Journal of Pathology and Translational Medicine

Yoon Kyung Sohn

23 Articles

Availability of Immunohistochemistry in the Diagnosis of Follicular Variant of Papillary Thyroid Carcinoma.: Ji Yun Jeong, Jung Sik Jang, Yoon Kyung Sohn, Jin Hyang Jung, Yi Kyeong Chun, Ji Young Park; Korean J Pathol. 2010;44(1):48-55.; DOI: https://doi.org/10.4132/KoreanJPathol.2010.44.1.48

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BACKGROUND
Making the diagnosis of the follicular variant of papillary thyroid carcinoma (FVPTC) is often difficult, and there are no accurate immunohistochemical or molecular markers. The purpose of this study is to evaluate performing immunohistochemistry to make the diagnosis of FVPTC.
METHODS
A total of 249 thyroid lesions were studied. We made the tissue microarray, and we assessed the expression of HBME-1, galectin-3, CD56, and p63.
RESULTS
Galectin-3, HBME-1, and p63 were positive in 79.7%, 79.7%, and 15.9% of the FVPTC, respectively. These immunohistochemical features of FVPTC were between those of classic papillary thyroid carcinoma (CPTC) and those of non-PTC. The CD56 expression was positive in 75.4% of the FVPTC, which is much higher than that of the CPTC (28.3%), and even higher than that of the non-PTC lesions (60%). Comparing FVPTC with CPTC, the expression of galectin-3 was significantly higher and the expression of CD56 was significantly lower in the CPTCs. Comparing the FVPTC with follicular carcinoma (FC), the expression of all the markers was significantly higher in the FVPTC. Comparing PTC with FC, the expression of CD56 was lower and the expressions of the other markers were higher in the PTCs.
CONCLUSIONS
Galectin-3, HBME-1, and p63 can help make the diagnosis of FVPTC, and a cocktail of these markers can be even more useful. But CD56 is not thought to be useful to make the diagnosis of FVPTC.

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A Case of Multifocal Papillary Thyroid Carcinoma Consisting of One Encapsulated Follicular Variant withBRAFK601E Mutation and Three Conventional Types withBRAFV600E Mutation
Wook Youn Kim, Young Sin Ko, Tae Sook Hwang, Hye Seung Han, So Dug Lim, Wan Seop Kim, Seo Young Oh
Korean Journal of Pathology.2013; 47(3): 293. CrossRef

Inactivation of TPEF Gene by Aberrant Methylation in Hepatocellular Carcinoma.: Woon Bok Chung, Soon Young Kim, So Young Chun, Ku Seong Kang, Hae Ahm Lee, Joung Ok Kim, Ji Young Park, Yoon Kyung Sohn, Jung Wan Kim; Korean J Pathol. 2008;42(1):9-15.

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Abstract PDF: BACKGROUND
Abnormalities of genomic methylation patterns have been shown to play a role in the development of carcinoma, and the silencing of tumor suppressor genes is related to local de novo methylation.
METHODS
Using methylation specific arbitrarily primed-Polymerase Chain Reaction (Ms AP-PCR), we identified a 322 bp sequence that contained a 5' un-translated and exon1 regions of the TPEF gene. To evaluate the inactivation of the TPEF gene through hypermethylation in hepatocellular carcinoma (HCC), we investigated the correlation between methylation patterns and TPEF expression in tumor tissues of human HCC and cell lines via a Combined Bisulfite Restriction Assay (CoBRA) and RT-PCR.
RESULTS
A dense methylation pattern of the TPEF was detected in most cell lines, as well as in 10 of the 14 (71.4%) HCC tissues. In addition, loss of heterozygosity (LOH) from the TPEF gene was observed in 5 of the 14 (36%) HCC tissues. Furthermore, RT-PCR analysis revealed TPEF expression in 5 of 8 (62.5%) cell lines. Finally, treatment with a demethylating agent, 5-Aza- 2'-deoxycitidine (5-AzaC), increased the expression of TPEF mRNA.
CONCLUSION
These results indicate that inactivation of the TPEF gene through hypermethylation may be a mechanism by which tumorigenesis occurs in HCC.

Genistein Induces G2/M Cell Cycle Arrest and Apoptosis in Rat Neuroblastoma B35 Cells; Involvement of p21(waf1/cip1), Bax and Bcl-2.: Ismail A Ismail, Ku Seong Kang, Jung Wan Kim, Yoon Kyung Sohn; Korean J Pathol. 2006;40(5):339-347.

