http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Lee, Hyun Joo,Lee, Woo Kyung,Kang, Chan Woo,Ku, Cheol Ryong,Cho, Yoon Hee,Lee, Eun Jig Elsevier 2018 Cancer letters Vol.417 No.-
<P><B>Abstract</B></P> <P>The RB-E2F1 pathway is an important mechanism of cell-cycle control, and deregulation of this pathway is one of the key factors contributing to tumorigenesis. Cyclin-dependent kinases (CDKs) and Cyclin D have been known to increase in aggressive thyroid cancer. However, there has been no study to investigate effects of a selective CDK 4/6 inhibitor, Ribociclib (LEE011), in thyroid cancer. Performing Western blotting, we found that RB phosphorylation and the expression of Cyclin D are significantly higher in papillary thyroid cancer (PTC) cell lines as well as anaplastic thyroid cancer (ATC) cell lines, compared with normal thyroid cell line and follicular thyroid cancer cell line. LEE011 dose-dependently inhibited RB phosphorylation and also decreased the expressions of its target genes such as <I>FOXM1, Cyclin A1,</I> and <I>Myc</I> in ATC. Furthermore, LEE011 induced cell cycle arrest in G0-G1 phase and cell apoptosis, and inhibited cell proliferation in ATC. Consistently, oral administration of LEE011 to ATC xenograft models strongly inhibited tumor growth with decreased expressions of pRB, pAKT and Ki-67, and also significantly increased tumor cell apoptosis. Taken together, our data support the rationale for clinical development of the CDK4/6 inhibitor as a therapy for patients with aggressive thyroid cancer.</P> <P><B>Highlights</B></P> <P> <UL> <LI> pRB and Cyclin D were expressed high in aggressive thyroid cancer. </LI> <LI> LEE011 suppressed pRB and also decreased the expressions of its target genes in ATC. </LI> <LI> LEE011 induced cell cycle G1 arrest and apoptosis, and inhibited cell proliferation. </LI> <LI> LEE011 inhibited in vivo tumor growth with decreased expressions of pRB and Ki-67. </LI> <LI> We could explain the anticancer effects with the RB-E2F pathway. </LI> </UL> </P>
다낭성 난소증후군 환자에서 L - dopa 및 Pyridostigmine 자극에 대한 성장호르몬 분비
이경미,배희동,이병석,허갑범,이현철,임승길,이은직,김경래,정윤석,박기현 대한내분비학회 1993 Endocrinology and metabolism Vol.8 No.3
Polycystic ovary syndrome (PCOS) is the combination of ovulatory failure, infertility, hirsutism, obesity, bilateral polycystic ovaries and large numbers of endocrine dysfunctions. In 12 women with PCOS and 9 control women with regular cycle, the Ghrespose to L-dopa and insulin response to oral glucose tolerence test were investigated. In PCOS, L-dopa test with phridostigmine pretreatment was also performed. GH response and GH response area under the curve(AUC) to L-dopa were significantly lower in PCOS (basal(ng/ml), maximum(ng/ml), GH resonse AUC(ng/mlxh), 0.5±0.2, 1.6±0.7, 2.1±0.7) than those(1.4±0.2, 6.9±1.1, 9.7±1.0) of controls (p$lt;0.05). Pyridostigmine pretreatment had significantly enbhanced the GH response to L-dopa (1.4±0.4, 7.7±1.3, 9.6±1.4) in PCOS (p$lt;0.05). Insulin response (uU/ml) and insulin response AUC (uU/mlxh) to glucose load were significantly higher in PCOS(8.0±1.8, 142.1±59.5, 1`94.3±73.7) than those (5.3±1.2, 24.9±2.6, 35.9±2.8) of controls(p$lt;0.05). Plasma IGF-1 levels of ug/L) were significantly higher than controls(287.3±27.1) (p$lt;0.05). BMI had a positive correlation with insulin response AUC (p$lt;0.01). Insulin respponse AUC had a positive correlation with plasma IGF-1 levels (p$lt;0.001) but inverse correlation with GH response AUC in PCOS and controls(p$lt;0.05). These data suggest that decreased GH secretion of PCOS may be associated with a high somatostatin activity and a high plasma IGF-1 level (J Kor Soc Endocrinol 8: 265~272, 1993)
Lee, Eun Jig,Ahn, Jung Yong,Noh, Taewoong,Kim, Se Hun,Kim, Tai Seung,Kim, Sun Ho WilliamsWilkins Co 2009 Neurosurgery Vol.64 No.3
<P>The microsurgical pseudocapsule can be found in the transition zone between an adenoma and the surrounding normal pituitary tissue. We investigated the precise histology of the pseudocapsule. Furthermore, we evaluated the remission rate, the changes in pituitary function, and the recurrence rate after intensive resection of the pseudocapsule.</P>
이경미,박기현,이병석,허갑범,이현철,임승길,이은직,김경래,정윤석,남문석 대한내분비학회 1993 Endocrinology and metabolism Vol.8 No.2
Bone minearal density (BMD) is generally known to decrease with age, especially in postmenoopausal women. We examined the correlation between the body composition and BMD with dual energy x-ray absorptiometry (DEXA) in 36 premenopausal and 96 postmenopausal women. There were no statistical differences in total lean body mass (TLBM), total body fat mass(TBRM) and % body fat between pre-and body mass index(BMI), but no correlation with TBFM. In postmenopausal women, BMD had a negative correlation with age and postmenopausal period, but positive correlation with BMI, TBRM and TLBM by simple regression analysis. Multiple regression analysis revealed that positive correlation was found between TBFM and BMD of lumbar spine and femoral neck in postmenopausal women but not in premenopausal women. We concluded that TBFM in postmenopausal women is an iportant factor in maintaining the BMD, however the mechanism unerlying this relationship will be further clarified. (J Kor Soc Endocrinol 8: 180~186, 1993)
