10月13-16日，第14届国际妇科肿瘤学会双年会（IGCS 2012）在加拿大温哥华举行。IGCS 2012一如既往地为参会者奉上妇科肿瘤学领域最新研究进展，提供发布、讨论和争辩最新科学信息的良机。金宝搏网站登录技巧 对本届年会进行了专题报道（http://zt.cmt.com.cn/zt/igcs2012/index.html）。

研究摘要：

Enhancement of the Cyclooxygenase 2YProstaglandin E2
Axis by Activated Lymphocytes Promotes the Activity
of Myeloid-Derived Suppressor Cells in Patients With
Ovarian Cancer
J Wong1, N Obermajer1, R Muthuswamy1, K Odunsi2, RP
Edwards3-5, P Kalinski1,5
1Department of Surgery, University of Pittsburgh, Pittsburgh,
PA; 2Department of Gynecologic Oncology and Immunology,
Roswell Park Cancer Institute, Buffalo, NY; 3Magee-Womens
Research Institute Ovarian Cancer Center of Excellence,
Pittsburgh, PA; 4Peritoneal/Ovarian Cancer Specialty Care
Center, Hillman Cancer Center, University of Pittsburgh,
5University of Pittsburgh Cancer Institute, Pittsburgh, PA;
University Pittsburgh School of Medicine, Pittsburgh, PA.
Background: Myeloid-derived suppressor cells (MDSCs)
are crucial contributors to tumor environment-associated
immune suppression, representing a key mechanism for tumor
progression and a significant barrier to effective immunotherapy.
Methods and Results:We demonstrate that the development,
accumulation, and persistent suppressive functions ofCD11b +
CD14 + CD33 + CD34 + CXCR4 + MDSCs in the tumor
ascites of patients with ovarian cancer critically depend on the

positive feedback between the tumor-associated inflammatory
mediator prostaglandin E2 (PGE2) and cyclooxygenase 2
(COX2), the key regulator of PGE2 synthesis. We further
demonstrate that activated T cells andNKcells enhanceMDSC
activity within the ovarian cancer environment through interferon
gammaYdependent activation of the COX2-PGE2 axis.
Inhibition of the COX2-PGE2 axis was capable of reversing
MDSC-associated immune suppression and the hyperactivation
of MDSCs by activated T cells and NK cells.
Conclusion: These data reveal the central importance of
COX2-PGE2 feedback in supporting MDSCs within the
human ovarian cancer environment and provide strong rationale
for the therapeutic targeting of PGE2 signaling in promoting
spontaneous and therapy-induced immune responses
in patients with ovarian cancer.