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Abstract PDF: BACKGROUND
The effect of genistein on different types of cells has been investigated. However, its effect on the nervous system is still unclear. The aim of the present work is to explore the effect of genistein on rat neuroblastoma B35 cells.
METHODS
The effect of genistein on the proliferation of B35 cells, its cytotoxicity, the cell-cycle distribution, the ultra-structural changes and the induction of apoptosis were determined using MTT assay, LDH assay, Flow-cytometric analysis, transmission electron microscopy and Hoechst staining, respectively. Furthermore, Real-time quantitative RT-PCR and Western blotting were used to examine the transcriptional and post-translational alterations of the G2/M cell-cycle arrest marker cyclin-dependent kinase inhibitor p21(waf1/cip1) and the apoptosis-related genes after genistein treatment.
RESULTS
Genistein significantly inhibits cell survival, slightly elevates the release of lactate dehydrogenase and induced apoptosis in B35 cells. Genistein increased the number of cells at S-phase and induced cells to accumulate at the G2/M phase. These G2/M arrested cells are associated with a marked up-regulation of p21(waf1/cip1) at both the mRNA and protein levels. We observed that genistein up-regulates pro-apoptotic Bax with concurrent down-regulation of the anti-apoptotic Bcl-2 protein.
CONCLUSION
These observations suggest that the anticancer effect of genistein on B35 neuroblastoma cells is mediated through multiple cellular pathways including G2/M cell-cycle arrest and the induction of apoptosis.

Effects of Selective Cyclooxygenase-2 Inhibitor NS-398 Pretreatment on the Rat Spinal Cord after Contusion Injury.: Hyeon Dae Cheong, Joo Kyung Sung, In Suk Ham, Ku Seong Kang, Joung Ok Kim, Jung Wan Kim, Tae In Park, Yoon Kyung Sohn; Korean J Pathol. 2006;40(4):255-262.

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Abstract PDF: BACKGROUND
Secondary spinal cord injury (SCI) that follows an initial mechanical insult can exacerbate the overall damage, limit the restorative processes and eventually lead to an in- creased neurological deficit. We hypothesized that selective inhibition of cyclooxygenase-2 (COX-2) may decrease the delayed cell death, and so this will contribute to decreased level of the secondary injury.
METHODS
The dorsal surface of the cord at the T9 level was subjected to weight drop impact using a 10 g rod. To block COX-2 activation, a selective COX-2 inhibitor (NS-398) was administered (5 mg/kg, i.p.) 15 min prior to SCI. The COX-1, COX-2, Caspase-3 and PGE2 expressions were measured by real time quantitative RT-PCR and fluorescence immunostaining.
RESULTS
Many activated caspase-3 positive cells were observed at 6 h and they increased until 72 h after SCI. The expression of COX-2 peaked at 6 h after SCI, while the COX-1 expression was unaffected. The principal cells that showed a COX-2 expression were the neurons and microglia. Pretreatment with NS-398 caused a significant decrease in the expression of prostaglandin E2 and activated caspase-3 positive cells after SCI.
CONCLUSION
These data suggest that COX-2 is one of the main factors related with the pathologic deficits from secondary SCI.

Effects of Genistein and Daidzein on the Growth of Human Colon Cancer HCT-116 Cells.: Jong Heon Shin, Ku Seong Kang, Joung Ok Kim, Ghil Suk Yoon, Tae Gyun Kwon, Jung Wan Kim, Yoon Kyung Sohn; Korean J Pathol. 2006;40(1):46-51.

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Abstract PDF: BACKGROUND
Genistein and daidzein are two major soybean isoflavones. They have received increasing attention because of their possible roles for cancer prevention. However, their mechanisms of action and molecular targets on the human colon cancer cells are not fully understood.
METHODS
Human colon cancer HCT-116 cells were treated with genistein and daidzein to investigate their effects on the cell growth and this was analyzed with MTT assay. TUNEL assay and Hoechst33342 stain were carried out to identify apotosis.
RESULTS
Daidzein was able to inhibit cell proliferation and induce apoptosis of the HCT-116 cells, but genistein didn't affect the cell growth. The ER antagonist ICI182780 didn't attenuate the antiproliferative and proapoptotic effects of daidzein: this means the effect of daidzein on the HCT-116 cells may not be dependent on the ER pathway. The other soybean isoflavone, genistein, attenuated the effects of daidzein on the HCT-116 cells and its mechanism should be elucidated.
CONCLUSIONS
These data suggest that daidzein may act as a preventive agent on human colon cancer, and its mechanism of action doesn't involve the ER-dependent pathway.

Correlation Between Neuronal Apoptosis and Expression of Inducible Nitric Oxide Synthase after Transient Focal Cerebral Ischemia.: Byoung Yuk Yi, Sung Kyoo Hwang, Ku Seong Kang, Hong Hua Quan, Young Mi Lee, Jung Wan Kim, Eun Kyoung Kwak, Ji Young Park, Yoon Kyung Sohn; Korean J Pathol. 2004;38(6):364-371.

