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Sang Hee Kim  (Kim SH) 4 Articles
Clinical Significance of Human Sodium Iodide Symporter mRNA Expressions in Primary and Metastatic Papillary Thyroid Carcinoma.
Seong Jin Lee, Hyun Joo Park, Eun Ju Lee, Ha Young Kim, Jin Kyu Koh, Ki Young Park, Sung Bae Kim, Gyung Yup Gong, Suk Joon Hong, Il Min Ahn, Sang Hee Kim
J Korean Endocr Soc. 1999;14(3):514-519.   Published online January 1, 2001
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BACKGROUND
The iodide transport into thyroid cells is an essential step in the biosynthesis of thyroid hormones. The sodium iodide symporter (NIS) which is responsible for iodide transport was cloned recently and identified as a plasma membrane glycoprotein. Recent report suggested the absence of human NIS (hNIS) mRNA expression of papillary carcinoma in thyroid indicates absence of response on radioiodine therapy for distant metastasis. To understand the change of hNIS expression at the stage of metastasis in papillary thyroid carcinomas, we evaluated the expression levels of hNIS mRNA in primary and lymph node metastatic papillary carcinoma tissues. METHODS: Seven pairs of primary and lymph node metastatic tissues were included in this study. The level of hNIS mRNA in lymph node metastatic tissues and primary tissues were evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR). The level of GAPDH mRNA was used as internal control. RESULTS: Two among 6 lymph node metastatic tissues did not show hNIS mRNA even with significant hNIS expressions in papillary carcinoma tissues in thyroid. The levels of hNIS expression of remaining 4 lymph node metastatic tissues were lower than those of corresponding primary tissues. Interestingly, one case showed no hNIS expression in primary tissue, but significant hNIS expression in lymph node metastatic tissue. There was no correlation in hNIS mRNA expression between primary and lymph node metastatic tissues. CONCLUSION: No correlation was found in hNIS mRNA expression between primary and lymph node metastatic tissues, suggesting the measurements of hNIS mRNA level in primary tissues may not predict therapeutic response to radioactive iodine.
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Allelotyping and Comparative Genomin Hybridization Studies in Papillary Thyroid Carcinomas and Follicular Adenomas.
Il Min Ahn, Eun Sook Kim, Hyun Soo Park, Ki Young Park, Seok Jun Hong, Kyung Yub Gong, Jin Yub Kim, Sung Bae Kim, Sang Hee Kim, Sung Jin Lee, Jung Hee Han, Kwan Ja Jee
J Korean Endocr Soc. 1999;14(2):314-322.   Published online January 1, 2001
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BACKGROUND
In our previous study, the prevalence of the known causes of thyroid tumorigenesis was relatively rare in Korean population, suggesting genetic and environmental differences exist. Screening of genetic alteration in papillary thyroid carcinoma(PTC) and follicular adenoma(FA) in whole genomic scale was needed prior to search on individual genes of possible causes. METHODS: Ten cases of PTC without ret/PTC-I, -2, -3 rearrangement and 5 cases of follicular adenoma were included in the study of microsatellite marker allelotyping. Sixty two microsatellite markers available, were chosen to cover the known sites of loss of heterozygosity(LOH) involved in thyroid tumors, tumor suppressor genes and terminal portion of each chromosomes. PCR was performed on tumor DNA and leukocytes DNA from each patient with MDE gel electrophoresis to detect LOH. Same specitnens as above, 3 case of normal thyroid tissues and NPA, ARO cell lines were included in the study of comparative genomic hybridization(CGH). Tumor and control DNAs were hybridized to metaphase chromosome with differential stainings with fluorescein and rhoda-mine-dUTP. Obtained results were analyzed by multicolor fluorescence computer assisted image analyzer. RESULTS: In allelotyping, LOH were detected in 5 cases of PTC, 2 cases on D10S1435, 1 case each on D2S1780, DSS1099, D11S1986, D16S539, 1 case of PTC revealed LOH on DSS1099, D11S1986. In FA, LOH were detected in 3 cases on D1S534, D1S226, Dl 1S907, D22S683, DXS9807. In CGH, Xp addition was noticed in 1 case of PTC, 12q and 10p addition was noticed in 1 case each, 16q deletion and 17q addition in 1 case of FA. CONCLUSION: No hot spot of LOH was noticed in microsatellite marker allelotyping, neither of common chromosomal change in CGH study suggesting unbalanced translocation or gene amplification more than 5-10 Mb may be involved in the genetic alteration of PTC and FA.
