狄文
妇科肿瘤的发病机理,肿瘤化疗的耐药机制及肿瘤治疗的新方法等。
个性化签名
- 姓名:狄文
- 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
- 职称:-
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学科领域:
妇产科学
- 研究兴趣:妇科肿瘤的发病机理,肿瘤化疗的耐药机制及肿瘤治疗的新方法等。
狄文,教授,主任医师,医学博士,博士生导师。1984年毕业于上海医科大学。现任上海交通大学医学院附属仁济医院妇产科主任、上海交通大学医学院妇产科学系主任、上海交通大学医学院妇产科学研究所副所长、中华医学会妇产科学分会副主任委员、上海医学会妇产科学分会副主任委员、上海抗癌协会妇科肿瘤专业委员会副主任委员、中华医学会妇科肿瘤学会委员、中国医师协会妇产科医师分会常委、上海市产科质量控制专家委员会委员。《上海医学》副主编、《中华妇产科杂志》、《现代妇产科进展》、《实用妇产科杂志》、《中华妇幼临床医学杂志》、《国外医学-妇幼保健分册》编委,《中国实用妇科与产科杂志》、《国外医学-计划生育分册》常务编委。全国五年制、七年制、八年制医学教材《妇产科学》编委。1998年狄文教授被入选 “上海市卫生系统百名跨世纪优秀学科带头人”培养计划,2008年入选上海市科委优秀学科带头人培养计划,2009年入选上海交通大学医学院优秀学科带头人培养计划。
早在90年代初期,狄文教授在妊娠合并系统性红斑狼疮的基础和临床研究中,打破了SLE妇女不能妊娠的禁区,使得许多许多SLE 女性患者也拥有了作一个母亲的权利和幸福。其医疗成果也具有了深远的社会价值。其研究成果曾获得上海市青年科技博览会铜奖,第二届全国妇产科青年优秀论文二等奖等奖项,并通过了上海市卫生局组织的科技鉴定,专家们认为其研究达到国际先进水平。2009年和仁济医院风湿病科合作获得国家科技进步二等奖。作为上海市产科心脏病监护中心的成员,狄文教授在妊娠合并心脏病、心衰的诊治上具有丰富的临床经验,心脏病监护中心吸引了华东地区许多患严重心脏病的孕妇前来就诊,效果显著,中心多次获得上海市卫生局表扬。狄文教授曾在美国作为期三年的博士后研究,专攻肿瘤分子生物学研究,其研究成果“维甲酸感应基因启动子”的研究获得1998年世界议会基金奖。由其领衔的仁济医院妇产科肿瘤小组近年来在妇科肿瘤的综合诊治方面取得了显著成绩。进一步规范和完善了肿瘤患者的手术指征、手术方式及手术后的化疗方案,使其5年生存率大大提高。有关上皮性卵巢癌的转移及其耐药机制和靶向治疗的系列研究获得2008年上海医学科技二等奖、2009年教育部科技进步二等奖、上海市科技进步三等奖。
科研上,狄文教授目前承担国家自然基金项目级多项市级以上科研课题,内容涉及妇科肿瘤的发病机理,肿瘤化疗的耐药机制及肿瘤治疗的新方法等。科研项目保持与世界发展潮流同步,项目先进、内容丰富,研究成果达国内领先水平,带动了本科室的科研发展,推动了整个妇产科学界的学术发展。在国外杂志、国家核心杂志发表论文100余篇。主编、参编专著十余部。曾获国家科技进步二等奖、教育部科技进步二等奖、上海市科技进步三等奖、上海医学二等奖。
至今已培养博士研究生4名,硕士研究生12名。目前在读研究生18人。2005年荣获“宝钢优秀教师奖”,荣获2007年第三届上海市高等学校名师奖、2007年上海市育才奖、2005~2007年度上海交通大学“师德标兵”、2007年上海交通大学名师奖、2007年上海交通大学医学院“院长奖”、2009年获得上海交通大学最受学生欢迎的老师。狄文教授主编的双语教材《妇产科学》获得2009年上海交通大学优秀教材特等奖。
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【期刊论文】CLINICAL DIAGNOSIS AND TREATMENT OF SMALL OVARIAN TUMOR IN POSTMENOPAUSAL WOMEN
狄文, WU Zhen-ming, DI Wen*
Chinese Journal of Cancer Research 18(3): 229-234, 2006,-0001,():
-1年11月30日
Objective: To investigate the clinical symptom, ultrasonographic scan finding, serum CA125 value, histopathological type and treatment of small ovarian tumor (<5 cm) in postmenopausal women. Methods: Retrospective analysis was carried out for 52 clinical materials of ovarian tumor cases in women more than one year after menopausal between Jan 1997 and Dec 2004. The largest diameter of the ovarian mass is less than 5 cm. Results: There were 11 ovarian cancers and 1 borderline ovarian tumor among 52 small ovarian tumors (23.1%). 10 ovarian cancers were epithelial neoplasms and 2 were sex cord-stromal tumors, and 8 cases were in late stage according to FIGO staging system (33.3%). Compared with benign tumor, there is no significant difference in the onset age, interval after menopausal and duration of history. The main clinical feature is abdominal symptoms, such as abdominal pain and distension in the malignant cases. The patients with benign tumors often showed the ovarian mass during the annual screening or admitted into hospital for other causes. The ultrasonography finding and serum CA125 level showed much difference between benign and malignant cases. Unilocular smooth-walled ovarian cysts mostly were found in benign