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Abstract PDF: BACKGROUND
Neuronal death in acute-phase cerebral ischemic injury is caused by necrosis. However, neuronal injury after reperfusion can be associated with apoptosis.
METHODS
We used Sprague-Dawley rats whose brains were reperfused after middle cerebral artery occlusion for either 30 min or 2 h. We examined a relationship between apoptosis and the expression of inducible nitric oxide synthase (iNOS) in the brain tissue from 3 h to 14 days after reperfusion in both groups.
RESULTS
TUNEL and iNOS positivity were closely related in both groups. The 2-h ischemia group exhibited increases in the amount of TUNEL and iNOS-positive cells for up to 3 days after reperfusion, at which the TUNEL and iNOS-positive cells decreased. The 30-min ischemia group exhibited peak positivity 24 h after reperfusion, followed by a similar decrease. iNOS mRNA expression peaked 3 h after reperfusion in the 30-min ischemia group, at which time it decreased. In the 2-h ischemia group, iNOS mRNA increased 3 h after reperfusion, peaked 24 h after reperfusion, and then decreased.
CONCLUSION
These results indicated the occurrence of delayed apoptosis in transient cerebral ischemia. Increased expression of iNOS is closely associated with this apoptosis, and oxygen free radical-producing materials, such as nitric oxide, may play an important role in the induction of this apoptosis.

Expression of Tumor Necrosis Factor-alpha, Interleukin-1beta and Inducible Nitric Oxide Synthase after Stereotaxic Injection of Lipopolysaccharide in Rat Hippocampus.: Hoon Kyu Oh, Ku Seong Kang, Ji Yeon Kim, Eun Kyoung Kwak, Jung Wan Kim, Ji Young Park, Yoon Kyung Sohn; Korean J Pathol. 2004;38(3):157-164.

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Abstract PDF: BACKGROUND
Brain inducible nitric oxide synthase (iNOS) might be detectable in several pathologic conditions, and it is thought to play an important role in their pathophysiology. Tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta are believed to be essential factors of iNOS induction of the brain.
METHODS
After intrahippocampal stereotaxic injection of lipopoly-saccharide (LPS), the rat brains were removed at 6, 12 and 24 h. The rat brain tissues were examined to clarify the expression patterns of TNF-alpha, IL-1beta and iNOS.
RESULTS
The inflammatory cells which were stained with anti-TNF-alpha antibody, appeared in 6 h and increased for 24 h after LPS injection. The iNOS positive cells appeared after 12 h of LPS injection. A semiquantitative analysis of reverse transcription-polymerase chain reaction (RT-PCR) revealed that the TNF-alpha and IL-1beta mRNA arose at 1 h, peaked at 6 h and then declined until 48 h after LPS injection. The iNOS mRNA arose after 6 h, peaked at 12 h, and declined until 48 h after LPS injection.
CONCLUSIONS
We conclude that the induction of inflammatory events by intrahippocampal injection of LPS activates TNF-alpha and IL-1beta secretion, and this is followed by an induction of iNOS expression. TNF-alpha and IL-1beta seem to be related with iNOS expression in brain inflammation.

The Effects of Ginsenoside Rb1 on the Apoptosis and the Production of Nitric Oxide in Rat C6 Glioma Cells.: Joo Hyeon Park, Yoon Hee Lee, Ku Seong Kang, Soo Kyoung Lee, Sun Zoo Kim, Ji Young Park, Eun Kyoung Kwak, Yoon Kyung Sohn; Korean J Pathol. 2004;38(1):1-7.

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Abstract PDF: BACKGROUND
Ginsenosides, the extract of Panax ginseng, exert various pharmacological effects such as anticancer activity by the mechanism that is not yet defined. In this study, we proposed that the anticancer effect of ginsenoside Rb1 is related to tumor cell apoptosis and ginsenoside Rb1 induces the tumor cell apoptosis via the nitric oxide (NO) production.
METHODS
Rat C6 glioma cells were activated by treating with lipopolysaccharide (LPS), interferon (IFN)-gamma , and tumor necrosis factor (TNF)-alpha on the culture medium to investigate the effects of ginsenoside Rb1.
RESULTS
Compared with C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha, C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha/ginsenoside Rb1 showed marked increase in the NO production and apoptosis. Ginsenoside Rb1 induces the NO production in C6 glioma cells in dose-dependent manner. When C6 glioma cells treated with LPS/IFN-gamma/TNF-alpha/ginsenoside Rb1 were incubated with the specific inhibitor of iNOS, S-Methyl-2-thiopseudoureasulfate (SMT), both NO production and apoptosis in C6 glioma cells was significantly decreased. Ginsenoside Rb1 induced the expression of iNOS mRNA and iNOS protein in C6 glioma cells.
CONCLUSIONS
These results suggest that the induction of iNOS expression and subsequent

Lipopolysaccharide/Interferon-gamma Induced Nitric Oxide Production in C6 Glioma Cells: Modulation by Dexamethasone.: Jong Heun Shin, Ku Seong Kang, Ji Yeoun Kim, Sun Zoo Kim, Ji Young Park, Eun Kyoung Kwak, Yoon Kyung Sohn; Korean J Pathol. 2002;36(6):406-411.

