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- 저자 : ( Joomyung Sung ) (검색결과 2 건)
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( Yeji Han ),( Eunmi Nam ),( Kyungeun Lee ),( Youngchul Moon ),( Joomyung Sung ),( Kyungmin Cho ),( Jungeun Choi ),( Jooyoung Kim ) 대한내과학회 2014 대한내과학회 추계학술발표논문집 Vol.2014 No.1
Background: Posterior reversible encephalopathy syndrome (PRES) is known to have symptoms of headache, visual disturbances, altered consciouseness and seizures, which can be result of acute hypertension, eclampsia, renal failure and the use of immunosuppressive or cytotoxic agents. We report a case of PRES ocurred as a result of FOLfiRI (irinotecan, 5-FU) chemotherapy in metastatic colorectal cacer/ Case Report: A 51-year old male with diagnosed of rectal cancer with liver metastasis, underwent an a low anterior resection on April,19, 2013.After operation, he has XELOX (capecitabine, oxaliplatin) as palliative chemotherapy. After sixth XELOX chemotherapy, chemotherapy as change of disease progression. When FOLfiRI chemotherapy administered, suddenly he appeared to have partial seizure with sudden eyeball deviation . The infusion of chemotherapy was stopped immediately ,he had treatment with anticonvulsants, such as phenytoin, levetiracetam. The brain MRI showed that white matter change in the bilateral occipital lobe, supported the diagnosis of PRES. The conservative treatment was continued for several days. After few days, the patient recovered from symptom and after that, he had chemotherapy XELOX and bevacizumab instead of FOLfiRI. The brain MRI after six months did not show any previous lesion, he is currently well being followed up as an outpatient. Conclusion: There are no known reports of the association between PRES and FOLfiRI chemotherapy.We postulate that FOLfiRI chemotherapy can disrupt the normal endothelial function of the brain leading to the development of PRES.
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Kim, Hyunkyung,Kim, Dongha,Choi, Seon Ah,Kim, Chang Rok,Oh, Se Kyu,Pyo, Ki Eun,Kim, Joomyung,Lee, Seung-Hoon,Yoon, Jong-Bok,Zhang, Yi,Baek, Sung Hee National Academy of Sciences 2018 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.115 No.46
<P><B>Significance</B></P><P>An aberrant covalent histone modification which drives dysregulation of transcriptional program is related to human diseases such as cancer. Thus, identifying signaling pathways modulating transcription factors and epigenetic enzymes are coming into view as attractive therapeutic targets. In this study, we provide evidence that KDM3A is tyrosine-phosphorylated by JAK2, and tyrosine-phosphorylated KDM3A acts as a coactivator for STAT3, thereby exerting increased cancer cell growth and motility. We propose that JAK2-dependent tyrosine phosphorylation of KDM3A could be a potential therapeutic target for epigenetic control of oncogenic effect governed by JAK2−STAT3 signaling pathway.</P><P>Janus tyrosine kinase 2 (JAK2)−signal transducer and activator of transcription 3 (STAT3) signaling pathway is essential for modulating cellular development, differentiation, and homeostasis. Thus, dysregulation of JAK2−STAT3 signaling pathway is frequently associated with human malignancies. Here, we provide evidence that lysine-specific demethylase 3A (KDM3A) functions as an essential epigenetic enzyme for the activation of JAK2−STAT3 signaling pathway. KDM3A is tyrosine-phosphorylated by JAK2 in the nucleus and functions as a STAT3-dependent transcriptional coactivator. JAK2−KDM3A signaling cascade induced by IL-6 leads to alteration of histone H3K9 methylation as a predominant epigenetic event, thereby providing the functional and mechanistic link between activation of JAK2−STAT3 signaling pathway and its epigenetic control. Together, our findings demonstrate that inhibition of KDM3A phosphorylation could be a potent therapeutic strategy to control oncogenic effect of JAK2−STAT3 signaling pathway.</P>
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