http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : ( David T Maclaughlin ) (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
-
David T. MacLaughlin 가톨릭중앙의료원 가톨릭암센터 1994 암심포지움 Vol.- No.1
It has been a long standing hypothesis of the Pediatric Research Laboratories and it's Director Professor Paticia K. Donahoe, that MIS, a fetal regressor of Müllerian tissue, could be useful to treat tumors of Müllerian origin in the auld. In particular, attention has focused on ovarian cancers which exhibit an overall poor survival. Our laboratory has developed a number of in vitro and ex vivo models to test this hypothesis using human tumor cell lines and biologically active recombinant human MIS preparation. Evidence to date supports the conclusion that MIS needs to be proteolytically processed to be active and that it appears to be a non-toxic agent capable of blocking cells in the G0/G1 phase of the cell cycle. MIS action is mediated by binding to it's receptor on the cell surface followed by the inhibition of dpidermal growth factor, EGF, receptor-autophosphorylation. Current work suggests that MIS blocks EGF receptor activation via stimulating a tyrosine phosphatase. In summarizing these studies we hope to convey our conclusions that MIS remains a candidate for future study as a novel chemotherapeutic.
-
( Jang Heub Kim ),( David T Maclaughlin ),( Patricia K Donahoe ) 대한산부인과학회 2014 Obstetrics & Gynecology Science Vol.57 No.5
Mullerian inhibiting substance (MIS), also called anti-Mullerian hormone (AMH), is a member of the transforming growth factor-β super-family of growth and differentiation response modifiers. It is produced in immature Sertoli cells in male embryos and binds to MIS/AMH receptors in primordial Mullerian ducts to cause regression of female reproductive structures that are the precursors to the fallopian tubes, the surface epithelium of the ovaries, the uterus, the cervix, and the upper third of the vagina. Because most gynecologic tumors originate from Mullerian ductderived tissues, and since MIS/AMH causes regression of the Mullerian duct in male embryos, it is expected to inhibit the growth of gynecologic tumors. Purified recombinant human MIS/AMH causes growth inhibition of epithelial ovarian cancer cells and cell lines in vitro and in vitro via MIS receptor-mediated mechanism. Furthermore, several lines of evidence suggest that MIS/AMH inhibits proliferation in tissues and cell lines of other MIS/AMH receptor-expressing gynecologic tumors such as cervical, endometrial, breast, and in endometriosis as well. These findings indicate that bioactive MIS/AMH recombinant protein should be tested in patients against tumors expressing the MIS/AMH receptor complex, perhaps beginning with ovarian cancer because it has the worst prognosis. The molecular tools to identify MIS/AMH receptor expressing ovarian and other cancers are in place, thus, it is possible to select patients for treatment. An MIS/AMH ELISA exists to follow administered doses of MIS/AMH, as well. Clinical trials await the production of sufficient supplies of qualified recombinant human MIS/AMH for this purpose.
-
Nam, Suk Woo,Jo, Yun Sung,Eun, Jung Woo,Song, Jae Yen,Ryu, Ki Sung,Lee, Jung Young,Lee, Joon Mo,Maclaughlin, David T,Kim, Jang Heub D.A. Spandidos 2009 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.23 No.5
<P>The purpose of this study was to investigate the large-scale characteristic molecular signature of Müllerian inhibiting substance (MIS) in human ovarian cancer cells through expression genomics. To understand the comprehensive molecular mechanisms by which MIS inhibits ovarian cancer cell growth, we identified the large-scale characteristic molecular changes elicited by MIS in the human ovarian cancer cell line OVCAR-8, using DNA microarray analysis. Combined serial gene expression analysis from 0 to 96 h after MIS treatment of OVCAR-8 cells resulted in 759 genes which showed at least a 2-fold change in overexpression or underexpression compared to non-treatment groups. Of the 759 outlier genes, 498 genes were mapped to known biological cellular processes, and the resultant major pathways included metabolism, signal transduction, cell growth and apoptosis. Among these pathways, 68 genetic elements were dissected as cell cycle-related genes induced by MIS. Although cellular phenotypic changes by MIS were observed after 24 h of treatment, the characteristic large-scale molecular changes were observed from 48 to 96 h of exposure to MIS. This finding may imply that the suppressive role of MIS on ovarian cancer cells could be cumulative in that the metabolic disturbance of MIS is followed by arrest at the G1/S cell cycle checkpoint. We suggest 759 outlier genes comprise the characteristic molecular signature of MIS, which may be responsible for the suppressive effect on OVCAR-8 cells. Although the precise biological mechanisms underlying these outlier genes should be validated, the genetic elements described herein provide promising therapeutic interventions for ovarian cancer.</P>
KISS연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