Absence of activating mutations of <i>CXCR4</i> in pituitary tumours
Lee, Yong-ho,Noh, Tae Woong,Lee, Mi Kyung,Jameson, J. Larry,Lee, Eun Jig Blackwell Publishing Ltd 2010 Clinical endocrinology Vol.72 No.2
<P>Summary</P><P>Objective </P><P>Mutations of the <I>gsp</I> oncogene are responsible for 30–40% of GH-producing pituitary adenomas and 10% of nonfunctioning pituitary adenomas (NFPAs). However, the pathogenetic mechanism of the remaining pituitary tumours still remains to be identified. Recently, the interaction between the chemokine stromal cell-derived factor 1 and its receptor CXCR4 was found to play an important role in GH production and cell proliferation in various pituitary adenoma cell lines. As CXCR4 is a Gi-coupled chemokine receptor, its constitutive activating mutations may be involved in pituitary tumour formation by cyclic adenosine monophosphate (cAMP)-independent, ERK-related pathways.</P><P>Patients and methods </P><P>We investigated whether somatic activating-mutations of <I>CXCR4</I> might be a possible tumourigenic mechanism for <I>gsp</I>-negative GH-secreting pituitary adenomas and NFPAs. Direct sequencing of polymerase chain reaction-amplified products for coding exons of <I>CXCR4</I> were performed using genomic deoxyribonucleic acid samples from 37 GH-producing pituitary tumour tissues that were negative for the <I>gsp</I> mutation and 14 CXCR4 expressing NFPAs.</P><P>Results </P><P>Immunohistochemical analyses and double immunofluorescent staining of sectioned paraffin-embedded pituitary tissues revealed that CXCR4 is highly expressed in GH-producing pituitary adenomas and NFPAs. Direct sequencing showed that two synonymous mutations in exon 2 (87 C > T and 414 C > T) were detected in 4 out of 51 pituitary tumours.</P><P>Conclusion </P><P>Our results indicate that an activating mutation of the <I>CXCR4</I> may not be a common pathogenetic mechanism in GH-producing pituitary tumours and NFPAs.</P>
Lee, Sung Jun,Rim, Tyler Hyung Taek,Jang, Sun Young,Kim, Chan Yun,Shin, Dong Yeob,Lee, Eun Jig,Lee, Sang Yeul,Yoon, Jin Sook Springer-Verlag 2013 Graefe’s archive for clinical and experimental oph Vol.251 No.1
<P>To evaluate the efficacy of subconjunctival triamcinolone injection for treating upper eyelid retraction caused by thyroid-associated ophthalmopathy (TAO).</P>
KSR1 is coordinately regulated with Notch signaling and oxidative phosphorylation in thyroid cancer
Lee, Jandee,Seol, Mi-Youn,Jeong, Seonhyang,Kwon, Hyeong Ju,Lee, Cho Rok,Ku, Cheol Ryong,Kang, Sang-Wook,Jeong, Jong Ju,Shin, Dong Yeob,Nam, Kee-Hyun,Lee, Eun Jig,Chung, Woong Youn,Jo, Young Suk Journal of Endocrinology (Ltd. by Guarantee) 2015 Journal of molecular endocrinology Vol.54 No.2
<P>Kinase suppressor of RAS1 (KSR1) is a scaffold protein implicated in RAS-mediated RAF activation. However, the molecular function of KSR in papillary thyroid cancer (PTC) is unknown. Thus, this study aimed to characterize the role of KSR1 in patients with PTC. qRT-PCR and immunohistochemistry (IHC) revealed inter-tumor heterogeneities in the expression of KSR1 in PTC tissues. Interestingly, BRAFV600E-positive PTC showed higher <I>KSR1</I> mRNA expression than BRAFV600E-negative PTC (<I>P</I><0.001). Gene Set Enrichment Analysis (GSEA) using public repositories showed that high KSR1 expression coordinately upregulated Notch signaling (nominal <I>P</I>=0.019, false discovery rate (FDR) <I>q</I>-value=0.165); this finding was supported by GeneNetwork analysis, indicating that <I>KSR1</I> expression is positively correlated with <I>NOTCH1</I> expression (<I>ρ</I>=0.677, <I>P</I>=6.15×10<SUP>−9</SUP>). siRNA against KSR1 (siKSR1) significantly decreased ERK phosphorylation induced by BRAFV600E, resulting in reduced expression of <I>NOTCH1</I> and <I>HES1</I>, targets of Notch signaling. GSEA revealed that high KSR1 expression was also associated with downregulation of genes related to oxidative phosphorylation (OxPhos). Consistent with this, electron microscopy showed that PTCs with high KSR1 expression exhibited structural defects of the mitochondrial cristae. Furthermore, siKSR1-transfected BCPAP and 8505C cells generated fewer colonies in colony-forming assays. In addition, GSEA showed that high expression of KSR2 and connector enhancer of KSR1 (CNKSR1) also coordinately upregulated Notch signaling (KSR2: nominal <I>P</I>=0.0097, FDR <I>q</I>-value=0.154 and CNKSR1: nominal <I>P</I><0.0001, FDR <I>q</I>-value=0.00554), and high CNKSR2 was associated with downregulation of the OxPhos gene set (nominal <I>P</I><0.0001, FDR <I>q</I>-value <0.0001). In conclusion, KSR1 is coordinately regulated with Notch signaling and OxPhos in PTC, because its scaffold function might be required to sustain the proliferative signaling and metabolic remodeling associated with this type of cancer.</P>