职有全国产前诊断技术专家组成员、中国优生学会医学遗传学专委会副主委、四川省医学遗传学会副主委、四川省遗传学会理事会理事、四川省计划生育技术专家委员会委员、成都市医学会优生优育分会主委等职务。曾在荷兰Erasmus大学临床遗传学系、莱顿大学人类分子遗传学所做访问学者,在美国密西根大学肿瘤中心做高级访问学者,美国杜克大学做副研究员。从事妇产科临床及基础研究工作多年。获国家自然科学基金、卫生部基金、博士点基金、CMB基金等科研基金资助,发表论文80余篇,也承担全国高等医学院校教材编写工作。指导和协助指导硕士生、博士生数十名,曾获四川省一、二、三等科技进步奖。
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207
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成果数
5
王和, Shanling Liu, , He Wang, Zhonghui Yang, Takashi Kon, Jiangao Zhu, Yiting Cao, Fang Li, John Kirkpatrick, Christopher V. Nicchitta, and Chuan-Yuan Li
Cancer Res 2005; 65: (20). October 15, 2005,-0001,():
-1年11月30日
Tumor-derived glucose-regulated protein 94 (GRP94/gp96) has shown great promise as a tumor vaccine. However, current protein-based approaches require the availability of large quantities of tumor tissue, which are often not possible. In addition, the efficacy of immunotherapy is often not ideal when used alone. In this study, we explored the therapeutic efficacy of a combined GRP94/gp96-based genetic immunotherapy and radiation therapy strategy in the weakly immunogenic and highly metastatic 4T1 murine mammary cancer model. An adenovirus encoding a modified, secretable form of GRP94 gene (AdsGRP94) was constructed and evaluated in various antitumor experiments. Lethally irradiated, virus-infected cells were used as vaccines. Adenoviral vectors were also injected directly into tumors in conjunction with tumor irradiation. Vaccination with lethally irradiated, AdsGRP94-infected 4T1 cells completely prevented subsequent tumor growth from challenge inoculations of as many as 107 cells per mouse. In established tumor models, vaccinations alone had minimal effect on local and metastatic tumor growth. However, when vaccination was combined with radiation therapy and i.t. AdsGRP94 injections, local tumor growth and pulmonary metastasis were markedly inhibited. In some cases, complete tumor regression was observed. In these cases, the mice were resistant to subsequent tumor challenge and remain tumor free up to 10 months after initial therapy. Our results indicate that combined AdsGRP94-based immunotherapy and radiation therapy may be a potentially effective strategy for cancer treatment.
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【期刊论文】A unique role of the DNA fragmentation factor in maintaining genomic stability
王和, Bin Yan*, †, Huili Wang†, ‡, Yuanlin Peng§, Ye Hu*, He Wang*, ¶, Xiuwu Zhang*, Qi Chen*, Joel S. Bedford§, Mark W. Dewhirst*, and Chuan-Yuan Li*
1504-1509 PNAS January 31, 2006 vol. 103 no.5,-0001,():
-1年11月30日
DNA fragmentation is a hallmark of apoptosis (programmed cell death). However, the biological function of apoptotic DNA fragmentation remains unclear. Here, we show that DNA fragmentation factor plays an important role for maintaining genomic stability. Inhibition or loss of the DNA fragmentation factor (DFF) caspase-activated DNase (CAD), whose nuclease activity is responsible for digesting genomic DNA during apoptosis, led to significant increases in spontaneous or induced gene mutations, gene amplifications, and chromosomal instability in primary mouse cells and transformed human cell lines. The mechanism underlying genetic instability in DFF CAD-deficient cells, at least in part, involves a small but significant elevation in the survival of cells exposed to ionizing radiation, suggesting that apoptotic DNA fragmentation factor contributes to genomic stability by ensuring the removal of cells that have suffered DNA damage. In support of this hypothesis are the observations of increased cellular transformation of mouse embryonic cells from the DFF CAD-null mice and significantly enhanced susceptibility to radiation-induced carcinogenesis in these mice. These data, in combination with published reports on the existence of tumor-specific gene mutations deletions in the DFF CAD genes in human cancer samples, suggest that apoptotic DNA fragmentation factor is required for the maintenance of genetic stability and may play a role in tumor suppression.