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Abstract PDF: BACKGROUND
Glial cell-derived nitric oxide (NO), and its regulation has significant implications for central nervous system pathophysiology. The aim of the present study was to see the production of NO in lipopolysaccharide (LPS)/interferon-gamma (IFN-)-treated C6 glioma cells and the effect of dexamethasone on NO production and apoptosis of LPS/IFN--treated C6 glioma cells.
METHODS
The apoptosis of LPS/IFN- treated C6 glioma cell was examined with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method and the production of NO in culture medium was measured. The expression of iNOS mRNA was examined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The effect of the N-monomethyl L-arginine (NMMA) and dexamethasone on the apoptosis and NO production was also examined.
RESULTS
Inducible nitric oxide synthase (iNOS) mRNA and NO production were markedly increased in LPS/IFN--treated C6 glioma cells. The expression of iNOS mRNA arose at 3 hours, peaked at 12 hours, and declined 24 hours after LPS/IFN--treatment. Accumulation of NO derivatives in the culture media was increased at least upto 48 hours after LPS/IFN-. The induction of iNOS expression and NO production in LPS/IFN--treated C6 cells was correlated with apoptotic cell death judged by TUNEL staining. After treatment of NMMA, one of the NOS inhibitors, NO production and apoptosis were markedly decreased. Dexamehasone treatment suppressed the NO production by concentration depenedent manner.
CONCLUSIONS
From the above results it is concluded that the LPS/IFN- induced apoptosis of C6 cells is mediated by iNOS-derived NO and NO production and apoptosis was suppressed by dexamethasone.

The Effect of Ischemic Preconditioning in Rat Liver: The Expression of Interleukin-1 and Nuclear Factor-B.: Kum Yoon Seup, Soo Kyoung Lee, Sun zoo Kim, Eun Kyoung Kwak, Ji Young Park, Tae In Park, Han Ik Bae, Yoon Kyung Sohn, In Soo Suh; Korean J Pathol. 2002;36(4):238-242.

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Abstract PDF: BACKGROUND
A short period of ischemia and reperfusion, called ischemic preconditioning, protects various tissues against subsequent sustained ischemic insult. Apoptosis of hepatocytes and sinusoidal endothelial cells are a critical mechanisms of injury in the ischemic liver. Because nuclear factor-B (NF-B) has a significant role in the cell survival, we hypothesized that ischemic preconditioning protects by inhibition of apoptosis through the expression of NF-B, induced by interleukin-1 (IL-1), which is known for enhancement of its transcription and activation.
METHODS
We induced ischemia and reperfusion on rat liver, and performed in situ terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labelling assay and polymerase chain reaction for IL-1 mRNA and NF-B mRNA.
RESULTS
Apoptosis of hepatocytes and sinusoidal endothelial cells, assessed by in situ TUNEL assay, was significantly reduced with preconditioning. The expression of IL-1 mRNA and NF-B mRNA are seen on discrete monoclonal bands around 344 and 356 base pairs, in comparison with normal rat liver, but, there was no significant difference between the ischemia-reperfusion group and the preconditioning group.
CONCLUSIONS
We suggest that ischemic preconditioning confers dramatic protection against prolonged ischemia via inhibition of apotosis through the expression of IL-1 inducing NF-B and its activation. However, we need further study in the activity of NF-B, such as nucleotide shift assay, because the activity of NF-B is regulated by binding of the inhibitory protein, IB.

Allelic Loss at the BRCA1 and BRCA2 Loci in Sporadic Breast Carcinoma Using Paraffin Embedded Tissue .: Ji Young Park, Myung Hoon Lee, Dong Ja Kim, Tae In Park, Young Ha Lee, Jung Wan Kim, Yoon Kyung Sohn; Korean J Pathol. 2002;36(2):100-105.

