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Suhyun Oh,김영관,Ji Hoon Seo,이금희,윤승수 대한화학회 2011 Bulletin of the Korean Chemical Society Vol.32 No.5
Blue fluorescent materials based on 9,9'-diethyl-2-diphenylaminofluorene derivatives were synthesized and characterized. These materials were used as the blue dopant materials for the emitting layer of organic lightemitting diode devices with the following device structure: ITO/DNTPD (40 nm)/NPB (20 nm)/MADN:dopants (2%, 20 nm)/Alq_3 (40 nm)/Liq (1.0 nm)/Al. All devices exhibited highly efficient blue emission. One of these devices exhibited a maximum luminance, luminous efficiency, power efficiency and CIE x, y coordinates of 8400 cd/m^2, 8.10 cd/A at 20 mA/cm^2, 3.36 lm/W at 20 mA/cm^2 and (0.151, 0.159), respectively. A deep blue device with CIE coordinates of (0.152, 0.139) showed the maximum luminance, luminous efficiency and power efficiency of 8630 cd/m^2, 6.31 cd/A at 20mA/cm^2 and 2.62 lm/W at 20 mA/cm^2,respectively
Targeting Cyclin D-CDK4/6 Sensitizes Immune-Refractory Cancer by Blocking the SCP3–NANOG Axis
Oh, Se Jin,Cho, Hanbyoul,Kim, Suhyun,Noh, Kyung Hee,Song, Kwon-Ho,Lee, Hyo-Jung,Woo, Seon Rang,Kim, Suyeon,Choi, Chel Hun,Chung, Joon-Yong,Hewitt, Stephen M.,Kim, Jae-Hoon,Baek, Seungki,Lee, Kyung-Mi American Association for Cancer Research 2018 Cancer Research Vol.78 No.10
<P>These findings reveal cyclin D1-CDK4/6 inhibition as an effective strategy for controlling SCP3<SUP>high</SUP> immune-refractroy cancer.</P><P>Immunoediting caused by antitumor immunity drives tumor cells to acquire refractory phenotypes. We demonstrated previously that tumor antigen–specific T cells edit these cells such that they become resistant to CTL killing and enrich NANOG<SUP>high</SUP> cancer stem cell-like cells. In this study, we show that synaptonemal complex protein 3 (SCP3), a member of the Cor1 family, is overexpressed in immunoedited cells and upregulates NANOG by hyperactivating the cyclin D1–CDK4/6 axis. The SCP3–cyclin D1–CDK4/6 axis was preserved across various types of human cancer and correlated negatively with progression-free survival of cervical cancer patients. Targeting CDK4/6 with the inhibitor palbociclib reversed multiaggressive phenotypes of SCP3<SUP>high</SUP> immunoedited tumor cells and led to long-term control of the disease. Collectively, our findings establish a firm molecular link of multiaggressiveness among SCP3, NANOG, cyclin D1, and CDK4/6 and identify CDK4/6 inhibitors as actionable drugs for controlling SCP3<SUP>high</SUP> immune-refractory cancer.</P><P><B>Significance:</B> These findings reveal cyclin D1-CDK4/6 inhibition as an effective strategy for controlling SCP3<SUP>high</SUP> immune-refractroy cancer. <I>Cancer Res; 78(10); 2638–53. ©2018 AACR</I>.</P>