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Volume 32(1); January 1998
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Original Articles
Pathology of Chronic Interstitial Lung Disease.
Dong Hwan Shin
Korean J Pathol. 1998;32(1):1-8.
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AbstractAbstract PDF
Interstitial lung disease is a generic term for a heterogeneous group of lung disease that primarily affect the interstitium although the disease is not clearly restricted to the interstitium. The majority of interstitial lung diseases represent inflammatory insults to the microscopic anatomic space bounded by the basement membrane of epithelial and endothelial cells, which may occur as slowly developing process and ultimately end up as end-stage honeycomb fibrosis. The currently prevalent classification of interstitial pneumonia with practical utility and easy reproducibility pertaining only to idopathic interstitial pneumonia encompasses several different entities some of which may represent different aspects of the same condition. Honeycomb fibrosis is usually caused by a variety of pulmonary disease including chronic interstitial lung disease. It is important to recognize that usual inter-stitial pneumonia and honeycomb fibrosis are not synonymous. In the era of chemotherapy for malignant tumor, aggressive immunosuppression for autoimmune diseases and transplant recipients and acquired immunodeficiency syndrome, lung disease in the immunocompromised host has been common. Diagnostic lung biopsy becomes increasingly needed because proper treatment of interstitial lung disease relies on correct morphologic diagnosis. This review summarizes the pathologic spectrum of idiopathic interstitial pneumonias together with other inflammatory process with known or suggestive etiologies simulating interstitial pneumonias.
The Expression of TGF-beta1 and TGF-beta Receptor I in Human Lung Cancer.
Hye Kyung Ahn, Young Hee Choi, Jung Weon Shim, Young Euy Park, Han Kyeom Kim, Jong Sang Choi, Joung Ho Han
Korean J Pathol. 1998;32(1):9-20.
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AbstractAbstract PDF
A majority of human lung cancer cell lines have developed resistance to growth inhibition via the activation of transforming growth facter-beta (TGF-beta). Previous studies have reported that growth inhibition of TGF-beta is linked to the expression of transforming growth factor-beta receptor type I (TGF-betaRI). Immunohistochemical studies of TGF-beta1 and TGF-betaRI have been carried out in 43 cases of lung neoplasm; including 25 cases of squamous cell carcinoma, 13 cases of adenocarcinoma, 2 cases of adenosquamous cell carcinoma, and 1 case each of undifferentiated carcinoma, small cell carcinoma and neuroendocrine carcinoma. Reverse transcriptase polymerase chain reaction (RT-PCR) for TGF-beta1 mRNA was also performed in 40 cases of tumors and 14 control cases of normal parenchyme. Immunohistochemically, TGF-beta1 and TGF-betaRI expression were noted in the cytoplasm of all type of tumor cells. The staining intensity and areas were examined and scored from 0 to 5. As a whole, TGF-beta1 staining scores in the neoplastic lesions were higher than that of the adjacent normal parenchyme, bronchial epithelium or alveolar epithelium. However, TGF-betaRI staining scores were generally lower than that of the adjacent normal components. The TGF-beta1 mRNA showed a higher percentage of expression in tumors than in normal control. Tumor size, lymph node metastasis, histological differentiation and histological type of tumors did not correlated with the staining score of TGF-beta1 and TGF-betaRI. These results indicate that although various types of human lung carcinoma cells produce TGF-beta1, they show a reduction in TGF-betaRI, resulting in an escape from growth inhibition by TGF-beta1.
A Comparative Study of Immunohistochemistry and PCR-SSCP for Detection of p53 Mutation In Gastric Carcinoma.
Jong Soon Kim, Jae Hyuk Lee, Min Cheol Lee, Chang Soo Park, Sang Woo Juhung
Korean J Pathol. 1998;32(1):21-28.