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Abstract PDF: BACKGROUND
Germline mutations in the breast cancer-associated genes BRCA1 and BRCA2 confer susceptibility and a lifetime risk of breast. Several morphological and clinical features have been attributed to hereditary tumors. However, in sporadic breast cancer, the interrelationship between the loss of heterozygosity (LOH) of these loci and clinical features remains to be fully elucidated.
METHODS
Microdissected paraffin-embedded tissue blocks of 48 cases of surgically resected breast carcinoma were investigated to identify the LOH of BRCA1 and BRCA2 using microsatellite markers.
RESULTS
Of 48 cases, 22 (45.9%) exhibited LOH at BRCA1 locus while in 29 out of 48 (60.4%) cases LOH was observed for the BRCA2 region. There was no significant correlation between LOH at BRCA1/2 and the patient's age, tumor size, histologic grade or lymph node metastasis. When comparing the frequency of LOH with the expression of several prognostic factors, such as p53, c-erb B2 protein, estrogen and progesterone receptor using immunohistochemical stain, there was only correlation with LOH at BRCA2 and the progesterone receptor.
CONCLUSIONS
Our results suggest that allelic deletion play a role to the development of sporadic breast cancers.

Fine Needle Aspiration Cytologic Diagnosis of Thymoma Presenting as a Thyroid Nodule: A Report of Two Cases.: Dong Ja Kim, Ji Young Park, Yoon Seup Kum, Tae In Park, Yoon Kyung Sohn; Korean J Cytopathol. 2000;11(1):41-46.

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Abstract PDF: Thymoma is the most common anterior mediastinal tumor in adults. Rarely, it is presented as the anterior neck mass, commonly located in the anterolateral aspect of the neck or adjacent to the thyroid. We experienced two cases of fine needle aspiration cytology of thymoma, mimicking thyroid mass. The first case was an ectopoic cervical thymoma in a 31-year-old female. The fine needle aspiration cytology was misinterpreted as reactive hyperplasia of lymph node. But the histologic diagnosis was thymoma, predominantly lymphocytic type. The second case was an invasive thymoma in a 66-year-old female, who complained a large anterior neck mass. The fine needle aspiration cytology revealed biphasic population of some clusters of epithelial cells and scattered lymphocytes. The cytologic diagnosis was thymoma and was confirmed as invasive thymoma after the biopsy. Therefore, when the cytologic feature of anterior neck mass shows the both lymphocyte and epithelial component, the differential diagnosis should include the possibility of thymoma.

The Relationship of Ki-67, Proliferating Cell Nuclear Antigen, AgNORs and p53 Protein Expression in Astrocytoma.: Dong Ja Kim, Jae Weon Lim, Yoon Kyung Sohn; Korean J Pathol. 1999;33(1):25-31.

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Abstract PDF: The grading of astrocytoma has traditionally relied on histological assessment, but there are some differences in their parameters, application, and reproducibility. Recently, numerous studies have attempted to correlate biological aggresiveness with tumor proliferation index using new immunohistochemical methods. The purpose of this study is to correlate the histopathological grades of astrocytoma with the expression of Ki-67, PCNA, p53 protein and AgNORs. The paraffin sections of 41 consecutive cases of astrocytomas were examined. Histologically the tumors were graded as three groups under the St. Anne-Mayo system and showed 14 cases in grade II, 15 cases in grade III and 12 cases in grade IV (glioblastoma multiforme). As a result, the Ki-67 labelling index and p53 protein expression tended to increase with increasing grade of malignancy. But the univariate analysis showed that there was no significant difference between the tumor grades (p>0.05). The PCNA labelling index and number of AgNORs revealed striking differences between the grade II and grade III astrocytomas (p<0.05). We concluded that the PCNA labelling index and AgNORs counting are useful markers for differentiation between grade II and III astrocytomas.

Intracranial Fibro-Osseous Lesion: A case report and literature review.: Jae Weon Lim, Seung Cheol Lee, Byoung Yuk Yi, Yoon Kyung Sohn; Korean J Pathol. 1997;31(8):798-801.

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Abstract PDF: Intracranial fibro-osseous lesion, also reported as calcifying pseudoneoplasm of the neural axis, is an uncommon lesion of the central nervous system. Since the discovery of this entity by Rhodes and Davis in 1978, there have been a total of 21 cases reported in the literature. We encountered one such case in a 28 year old male, who presented with left hemiparesis for 1 year. By the MR images, a 1.5 cm sized round mass was found at right parietal lobe near motor cortex. The mass lesion enhanced well, homogenously and revealed clear, slightly irregular margin. Excisional biopsy of the mass was performed. Microscopically the lesion was composed of calcified fibrous tissue with an amorphous gray-blue, coarsely fibrillar to chondromyxoid nodular areas. Sparse spindle cells, immunohistochemically negative for GFAP, vimentin and S-100, were scattered within the amorphous material. Palisading spindle or polygonal cells were present at the more cellular periphery of the lesion, which were vimentin positive but S-100 negative. There was no evidence of the pilocytic astrocytes, Rosenthal fibers, or GFAP positive hypertrophic astrocytes. Intracranial fibro-osseous lesions are apparently slow-growing with generally excellent prognosis after wide excision. The etiology remains unclear, but most investigators favor a reactive rather than neoplastic process.