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The Expression of the Bcl-2 Family Proteins in Thyroid Neoplasms.
Il Min Ahn, Eun Sook Kim, Seok Jun Hong, Kyung Yub Gong, Tae Jin Lee, Jin Yub Kim, Sung Bae Kim, Sang Hee Kim
J Korean Endocr Soc. 1998;13(3):359-365.   Published online January 1, 2001
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BACKGROUND
Proteins of the Bcl-2 family are intracellular membrane-associated proteins that regulate programmed cell death either positively or negatively by as yet unknown mechanism. Bcl-2 family proteins have an antiapoptotic function, such as the Bcl-2, the long form of Bcl-x and Mcl-l, or a proapoptotic function, like the short form of Bcl-x and Bax. To investigate the potential role of Bcl-2 family proteins in thyroid tumorigenesis, the authors examined the pattern of expression of the Bel-2 family proteins in various thyroid neoplasms. METHODS: Bcl-2 family proteins, including Bcl-2, Bcl-x, Mcl-1 and Bax proteins were immunohistochemically stained in 57 cases of various thyroid neoplasms using formalin-fixed and paraffin embedded tissues; 18 cases of papillary carcinoma, 6 cases of medullary carcinoma, 4 cases of anaplastic carcinoma, 10 cases of follicular adenoma, 9 cases of adenomatous goiter, and 10 autopsy cases of fetal thyroid galnd. The intensity and frequency of the immunostaining were evaluated with the program of Image-Pro Plus Version 3.0 for image analysis. RESULT: Consistent expression of Bcl-2, Mcl-1, and Bax proteins were present in the surrounding normal thyroid tissue, however the expression of Bcl-x protein was not observed. Compare to the expression patterns of adenomatous goiter, and fetal and surrounding normal thyroid tissues, papillary and anaplastic carcinomas showed the decreased Bcl-2 and increased Bcl-x protein expressions(p (0.05). Medullary carcinoma revealed the increased Bcl-x protein expression only(p 0.05). CONCLUSION: These data suggest that combined patterns of decreased Bcl-2 and increased Bcl-x protein expressions may eontribute to the carcinogenesis of thyroid cancers originated from thyroid follicular cells, and an increased expression of Bcl-x protein may be related to the pathogenesis of medullary carcinoma from parafollicular C cells.
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A Case of Primary Thyroid Lymphoma Involving Bone Marrow (Stage IVE) Assoeiated with Hashimoto's Thyroiditis.
Young Kee Shong, Joong Yeol Park, Ghi Su Kim, Jae Kun Cho, Yun Ho Chu, Wan Sik Eom, Sang Hee Kim, Hyun Sook Chi, Gyung Yub Gong, Ki Up Lee
J Korean Endocr Soc. 1994;9(4):390-394.   Published online November 6, 2019
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Primary lymphoma of the thyroid is a relatively rare malignant tumor of the thyroid. It is known to be frequently associated with Hashimoto's thyroiditis. In Korea, a few cases of primary lymphoma of the thyroid have been reported and most of these cases were in the stage I E or II E. Recently, we experienced a case of the primary thyroid lymphoma, stage IV E associated with Hashimoto's thyroiditis in a 70-year-old woman who presented with dysphagia and dyspnea due to rapidly enlarging neck mass.She was treated with combination chemotherapy(cyclophosphamide, adriamycin, vincristine and methylprednisolone) and local radiotherapy and achieved partial response with resolution of dysphagia and dyspnea.
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