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AbstractAbstract PDF
Mutation of the p53 tumor-suppressor gene in exons 4 through 9 was examined in 34 cases of primary advanced gastric cancer using PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism) and the results were compared with p53 protein expression as determined by immunohistochemistry (IHC) using a monoclonal antibody(DO-1). p53 protein detected by IHC was observed in 14 cases (41.2%) and genotypic mutation detected by PCR-SSCP in exons 4-9 was observed in 13 cases (38.2%) One case showed an aberrant band on PCR-SSCP both in Exon 7 and Exon 8/9. p53 alteration detected by either IHC or PCR-SSCP was observed in 19 cases (55.9%), but only 8 cases (23.5%) showed both p53 mutation and protein expression. We also tried to obtain the correlation between relative intensity of the shifted bands on PCR-SSCP and percentage of positive cells by IHC, but a significant correlation was not seen between relative intensity of shifted bands on PCR-SSCP and positve cell ratio. A discrepancy between p53 protein expression and p53 mutation is observed in primary gastric carcinomas. The reason for this discrepancy are not apparent. However, examination of gastric carcinomas for mutations in other exons may identify a better correlation with protein overexpression. The results obtained in this study suggest that the negative reaction for p53 immunohistochemistry may not necessarily mean no genetic alteration of the p53 locus.
Expression of the nm23 and E-cadherin Proteins in Breast Carcinoma.
Jean a Kim, Won Il Kim, Sang In Shim, Chang Suck Kang, Kyo Young Lee, Young Shin Kim
Korean J Pathol. 1998;32(1):29-34.
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AbstractAbstract PDF
Expression of the nm23 and E-cadherin proteins has been studied in a number of tumors. Reduced expression of the nm23 and E-cadherin proteins seems to be associated with metastasis or disease progression in some tumors, including breast carcinoma. To assess the role of nm23 and E-cadherin in tumor differentiation and metastasis of breast carcinoma, immunohistochemical staining for the nm23 and E-cadherin proteins was performed in paraffin embedded tumor samples from 86 breast carcinomas. The results were as follows: 1) Expression of the nm23 protein in breast carcinoma was strong positive in 32 cases (37.2%), weak positive in 26 cases (30.2%), and negative in 28 cases (32.6%) of the cases. Expression of the nm23 protein in breast carcinoma decreased according to histological grade and lymph node metastasis, but was not statistically significant. 2) Expression of the E-cadherin protein in breast carcinoma was strong positive in 50 cases (58.1%), weak positive in 24 cases (27.9%), and negative in 12 cases (14%) of the cases. Expression of the E-cadherin protein in breast carcinoma decreased according to histological grade and lymph node metastasis, but was not statistically significant. 3) There was a statistically significant correlation between the expression of the nm23 protein and the E-cadherin protein in breast carcinoma (p<0.05). These results suggest that the expression of the nm23 and E-cadherin proteins is related to tumor differentiation, and may also be an useful prognostic factor in breast carcinoma.
Expression of Transforming Growth Factor-beta and Morphologic Changes of Glomerulosclerosis in FGS/NgaKist Mouse.
Hoon Kyu Oh, Yong Jin Kim, Mi Ok Park, Chul Ho Lee, Byung Hwa Hyun, In Soo Shu
Korean J Pathol. 1998;32(1):35-42.
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AbstractAbstract PDF
Focal segmental glomerulosclerosis (FSGS) is presented as not only one of the primary glomerular diseases but also as a secondary phenomenon for chronic irreversible renal diseases. The main pathological feature of FSGS is the accumulation of extracellular matrix in the glomeruli, for which overexpression of transforming growth factor-beta (TGF-beta) may be responsible for the accumulation of pathological matrix. A new animal model (FGS/NgaKist mouse) of renal failure by spontaneously generating glomerulosclerosis was developed. To elucidate the role of TGF-beta for FSGS, authors observed glomeruli of FGS/NgaKist mouse periodically. FGS/NgaKist mouse strain showed progression of proteinuria and focal glomerular sclerosis with the aging. The glomeruli showed anti IgG, IgA, IgM and complement complex deposits and extracellular matrix accumulation in the mesangium. TGF-beta mRNA and beta2antibody expressions were increased with the advance of glomerular sclerosis. The results suggest the following; FSGS of FGS/NgaKist strain is immune mediated disease and this stimuli on mesangial or endothelial cells may activate TGF-beta gene in their nuclei. This activation, in turn, can cause sclerosis by increasing TGF-beta mRNA transcription followed by secretion of TGF-beta and its action as cytokine for making collagen fibrils.
Ultrastructural Feature of Proximal Convoluted Tubular Cells of Rat Induced by Gentamicin.
Byoung Yuk Lee, Tae Jung Shon, Jong Min Chae
Korean J Pathol. 1998;32(1):43-50.