Prognostic Value of CD44v6 Isoform in Infiltrating Ductal Carcinoma of Breast.: Seung Cheol Lee, Yoon Kyung Sohn, Jung Sik Kwak, Woon Bok Jhung, Jung Wan Kim; Korean J Pathol. 1997;31(7):635-643.

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Abstract PDF: CD44 is a family of transmembrane glycoproteins involved in cell-cell and cell-matrix interactions. Expression of CD44 isofonns (splice variants) has been shown to be associated with poor prognosis in several human cancers. We evaluated the expression patterns of the CD44 isofortn (CD 44 splice variant v6) in infiltrating ductal carcinoma of the breast by immunohistochemical and RT-PCR method. Paraffin embedded blocks from seventy-five cases of mastectomized samples were analyzed immunohistochemically using monoclonoal antibody against CD44v6. CD44v6 was detected in fifty-seven cases (76%) of the tumor samples. Adjacent normal myoepithelial cells and ductal epithelial cells revealed focal positive reaction to CD44v6. Thirtytwo cases (80.0%) with lymph nodal metastasis revealed overexpression of CD44v6 monoclonal antibody, but twenty-five cases (71.4%) without nodal metastasis also showed positive reaction to CD44v6 monoclonal antibody, and there is no statistically significant value. Other prognostic factors of infiltrating ductal carcinoma, such as tumor size, histologic grade and hormonal receptors did not show any significant correlation with CD44v6 expression. The RT-PCR studies for 9 cases of infiltrating ductal carcinoma showed the same band patterns both in the normal and tumor tissues. From the above results, it is concluded that the expression of CD44v6 is not a valuable prognostic marker of infiltrating ductal carcinoma of breast.

Immunohistochemical Analysis of nm23 Protein in Infiltrating Ductal Carcinoma of the Breast.: Min Hee Jung, Seung Cheol Lee, Yoon Kyung Sohn, In Soo Suh; Korean J Pathol. 1997;31(2):145-151.

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Abstract PDF: The nm23 gene was originally identified from murine melanoma cell lines of varying metastatic potential. A strong association has been observed between reduced expression of nm23 gene and acquisition of metastatic behavior in some tumor cells including breast cancer and melanoma, but not in others such as colon cancer, neuroblastoma, and cervical cancer. It was proposed that nm23 may function as a suppressor gene for tumor metastasis. It has recently been found that the sequence of nm23 and NDP-kinase(NDP-K) was identical. Mortality associated with human breast carcinoma is almost entirely due to subsequent metastasis, but the molecular basis of this metastasis is not understood. Elucidation of the genetic control of metastatic propensity of a tumor is important in determining prognosis and choice of therapy. The purpose of this study was to investigate the relationship of nm23 protein expression with axillary lymph node metastasis and other prognostic factors. Using an immunohistochemical technique and employing a polyclonal antibody to nm23 protein, we have determined nm23 expression in a series of 72 infiltrating ductal carcinomas of the breast. Immunostaining for the nm23 gene product have heterogenous cytoplasmic and nuclear staining in 61 patients(84.7%). Sections were scored according to relative abundance(1 = less than 25% of the cells, 2 = 26-75%, 3 = 76-100%). In 61 patients with positive immunostaining, the staining was scored as 1 in 41.6%, 2 in 18.0%, and 3 in 40.2%. The staining of tumor cells was greater than that in normal epithelial cells and stromal cells. No relationship was found between nm23 expression and lymph node metastasis, histologic grade, tumor size, estrogen receptors or progesterone receptors. Therefore, nm23 protein is increased in neoplastic tissues but no correlation with metastatic potential could be demonstrated. The biological mechanism of over-expression of nm23 in malignant cells and its role in tumor progression remain to be determined.

Primary Signet Ring Cell Carcinoma of the Lung: Report of Two Cases .: Dong Ja Kim, Sook Hee Lee, Yoon Kyung Sohn; Korean J Cytopathol. 1997;8(1):83-86.

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Abstract PDF: Signet ring cell carcinoma is a variant of adenocarcinoma and has been rarely reported in the lung as a primary site. Recently, we experienced two cases of primary signet ring cell carcinoma in the lung without any other extrapulmonary lesion. Sputum cytology was performed and the tumor cells which have eccentrically located nuclei and abundnat mucinous cytoplasm were dispersed in diffuse sheets. On resected specimen, the signet ring cells occupied about 50~80% of all tumor cell nests. HIstochemical staining revealed that the mucin produced by tumor cells was mostly carboxylated acid mucins. Ultrastructurally, the tumor cells contained variable sized membrane-bound mucin granules with weak central osmiophilic density and showed numerous surface microvilli, which represented that tumor cells arose from bronchial epithelial cells. In general, this tumor has diffusely infiltrative nature and the prognosis is fatal due to widespread metastasis before clinical discovery.

