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S-68 A Primary Hepatic Leiomyoma in a Gastric Cancer Patient
( Sung Ju Kang ),( Suk Hyun Jang ),( Hyung Bin Yuk ),( Jang Sihn Sohn ),( Ki Hyun Ryu ),( Sun Moon Kim ) 대한내과학회 2016 대한내과학회 추계학술발표논문집 Vol.2016 No.1
An asymptomatic, 57-year-old man without any significant medical history was referred to our hospital because of early gastric cancer and a hepatic mass. Esophagogastroduodenoscopy revealed a superficial elevated lesion with central depression approximately 20 mm in size in the posterior wall of the antrum of the stomach. Pathologic examination confirmed well-differentiated adenocarcinoma. The laboratory tests and tumor markers, including AFP, CA19-9, and CEA, were within the normal range. Computed tomography (CT) revealed the hepatic mass was approximately 33 mm in size in segment Ⅱ/Ⅲ of the liver. However, the imaging cannot reliably differentiate between sclerosing hemangioma and metastasis. He underwent a US-guided needle biopsy, but we couldn't obtain a biopsy specimen, as the firmness of the liver mass made it impossible to put the needle through into the core. Subsequently underwent a diagnostic laparoscopic wedge resection. The mass was histologically typical for a leiomyoma. Primary hepatic leiomyoma (PHL) is a very rare benign tumor, with only 36 cases reported in the world literature. Surgical resection is both diagnostic and curative. This is the first report describing PHL in the domestic literature and the first report describing PHL diagnosed with coexisting gastric cancer in the world literature. In conclusion, when the patient presents a hepatic mass with another malignancy, reliable tissue diagnosis is necessary to exclude this rare entity, especially if the imaging cannot reliably differentiate between hemangioma and metastasis.
A Murine Model of Toluene Diisocyanate-induced Contact Hypersensitivity
Chai, Ok Hee,Park, Sung Gil,Sohn, Jang Sihn,Hwang, Seung Soo,Li, Guang Zhao,Han, Eui-Hyeog,Kim, Hyoung Tae,Lee, Moo Sam,Lee, Hurn-Ku,Lee, Yong Chul,Song, Chang Ho The Korean Association of Immunobiologists 2002 Immune Network Vol.2 No.3
Background: Toluene diisocyanate (TDI) can cause contact allergy and occupational asthma, but the mechanism underlying sensitization to this chemical compound remains controversal. Also the correlation of mast cell with contact hypersensitivity (CHS) and the role of mast cell in the TDI-induced CHS is unknown. This issue was investigated by administrating TDI on the skin of genetically mast cell-deficient WBB6F1/$J-Kit^{W}/Kit^{W-v}$ ($W/W^{V}$) and congenic normal WBB6F1/J-Kit+/+ (+/+) mice. Methods: To development of animal model of TDI-induced CHS and to investigate the correlation of mast cell with CHS and the role of mast cell in the TDI-induced CHS, $W/W^V$ and +/+ mice were sensitized with TDI on the back skin at day 1 and day 8, and then challenged with 1% TDI on the ear at day 15. At 1, 2, 4, 8, and 24 hours after 1% TDI challenge, the ear thicknesses were measured. It was investigated the histologic changes of dermis in the ear of $W/W^V$ and +/+ mice at 24 hours after 1% TDI challenge. Results: TDI induced a significant ear swelling response in $W/W^V$ and +/+ mice. TDI induced the significant infiltrations of polymorphonuclear leukocytes and eosinophils in $W/W^V$ and +/+ mice, but not of mast cells in normal mice. And TDI increased a characteristic extent of mast cell degranulation in normal mice. There were no significant differences in the ear swelling and the infiltrations of polymorphonuclear leukocytes and eosinophils of normal versus $W/W^V$ mice, either at baseline or after TDI-induced CHS. Conclusion: From the above results, TDI can be used as a murine CHS model, and the mast cells may not be essential in TDI-induced CHS.
Nuclear EpICD expression and its role in hepatocellular carcinoma
PARK, SHIN YOUNG,BAE, JUN SANG,CHA, EUN JUNG,CHU, HYUN HEE,SOHN, JANG SIHN,MOON, WOO SUNG Spandidos Publications 2016 ONCOLOGY REPORTS Vol.36 No.1
<P>Regulated intramembrane proteolysis of epithelial cell adhesion molecule (EpCAM) results in shedding of the extracellular domain (EpEX) and release of the intracellular domain (EpICD) into the cytoplasm. Released EpICD associates with FHL2, beta-catenin and Lef-1 to form a nuclear complex and triggers oncogenic signaling. This study was conducted to examine the nuclear expression of EpICD in hepatocellular carcinoma (HCC) and to assess the role of EpICD in HCC. EpICD immunoexpression was examined in 100 cases of HCC using tissue microarrays and correlated with clinicopathological parameters. We also examined the role of EpICD in HCC using EpICD cDNA transfected HCC cell line and EpCAM silenced HCC cell line by small interfering RNA (siRNA). Nuclear expression of EpICD was observed in 19 of 100 (19%) cases. Nuclear expression of EpICD significantly correlated with nuclear expression of p-catenin, and Ki-67 labeling index. In addition, nuclear expression of EpICD was associated with higher histologic grade and advanced T category. Forced overexpression of EpICD in the HCC cell significantly increased the cell proliferation, migration and invasion. The overexpression of EpICD also increased the expression levels of the active form of beta-catenin and c-myc and cyclin Dl. In contrast, downregulation of EpCAM by siRNA decreased the cell proliferation, migration, invasion and the expression of active form of beta-catenin, c-myc and cyclin Dl. Our present data suggest that EpICD plays important roles in HCC progression by modulating expression of target genes of EpCAM.</P>
Kwon, Seyong,Kim, Minseok S.,Lee, Eun Sook,Sohn, Jang Sihn,Park, Je-Kyun Oxford University Press 2014 Integrative biology Vol.6 No.4
Conventional molecular profiling methods using immunochemical assays have limits in terms of multiplexity and the quantification of biomarkers in investigation of cancer cells. In this paper, we demonstrate a quantum dot (QD)-based microfluidic multiple biomarker quantification (QD-MMBQ) method that enables labeling of more than eight proteins immunochemically on cell blocks within 1 h, in a quantitative manner. An internal reference, beta-actin, was used as a loading control to compensate for differences in not only the cell number but also in staining quality among specimens. Furthermore, the microfluidic blocking method exhibited less nonspecific binding of QDs than the conventional static blocking method.