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AbstractAbstract PDF
Myeloid body formation is an ultrastructural feature of gentamicin induced nephrotoxicity in human being and experimental animals. The origin of the myeloid body is not satisfactorily understood and morphological verification of the developing process of this structure is not fully accomplished. We injected 100 mg/kg/12 hour of gentamicin in 20 Spraque-Dawley rats and examined the ultrastructural feature of the proximal convoluted tubular cells of the kidney every 30 minutes in the first 4 hours, and in 5 hours, 6 hours, 12 hours, 24 hours and 48 hours after injection of gentamicin, with a TEM and a SEM. Myeloid bodies were noted as concentric layers of membranous structures of degenerated endoplasmic reticulum and mitochondria in the lysosome. The number and size of the myeloid body containing lysosomes were increased with time. We can deduce from this observation that injured cell organelles by diffusible gentamicin within the cells are autophagocytosed by lysosomes which were also injured by the drug from pinocytotic vesicles, and incompletely digested organellar remnants are retained in the lysosomes as myeloid bodies. So we think that the myeloid body formation is a result of an exaggerated and a pathologic autophagocytic process due to cell injury induced by gentamicin.
Expression of Alpha Smooth Muscle Actin and Lysozyme in Various Glomerular Diseases.
Sun Hee Sung, Woon Sup Han
Korean J Pathol. 1998;32(1):51-57.
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AbstractAbstract PDF
The cells of glomerular mesangium is composed mostly of intrinsic contractile mesangial cells and a few macrophages. Injury to the mesangium is central to many glomerular diseases. This study was aimed to evaluate and compare the expressions of alpha-smooth muscle actin (ASMA) and lysozyme in the mesangium of various human glomerular diseases and also of according to the severity of their progressions. We performed immunohistochemical and transmission electromicroscopic examinations in 51 cases of renal biopsy including 5 normal kidneys. The results were as follows; (1) ASMA staining was negligible in normal glomeruli. (2) Increased ASMA staining was observed in the mesangium of glomeruli from all specimens of primary glomerular disease, regardless of their diagnosis. (3) The staining intensity of ASMA in mesangium was mild in minimal change disease and membranous glomerulonephritis, and strong in focal segmental glomerulosclerosis (FSGS), diffuse mesangial hypercellularity, membranoproliferative glomerulonephritis (MPGN), and IgA nephropathy (IgAN). (4) The staining intensity of ASMA have no correlation with mesangial immune deposits. (5) The staining intensity of ASMA in mesangium was inversely correlated with the disease progression in FSGS and IgAN. (6) Glomeruli showing global or segmental sclerosis invariably lacked ASMA. (7) Compared with ASMA, the mesangial cells with lysozyme expression were very rare, even though it was in proportion to ASMA staining. Interstitial ASMA expression was confined to fibrotic area in various glomerular diseases. In conclusion, the expression of ASMA and lysozyme in mesangium are increased in a variety of glomerular diseases, regardless of disease entity. Their intensity was in proportion to the mesangial cell proliferation. In progressive glomerulonephritis, such as IgAN and FSGS, the increased expression of ASMA was prominent in the early lesion, and decreased with the progression of the glomerular sclerosis.
Case Reports
Normoblasts and Lymphocytes Carry the Fused Bcr-Abl Gene in Chronic Myelogenous Leukemia: Two Color Fluorescence in Situ Hybridization(FISH) Analysis on the Blood Smears.
Chang Suk Kang, Eun Jung Lee, Won bae Lee, Yong goo Kim, Kyung Ja Han, Kyung Soo Lee, Sang In Shim
Korean J Pathol. 1998;32(1):58-62.
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AbstractAbstract PDF
We performed dual color fluorescence in situ hybridization (FISH) for the bcr/abl fusion in CML using the peripheral blood smears without destruction of cell morphology to determine the bcr/abl fusion. Two patients of CML, one patient in accelerated phase and one patient in chronic phase, were selected. The blood smears were fixed in absolute methanol. FISH was performed with the Mbcr/abl translocation DNA probe mixture and the slides were stained with Wright's stain after FISH. The blood smears of both cases revealed distinct signals without destruction of cellular morphology. The normoblasts and lymphocytes revealed beautiful fused bcr/abl signals as well as granulocytes in both cases. The results provide a novel finding that the normoblasts and lymphocytes in CML are also neoplastic clonal cells which has not been demonstrated with a single-cell approach before.
Granular Cell Tumor of the Thyroid.
Haeng Ji Kang, Eun Kyung Hong, Moon Hyang Park, Jung Dal Lee
Korean J Pathol. 1998;32(1):63-67.