Ultrastructural Study of Amiodarone-Associated Lung Injury.: Eun Yung Kim, Sang Han Lee, Yoon Kyung Sohn, Tae Joong Sohn; Korean J Pathol. 1995;29(1):10-23.

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Abstract PDF: Amiodarone, an antiarrhythmic drug, may exert pulmonary toxicity in some patients but the pathogenesis is not clear. This study was carried out to investigate the pathogenetic mechanism of pulmonary injury induced by amiodarone at dose of 100 mg/kg/day given to rats by intraperitoneal injection for 3 weeks. And the preventive effects of concomitantly injected steroid (10 mg/kg/day) on amiodarone induced pulmonary injury was also studied using bronchoalveolar lavage, light microscopy and transmission electron microscopy. The results obtained were summarized as follows: Mild lymphocytosis of bronchoalveolar lavage fluid was found in all experimental groups. Intracytoplasmic lamellar body formation was found in all types of pulmonary cells and type II pneumocytes revealed the earliest abnormal lamellar body formation. The capillary endothelial cells showed cellular swelling and detachment from underlying basement membrane at early phase of experiment and the edema of alveolar wall and interstitium were noted. Interstitial fibrosis and proliferation of type II pneumocytes were noted at late phase. The lungs of steroid injected groups revealed accumulation of lamellar bodies in all types of pulmonary cells but interstitial fibrosis was not occurred. These findings support the concept that amiodarone is responsible for a drug-induced phospholipidosis and directly toxic to pulmonary endothelial and epithelial cells. And steroid may regress the progression of amiodarone induced pulmonary injury.

The effects of Broad Spectrum Antibiotics and Endotoxin to the Carbon Tetrachloride-induced Liver Injury.: Hyun Ho Shin, O Joon Kwon, Yoon Kyung Sohn, In Soo Suh, Tae Joong Sohn; Korean J Pathol. 1992;26(4):329-337.

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Abstract PDF: This study was performed to investigate the effect of endotoxin to the CCl4-induced liver injury. Twelve Sprague-Dawley rats were intraperitoneally injected 1.6 g/kg CCl4 as control group. Another 24 rats were orally administrated 300 mg/kg of neomycin at 16 and 3 hours prior to CCl4 injection as experimental group. Twelve among them were intraperitoneally infected 1.0 mg/kg of endotoxin(E-Coli, 0111:B4, No L-2630, lipopolysaccharide, Sigma, USA) and CCl4 simultaneously for offsetting neomycin effect. The rats were sacrificed at 1, 4, 10, and 24 hours after CCl4 injection. The liver tissues from all experimental groups were observed by light and electron microscopy. The results obtained were summarized as follows: In the CCl4 only group, the hepatocytes revealed sweling of ER and mitochondria with many lipid droplet in the cytoplasm. Focal cellular necrosis was seen at the later phase. The Kupffer cells were activated and showed many cytoplasmic processes, secondary lysosomes, and vaculoles. The endothelial cells were edematous. Several neutrophils, platelets, and microthrombi were scattered in the sinusoid. In the neomycin-CCl4-endotoxin administrated group, both hepatocytic destruction and intrasinusoidal microthrombi formation were more pronounced. In the neomycin pretreated group, the hepatocytes revealed mild cellular destruction without necrosis. There is no intrasinusoidal microthrombi. According to these results, it would be concluded that the small dosage of gastrointestinal tract-derived endotoxin affects to the liver injury caused by CCl4. The synergistic effects of CCl4 and gastrointestinal tract-derived endotoxin which can not be detoxified by damaged Kupffer cells, may be more important in the pathogenesis of CCl4-induced liver injury.

Pulmonary Alveolar Proteinosis: A case report.: Chang Ho Cho, Yoon Kyung Sohn, Jyung Sik Kwak, Jung Yoon Choi, Won Sik Lee, Tae Hoon Jung; Korean J Pathol. 1991;25(3):263-268.

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Abstract PDF: A case of pulmonary alveolar proteinosis is reported. Most of the alveolar spaces were filled with amorphous deep eosinohilic material which revealed strong positive reaction to periodic acid-Schiff staining. Electron microscopic observation of this material showed numerous lamellar bodies in the alveolar spaces and cytoplasms of alveolar macrophages. A part of them were concentric multilamellated type A lamellar bodies and the other were finger printlike type B bodies. Combined type A and type B lamellar bodies were rarely present. From the above features it is suggested that both type A and B lamellar bodies could be transformed one another and those lamellar bodies may be originated from pulmonary surfactant.

