郑文新
基于WHO疾病分类的诊断标准的建立,分子病理学的发展以及组织库的建立
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- 姓名:郑文新
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学术头衔:
博士生导师
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学科领域:
病理学
- 研究兴趣:基于WHO疾病分类的诊断标准的建立,分子病理学的发展以及组织库的建立
郑文新,兼职杰出PI复旦大学讲座特聘教授,病理学、妇科学及肿瘤学教授,复旦大学上海医学院病理中心和病理学系主任,美国亚利桑那大学医学院分子病理和妇产科病理学主任。
郑教授1982年毕业于复旦大学上海医学院,随后作为住院医生任职于妇产科医院。其后在复旦大学完成研究生课程,主修妇科内分泌学。1986年至2000年作为博士后和副研究员在美国哥伦比亚大学从事生殖医学研究。郑教授以服务病人为己任,在 1991年于Cornell大学附属纽约医院接受病理住院医生培训。由于主修妇产科学,郑教授选择妇产科病理为其专业。1995年至1996年,接受了妇产科病理专业训练。1996年成为南加利福尼亚大学助理教授和病理主治医师,2000年任耶鲁大学副教授和妇产科病理主任,2005年任亚利桑那大学病理和妇科教授以及妇产科病理和分子病理学主任。
由于其在病理学领域的杰出成就,郑教授于2005年五月被任命为复旦大学上海医学院病理研究中心和病理学系主任。郑教授在复旦的主要目标是在未来的10年内使复旦病理成为国际认可的成员之一,统一复旦系统的所有病理资源包括8所附属医院的外科病理。在郑教授的领导下,复旦病理学目前主要致力于基于WHO疾病分类的诊断标准的建立,分子病理学的发展以及组织库的建立。复旦病理学改革在不久的将来可能对中国病理学领域产生深远影响。
郑教授是一个国际著名的妇产科病理学家。他参与过世界各地的多次妇产科病理会诊,是美国妇产科肿瘤学组织癌症预防委员会的少数成员之一,获得过多个研究基金,包括NIH RO1基金,研究卵巢、子宫内膜和子宫颈癌。郑教授的主要研究贡献包括他定义了Ⅱ型子宫内膜癌的先兆病变,提出了卵巢上皮性癌发生的激素平衡理论以及描述了子宫内膜异位的起始过程,同时也是许多权威病理学和妇科学杂志的特邀评论家。
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郑文新, Wenxin Zhenga, b, *, Peter E. Schwartzb
Gynecologic Oncology 96(2005)579-582,-0001,():
-1年11月30日
Uterine papillary serous carcinoma (UPSC) is an aggressive form of endometrial cancer, that has a dismal prognosis [1-3]. Since its etiology is virtually unknown, physicians and research scientists who battle this disease have tried to identify its precursor lesions in order to improve disease management through early detection.
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郑文新, Peter E. Schwartz, M.D.a, * and Wenxin Zheng, M.D.b
Gynecologic Oncology 90(2003)644-650,-0001,():
-1年11月30日
Objective. The objective was to determine the role of cytology in the pretreatment evaluation of women with clinical findings consistent with ovarian cancer who are being considered for neoadjuvant chemotherapy. Methods. Pretreatment cytology slides were available for review from 60 of 72 consecutive patients treated with platinum-based neoadjuvant chemotherapy who were believed to have ovarian cancer based on clinical findings. Fifty of the 72 patients had evidence of both intraabdominal and extraabdominal tumor spread prior to treatment. Fifty-three of 66 patients had CA125 values >500 U/mL, 34 being >1500 U/mL. Pretreatment cytology was compared to surgical specimens obtained following chemotherapy. Results. Cytologic findings were consistent with ovarian cancer in 55 patients, not consistent with ovarian cancer in 4 cases, and insufficient for diagnosis in one case. Forty-seven of the 60 patients underwent surgery. Forty-two of 43 patients with cytology consistent with ovarian cancer had epithelial ovarian cancers at surgery. One had no pathologic evidence of disease. Three of the 4 patients thought not to have cytology consistent with ovarian cancer underwent surgery following neoadjuvant chemotherapy. Two had ovarian epithelial cancers and one had a mesonephric adenocarcinoma. The one patient with cytology insufficient for diagnosis also had an epithelial ovarian cancer at diagnosis. Conclusions. Cytology proved to be extremely helpful in supporting the clinical impression of an apparent advanced ovarian cancer. When the cytologic diagnosis does not match the clinical impression, communication between the cytologist or pathologist and the clinician is essential.