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AbstractAbstract PDF
Granular cell tumor is not uncommon and is a well recognized entity which may arise at virtually any site of the body. However, occurrence in the thyroid is extremely rare and has not been described well. Only three cases could be found in the English literatures. We report a case of granular cell tumor of the thyroid in a 30 year-old woman. The tumor was illdefined, infiltrative and was composed of diffuse sheets of polygonal to fusiform cells with abundant eosinophilic granular cytoplasm. The tumor showed evidence of Schwann cell differentiation in immunohistochemical and ultrastructural examinations. Differentiation from more common thyroid tumors having oncocytic granular cytoplasm should be made by immunohistochemistry or electron microscopy.
Granulomatous Inflammation of Hand following Sea Urchin Sting: 2 cases report.
Jung Ran Kim, Dong Hoon Kim, Tae Jung Jang, Jong Im Lee, Hyun Sul Lim, Hyeon Kyeong Lee, Sung Han Bae
Korean J Pathol. 1998;32(1):68-71.
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AbstractAbstract PDF
Injuries from sea urchins are induced by from penetration of the calcareous spines into the skin. Apart from the transient episode of excruciating pain, there is usually no residual disability. Complications arise, however, when spines are embedded over bony prominences, or within joints. Two cases are reported with injury and protracted disability of fingers resulting from contact with the purple sea urchin, Anthocidaris crassispina, a common echinoderm inhabitant of the Korean east coast. After a latent period of several months in both cases, Case 1 presented as caseating granulomas in the synovium and case 2 exhibited as the usual soft tissue nonsynovial foreign body and noncaseating granulomas. There appears to be a paucity of published data regarding the effects of puncture wounds caused by the spines of this animal. The granulomas have appeared after a latent interval of several months in a proportion of the sufferers, suggests a delayed hyperserisitivity reaction similar to that produced by Mycobacterium species.
Metanephric Adenoma of the Kidney.
Yoon La Choi, Jung Won Lee, Jai Hyang Go, Cheol Keun Park
Korean J Pathol. 1998;32(1):72-75.
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AbstractAbstract PDF
Metanephric adenoma is a rare renal epithelial tumor. Its light microscopic features are very characteristic, and immunohistochemical and electron microscopic studies are not critical to the diagnosis. The literature indicate that, to date, the tumor has behaved in a benign fashion, and predominantly but not exclusively occurred in middle-aged women. It occurs in a wide range up to 11 cm and is usually an incidental finding but may be symptomatic with hematuria or flank pain. Recently, we have experienced a case of renal tumor showing distinctive adenomatous features, which is incidentally found in a 52-year-old female. This tumor is confined to the renal cortex and is well-circumscribed with a characteristic uniform and orderly proliferation of compact well-differentiated small tubules lined by bland oval cells with a very low level of mitotic activity. The term metanephric adenoma is appropriate for this tumor because it accurately describes its bland proliferation of tubules and reflects the embryonic architectural and cytological appearance of this proliferation. The pattern of the tumor, with its occasional papillary glomeruloid- like bodies and foci of elongated tubules, is reminiscent of the fetal metanephric kidney.
Pigmented Squamous Cell Carcinoma Arising from Pigmented Actinic Keratosis.
Hyun Joo Choi, Gyeong Sin Park, Seok Jin Kang, Yeong Jin Choi, Byung Kee Kim, Sun Moo Kim, Sang In Shim
Korean J Pathol. 1998;32(1):76-79.
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AbstractAbstract PDF
Pigmented squamous cell carcinoma is a very rare malignant, pigmented, epidermal tumor. The rarity of pigmented squamous cell carcinomas may reflect in part their misdiagnosis as other pigmented neoplasms, particularly malignant melanoma. To our knowledge, only five cases have been reported in literature. We recently experienced a case of pigmented squamous cell carcinoma arising from pigmented actinic keratosis in a 77 years old female. Physical examination showed a 0.8 0.6 cm, smooth, dark brown pigmented patch with irregular but sharply defined borders located on the upper left chest. The biopsy specimen showed histologic findings of pigmented actinic keratosis with abundant melanin pigments, which became pigmented squamous cell carcinoma. Most of pigments in the squamous cell carcinoma were contained within the melanocytes along with the neoplastic squamous cells.

JPTM : Journal of Pathology and Translational Medicine