정재욱

인사말

정재욱교수

전문분야 |  분자생식생리학
여성질환동물모델
Uterine Biology & Maternal Fetal Interactions
Endometriosis and Infertility

E – mail | jeongj@msu.edu

학력

고려대학교 공학사
고려대학교 이학박사

주요경력

미국베일러의과대학, 박사후연구원
미국베일러의과대학, 조교수
미국미시간주립대학, 부교수
서울대 농업생명과학대학, 겸임교수

주요연구내용

Normal endometrial function requires a balance of progesterone (P4) and estrogen (E2) effects. An imbalance caused by increased E2 action and/or decreased P4 action can result in abnormal endometrial proliferation and, ultimately, endometrial adenocarcinoma, the fourth most common cancer in women. Jeong’s laboratory has special interests in research relating to women’s health, particularly infertility and cancer using genetically engineered mouse models. We have identified mitogen-inducible gene 6 (Mig-6) as a down stream target of progesterone receptor (PR) action in the uterus. Mig-6 plays a critical role in the regulation of uterine function and the development of endometrial hyperplasia and cancer in the presence of steroid hormones. Importantly, the observation that endometrial carcinomas from women have a significant reduction in MIG-6 expression provides compelling support for an important growth regulatory role for Mig-6 in the uterus of both humans and mice. This demonstrates that Mig-6 is a critical regulator of the response of the endometrium to steroid hormones in regulating tissue homeostasis. Furthermore, this identifies a PR/Mig-6 regulatory pathway that is critical for the suppression of endometrial cancer. Current studies are aimed at the application of these genetic model systems to further study and understand the role of steroid hormone in women cancers, with the ultimate goal of developing therapies effective against tumors. These studies have broader implications for clinical application because of the benefits of animal models of translational research in women cancer.

[논문]

http://www.ncbi.nlm.nih.gov/sites/myncbi/1NGTVcAy2Q5/bibliography/40251047/public/?sort=date&direction=ascending