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郑文新, Sa Wang, a, Jeffery Pudney, b, Joon Song, c, Gil Mor, Peter E. Schwartz, c and Wenxin Zhenga, *
Gynecologic Oncology 88(2003)108-117,-0001,():
-1年11月30日
Background. Successful treatment of endometrial hyperplasia with progestins is commonly accompanied by the finding of an inactive or suppressed endometrium after therapy. However, approximately 30% of the endometrial hyperplasia cases do not respond to progestins and hyperplastic glands persist. The Fas/FasL system is known to play a role in tissue remodeling as a result of changes in menstrual hormone levels. The aims of this study are to examine Fas/FasL expression in endometrial hyperplasia of pre-and postprogestin treatment samples and to study the Fas/FasL regulation in vitro with Ishikawa cells after progestin stimulation. Design. Pre-and posttreatment paraffin-embedded endometrial hyperplasia tissue samples from 26 women were examined by immunohistochemistry for changes in Fas/FasL expression related to the administration of progestins. Among 26 patients, 18 were successfully treated with progestins and 8 failed treatment. Fas/ FasL positivity was defined by the presence of 10% or more immunoreactive epithelial cells in each specimen. In positive cases, a percentage or an immunoscore of immunoreactive cells was given by counting 500 cells. Cell viability was evaluated by the MTT assay. The in vitro effects of progesterone on Fas/FasL expression and apoptosis in Ishikawa cells were examined by using Western blot and TUNEL assays, respectively. Results. Fas immunoreactivity was present in 4/26 (15%) preprogestin cases with an average of 16% of the epithelial cells expressing Fas. FasL was expressed in 21/26 (80%) pretreatment cases with an average of 42% of the hyperplastic glandular cells being positive. In postprogestin cases, an increase of Fas expression (14/18, 77%) with an average of 47% stained cells was seen in responders (P<0.001), while FasL was found in 16/18 (89%) responders with an average of 65% of cells positive (P=0.587). In nonresponders, no significant changes in Fas/FasL expression were detected compared to pretreatment samples. With in vitro Ishikawa cells, a slight increase (10–20%) of Fas and FasL protein expression was detected after 24 h of progesterone treatment, but a more significant increase (220–343%) of both Fas and FasL expression was found after 48 h of withdrawing progesterone, which parallels apoptotic activity. Conclusions. The Fas/FasL system may be involved in the development of endometrial hyperplasia. Part of the molecular mechanisms of progestin therapy for endometrial hyperplasia is through upregulation of Fas/FasL expression. Dysregulation of Fas/FasL expression in hyperplastic endometrium may be part of the molecular mechanisms for nonresponders to progestin treatment. Intermittent, rather than continuous, progestin treatment may be more effective clinically for the treatment of endometrial hyperplasia.