The Effects of Proteolytic Agent on the Lung Injured by Endotoxemia.: Chang Ho Cho, Yoon Kyung Sohn, Jyung Sik Kwak, Tae Joong Sohn; Korean J Pathol. 1991;25(3):215-222.

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Abstract PDF: The authors studied the lung injury induced by endotoxemia and the effects of proteolytic agent on the lung changed by endotoxemia. Sprague-Dawley rats were intraperitoneally administrated with a single dose of endotoxin (4 mg/kg, E. coli 025 : B6 lipopolysaccharide) or with endotoxin and gabexate mesilate (200 mg/kg), a proteolytic agent, concomitantly. Rats of each group were scarificed at 9, 18, and 27 hours after injection. Light and electron microscopic examination were done. The results obtained were summarized as follows: Light microscopic exmination revealed congested capillaries and neutrophilic infiltration in both groups. Electron microscopic findings were interstitial and alveolar neutrophilic infiltration, endothelial swelling with increased pinocytotic vesicles and cytoplasmic process formation, and interstitial edema. Decrease of osmiophilic bodies in the type II pneumocytes had appeared at 9 hours after endotoxin injection. These changes were increased in severity at 18 hours and 27 hours after endotoxin injection. In the group of concomitant treatment of gabexate mesilated and endotoxin, there was no edema at 9 hours after injection. After 18 hours welling of endothelial cell and interstitial edema had appeared. However, the severity of the edema was markedly decreased. Type II pneumocytes showed well preserved osmiophilic bodies. According to these results, it is considered that administration of gabexate mesilate can significantly redeced the lung injury induced by endotoxemia.

The Formation of Giant Mitochondria in the Liver Cells Induced by Hydrazine.: Il Hoon Kwon, Jong Gi Lee, Yoon Kyung Sohn, Tae Joong Sohn; Korean J Pathol. 1986;20(3):288-294.

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Abstract PDF: The authors studied the formation of giant mitochondria in liver cell. The Sprague Dawley rats were sacrificed following intervals; 5, 10, 20, 30, and 60 minutes after intraperitoneal injection of hydrazine in the amount of 200 microliter/kg. And the extracted liver tissues were examined with light and electron microscopes. The results obtained were summarized as follow; Light microscopically, there is little difference between control and experimental groups. Electron microscopically, elongated, bizzare shaped mitochondria are appears 5 minutes after hydrazine injection. Those show attenuated portion, Y, U, or C shaped feature suggesting fusion or budding mitochondria. The number of giant mitochondria is decreased after 10 minutes group and rarely present in 60 minutes group. The results suggest in this experiment that the formation of giant mitochondria is kind of reversible change and it is different from the mitochondrial swelling of cellular injury. Intermitochondrial fusion and mitochondrial budding may be related with the formation of giant mitochondria.

Ultrastructural Changes of Liver Cell Mitochondria in Autolysis.: Yoon Kyung Sohn, Il Hoon Kwon, Tae Joong Sohn; Korean J Cytopathol. 1985;19(3):290-301.

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Abstract PDF: The authors studied the ultrastructural changes of liver cell mitochondria in autolysis. The male Sprague-Dawley rats, weighting 140~160 gm were sacrificed for extract liver tissue. The slices of the liver tissue were incubated in 37 degrees C aseptic normal saline, and those were examined by following intervals; 10, 20 and 30 minutes and 1, 2, 6, 12 and 24 hours with light and electron microscope. The results obtained by light microscopy were summerized as follow. Several fine intracytoplasmic vacuoles were observed 1 hour after incubation. After 3 hours, focal destruction of cytoplasmic membrane with pyknosis of nuclei were observed. More delicate intracytoplasmic architectural changes could not be detected at light microscopic studies. The cord arrangement and cellular boundaries were relatively well preserved until 24 hours after incubation. Electronmicroscopically, mild intramitochondrial swelling with diminution of intramatrical granules were observed at 20 minutes. These were the earliest findings. Both high amplitude swelling and destruction of mitochondrial membrane were observed concurrently at 1 hour after incubation. The earlier membrane changes were observed at inner membrane with cristae and followed by degeneration of the outer membrane. The intramatrical amorphous dense deposits were observed at 30 minutes when the membranes were not destroyed. These deposits were noted in the other experimental groups which were incubated longer than 30 minutes. More electron dense deposits were observed after 1 hour at that time the membrane changes appeared. Vhe results suggest in this experiment that the earliest autolytic changes of liver cell mitochondria is loss of intramitochondrial granules and the membraneous changes led to the irreversible mitochondiral injury. The appearance of two types of intramitochondrial dense deposits would be an interesting finding needed to require further investigation for the chemical stucture and mechanism of dense deposit formation.

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