tumor and the CA125 values were always less than 35 U/ml; but the solid or complex sonographic structures (multilocular, or with a papillary projections on the wall) often indicated a high risk of cancer, especially there was ascites in the pelvic cavity. Serum CA125 level in many cancer cases was elevated (>35 U/ml), over 300 U/ml in more than half of the patients. Surgery is still the first choice to treat ovarian cancer, and chemotherapy would be an auxiliary method. Till now, 3 ovarian cancer patients died of complications of cancer and 2 cases had recurrence. Conclusion: Small ovarian tumor in postmenopausal women has a comparatively low malignant occurrence but more in later stage. Many are epithelial carcinoma. If there is complex or parenchymal sonographic structure accompanied with a high serum CA125 level, operation should be considered, while it can be followed up when the ultrasound shows a smooth cyst with normal CA125 value.
Ovarian tumor, Postmenopausal, CA125, Ultrasonography
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狄文, Cong Cao a, b, Shan Lu a, Alex Sowa a, Rebecca Kivlin a, Ashley Amaral a, Wenming Chu b, Hui Yang c, Wen Di c, *, Yinsheng Wan a
Cancer Letters 266(2008)249-262,-0001,():
-1年11月30日
Over-expression of EGFR, as in most cases of ovarian cancer, is associated with advanced-stage disease and poor prognosis. Activation of EGFR signaling pathway is involved in increased cell proliferation, angiogenesis, metastasis and decreased apoptosis. Tyrosine kinase activity is essential for signal transduction and receptor down-regulation. However, we found in this study that tyrosine kinase activity is not necessary in ligand-induced EGFR down-regulation in ovarian cancer cell line CaOV3 cells. EGFR tyrosine kinase inhibitors, such as PD153035, AG1478, as well as non-specific tyrosine kinase inhibitor PP2 cannot reverse EGF-induced down-regulation of EGFR. These findings thus permit us to develop the following exciting but unconventional strategy to sensitize cancer cells, namely, by priming ovarian cancer cells with EGF and EGFR inhibitor PD153035, before chemotherapy. This priming procedure down-regulates EGFR without induction of mitogenic signals such as ERK and PI3K/AKT. EGF plus EGFR inhibitor-primed ovarian cancer cells display increased sensitivity to taxol-induced cell death, resistant to EGF-induced cell migration and cell proliferation as well as ERK and PI3K/AKT activation. Further studies showed that PD153035, which does not reverse ligand-induced EGFR down-regulation, blocks EGF-induced EGFR activation as well as EGFR’s binding to c-cbl and Grb2. Taken together, we contend that priming with EGFR inhibitors plus EGF inhibits cell signaling pathways leading to cell proliferation and survival, while down-regulating EGFR. This priming approach sensitizes ovarian cancer cells and would ultimately result in better chemotherapeutical outcome.
EGF, EGFR inhibitor, Down-regulation, Tyrosine kinase, Ovarian cancer
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