Endometrial hyperplasia, Progestin, Apoptosis, Fas/, FasL
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【期刊论文】Involution of PTEN-null endometrial glands with progestin therapy
郑文新, Wenxin Zheng, a, b Heather E. Baker, c and George L. Mutterc, *
Gynecologic Oncology 92(2004)1008-1013,-0001,():
-1年11月30日
Objectives. Loss of PTEN tumor suppressor gene function characterizes most (63%) endometrial precancerous lesions (endometrial intraepithelial neoplasia, EIN) and up to 83% of endometrioid endometrial cancers. Because systemic progestins are known to promote involution of precancerous endometrial lesions, we tested the hypothesis that this therapy preferentially leads to clearance of immunohistochemically detected PTEN-null endometrial glands in a variety of histopathologic settings. Methods. PTEN immunohistochemistry of pre and postprogestin-treated endometria was successfully performed on 17 women presenting with an intake endometrial biopsy diagnosis of "hyperplasia". Intake biopsies were rediagnosed using EIN criteria as 5 normal (proliferative or secretory), 4 anovulatory, 3 polyps, and 5 EIN endometria. The persistence of PTEN-null glands in progestin-treated patients was compared to that seen previously in rebiopsied normal proliferative endometrium of endogenously cycling premenopausal women. Results. Ten of 17 women prehormonal therapy had PTEN-null glands in the initial biopsy, and 90% (9/10) of these disappeared in the postprogestin sample. This contrasts with only 17% (2/12) involution in the endometria of normal cycling women (Fishers exact test P=0.002, Odds Ratio 45). Conclusions. We conclude that progestin therapy promotes involution, or disappearance, of PTEN-null endometrial glands relative to the persistence rate seen for normal cycling women. This effect occurs among PTEN-null glands having a variety of histopathologic presentations.
Endometrial hyperplasia, EIN, PTEN, Progesterone
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【期刊论文】Apoptosis May Be an Early Event of Progestin Therapy for Endometrial Hyperplasia
郑文新, Charlie A. Amezcua, M.D., *, Jean J. Lu, Juan C. Felix, †, Frank Z. Stanczyk, Ph.D., † and Wenxin Zheng, M.D.*,
Gynecologic Oncology 79, 169-176(2000),-0001,():
-1年11月30日
Objective. The aim of this study was to investigate the role of apoptosis during progestin therapy for the treatment of endometrial hyperplasia. Methods. Pre-and posttreatment paraffin-embedded endometrial tissue samples from 19 women with endometrial hyperplasia were examined for changes in glandular cellularity and apoptotic activity related to the administration of progestins. Twelve patients were successfully treated with progestin therapy and 7 patients failed treatment. Glandular cellularity was assessed based on calculating the average number of cells per gland obtained on histologic examination of hematoxylin and eosin stained tissue sections. Apoptotic activity was assessed on the same tissue sections by counting the average number of apoptotic cells per 10 high power fields (hpf) using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) assay. The effects of progesterone on apoptotic activity in a low-grade endometrial adenocarcinoma cell line (Ishikawa cells) was also examined using an ELISA cell death detection kit. Results. Glandular cellularity significantly decreased with progestin therapy in both treatment outcome groups. The reduction in cells per gland was significantly greater in the group of successfully treated cases compared to the treatment failures (P 5 0.005). However, within the successfully treated group, in situ detection of apoptotic cells using the TUNEL assay showed no statistical difference between pre-and posttreatment endometrial samples. Interestingly, a significant decrease in apoptosis was found in posttreatment samples of the group with persistent hyperplasia. The average number of apoptotic cells detected in 10 hpf was reduced from 7.9 prior to treatment to 3.1 after progestin therapy (P 5 0.03). In the progesterone-treated Ishikawa cell line, an increase in apoptotic activity started at 24 h, reached a peak at 48 h, and continued up to 72 h of hormone treatment. At 48 h, apoptotic activity was 42.6% greater than in the untreated control (P 5 0.04). By 72 h of progesterone treatment, apoptosis was 37.2% greater in the treated cells compared to the noninoculated cells (P 5 0.04). Conclusions. Progestin-induced apoptosis may occur during the early period of treatment for endometrial hyperplasia. Compared to the fully responsive group, persistent endometrial hyperplasia may have intrinsically different molecular mechanisms in response to progestin therapy.
endometrial hyperplasia, endometrial cancer, progestin, apoptosis.,
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