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王和, Xiuwu Zhang, Takashi Kon, He Wang, Fang Li, Qian Huang, Zahid N. Rabbani, John P. Kirkpatrick, Zeljko Vujaskovic, Mark W. Dewhirst, and Chuan-Yuan Li
CANCER RESEARCH 64, 8139-8142, November 15, 2004,-0001,():
-1年11月30日
Hypoxia-inducible factor-1α (HIF-1α) is an important transcriptional factor that is activated when mammalian cells experience hypoxia, a tumor microenvironmental condition that plays pivotal roles in tumor progression and treatment. In this study, we examined the idea of downregulating HIF-1α in tumor cells for therapeutic gain. We show that the expression levels of HIF-1α can be significantly attenuated by use of the recently established small interfering RNA technology in combination with adenovirus-mediated gene transfer. Down-regulation of the HIF-1α protein enhanced hypoxia-mediated tumor cell apoptosis in vitro. Subcutaneous tumor growth was also prevented from cells with attenuated HIF-1α expression. In addition, intratumoral injection of adenovirus encoding the HIF-1α-targeted small interfering RNA had a small but significant effect on tumor growth when combined with ionizing radiation. Therefore, our results provide proof of HIF-1α as an effective target for anticancer therapy. They also suggest that an adenovirus-based small interfering RNA gene transfer approach may be a potentially effective adjuvant strategy for cancer treatmen
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【期刊论文】A Novel Conditionally Replicative Adenovirus Vector Targeting Telomerase-Positive Tumor Cells
王和, Qian Huang, , Xiuwu Zhang, He Wang, Bin Yan, John Kirkpatrick, Mark W. Dewhrist, and Chuan-Yuan Li
Vol. 10, 1439-1445, February 15, 2004,-0001,():
-1年11月30日
Purpose: To develop a novel conditionally replicative adenovirus vector that targets telomerase-positive cancer cells. Experimental Design: A telomerase gene-derived promoter was used to control the expression of the E1a gene so that the E1a gene is only expressed in telomerase-positive tumor cells. In addition, a reporter gene was also engineered into the vector so that its infection and replication can be monitored easily. Results: A novel recombinant adenovirus vector that could selectively replicate in telomerase-positive cancer cells was made successfully. This vector showed active replication in a panel of cancer cells and minimal replication in normal human fibroblast or epithelial cells. The recombinant vector could effectively lyse various cultured tumor cells even at very low multiplicity of infection. The replication efficiency in tumor cells is over 103-fold more than normal fibroblast and epithelial cells. In s.c. tumor models, the newly developed telomerase-selective adenovirus vectors exhibited significantly more virus replication and reporter gene expression. Conclusions: The telomerase-targeted adenovirus vector has significant potential as an oncolytic virus as well as a tumor-specific therapeutic gene delivery vehicle.
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王和, Yong Wang, He Wang, Chuan-Yuan Li, and Fan Yuan
Mol Cancer Ther 2006; 5 (2): 362-6,-0001,():
-1年11月30日
Recent studies have shown that up to 90% of viral vectors could disseminate to normal organs following intratumoral infusion. The amount of dissemination might be dependent on the infusion conditions. Therefore, we investigated the effects of infusion rate, volume, and dose on transgene expression in liver and tumor tissues after intratumoral infusion of an adenoviral vector encoding luciferase. Luciferase expression was determined through bioluminescence intensity measurement. We observed that the luciferase expression in the liver was independent of the infusion rate but increased with the infusion dose, whereas the luciferase expression in the tumor was a bell-shaped function of the infusion rate. The latter observation was consistent with the distribution pattern of Evans blue-labeled albumin after its solution was infused into tumors at the same infusion rates. We also observed that the infusion volume could affect luciferase expression in the tumor but not in the liver. These observations implied that virus dissemination was determined mainly by the infusion dose, whereas the amount of transgene expression in the tumor depended on the distribution volume of viral vectors in the tumor as well as the infusion dose.
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