75 results on '"Jang, J.-J."'
Search Results
2. Runx3 is required for the differentiation of lung epithelial cells and suppression of lung cancer
- Author
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Lee, K-S, Lee, Y-S, Lee, J-M, Ito, K, Cinghu, S, Kim, J-H, Jang, J-W, Li, Y-H, Goh, Y-M, Chi, X-Z, Wee, H, Lee, H-W, Hosoya, A, Chung, J-H, Jang, J-J, Kundu, J K, Surh, Y-J, Kim, W-J, Ito, Y, Jung, H-S, and Bae, S-C
- Published
- 2010
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3. Expression of heat shock protein 70 blocks thymic differentiation of T cells in transgenic mice
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LEE, W.-H., PARK, Y.-M., KIM, J.-I., PARK, W.-Y., KIM, S.-H., JANG, J.-J., and SEO, J.-S.
- Published
- 1998
4. Spatial Information in local society’s cultural conservation and research
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Jang, J.-J, primary, Liao, H.-M., additional, and Fan, I.-C., additional
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- 2015
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5. P-218ASSESSMENT OF ISCHAEMIA REPERFUSION INJURY BY MICRO-COMPUTED TOMOGRAPHY AND ULTRA-SHORT ECHO-TIME MAGNETIC RESONANCE IMAGING AFTER MOUSE LUNG TRANSPLANTATION
- Author
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Tsushima, Yukio, primary, Wurnig, M., additional, Jang, J.-J., additional, Boss, A., additional, Weder, W., additional, and Jungraithmayr, W., additional
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- 2013
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6. Nuclear overexpression of bcl-2 oncoprotein during the progression of human stomach cancer
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Lee, S S, primary, Cho, K J, additional, Hong, S I, additional, Myoung, N K, additional, and Jang, J J, additional
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- 1998
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7. Cell proliferation not associated with carcinogenesis in rodents and humans.
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Ward, J M, primary, Uno, H, additional, Kurata, Y, additional, Weghorst, C M, additional, and Jang, J J, additional
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- 1993
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8. A 4-week feeding study of ground red chilli (Capsicum annuum) in male B6C3F1 mice
- Author
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Jang, J.-J., primary, Devor, D.E., additional, Logsdon, D.L., additional, and Ward, J.M., additional
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- 1992
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9. ADMA regulates angiogenesis: genetic and metabolic evidence.
- Author
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Achan, V., Ho, H. K., Heeschen, C., Stuehlinger, M., Jang, J. J., Kimoto, M., Vallance, P., and Cooke, J. P.
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NITRIC oxide ,NEOVASCULARIZATION ,NITRIC-oxide synthases ,ISCHEMIA ,TRANSGENIC mice - Abstract
Endothelium-derived nitric oxide (NO) plays an important role in transducing the effects of angiogenic factors. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase (NOS). We used a murine model of hindlimb ischemia to investigate whether genetic or metabolic changes in ADMA levels could impair angiogenic response in vivo. Hindlimb ischemia was surgically induced in C57BL/6J mice, apo E-deficient mice, or transgenic mice overexpressing dimethylarginine dimethylaminohydrolase (DDAH). Some animals were also treated with the NOS antagonist L-nitro-arginine, or the NO precursor L-arginine. Angiogenesis was quantified in the hindlimb skeletal muscle by capillary/myocyte ratio. Plasma or tissue ADMA levels were measured by HPLC. In normal mice, hindlimb ischemia increased tissue ADMA twofold, and reduced DDAH and NOS expression. This was associated with a reduced NOS activity (by over 80%) three days following surgery. On day seven, a threefold increase in DDAH expression and a fall in tissue ADMA levels were associated with a sevenfold increase in NOS activity, whereas NOS expression did not increase above baseline. In DDAH transgenic mice, the elevation of ADMA and decrement in NOS activity was blunted during hindlimb ischemia. Plasma ADMA levels were increased in apo E-mice (1.79 ± 0.45 versus 1.07 ± 0.08 μmol/l; p = 0.008). Capillary index was significantly reduced in apo Emice up to seven weeks after surgery (0.25 ± 0.05 versus 0.62 ±; 0.08; p > 0.001). The effect of hypercholesterolemia on capillary index was reversed by L-arginine, and (in wild-type mice) mimicked by administration of the NOS antagonist L-nitro-arginine. In conclusion, metabolic or genetic changes in plasma and tissue ADMA levels affect tissue NO production and angiogenic response to ischemia. [ABSTRACT FROM AUTHOR]
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- 2005
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10. Interferon-alpha treatment of chronic hepatitis C in children with hemophilia.
- Author
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Ko, J S, Choe, Y H, Kim, E J, Lee, E H, Jang, J J, and Seo, J K
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- 2001
11. The effect of tumor size on F-18-labeled fluorodeoxyglucose and fluoroerythronitroimidazole uptake in a murine sarcoma model.
- Author
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Chung, June-Key, Chang, Young, Lee, Yong, Kim, Young, Jeong, Jae, Lee, Dong, Jang, Ja, Lee, Myung, Chung, J K, Chang, Y S, Lee, Y J, Kim, Y J, Jeong, J M, Lee, D S, Jang, J J, and Lee, M C
- Abstract
The purpose of this study was to evaluate the effect of tumor size on the uptake of 18F-fluorodeoxyglucose (FDG) and fluoroerythronitroimidazole (FETNIM) in a murine sarcoma model. ICR mice were xenografted with sarcoma 180 cell line and tumors were allowed to grow to a weight of 0.26-5.82 grams. 18F-FDG and 18F-FETNIM were injected intravenously in separate groups of mice, and after 1 hr, the tumors were excised and radiotracer uptake was measured. In another group of mice tumors were autoradiographically analyzed and subjected to H & E staining. In both the FDG and FETNIM group, per-gram radiotracer uptake by a tumor was inversely proportional to tumor weight. 18F-FETNIM correlated more (r = -0.593, p < 0.05) than 18F-FDG (r = -0.447, p < 0.05). Autoradiographic studies revealed that FDG accumulated in viable tumor areas, whereas FETNIM accumulated in both viable and partially necrotic areas. In the case of 18F-FETNIM, a direct correlation between tumor weight and the no-uptake-area to total-tumor-area was demonstrated. We concluded that increased tumor size is associated with decreased uptake of 18F-FDG and FETNIM, though this depends on the type of radiotracers and distribution of necrosis. [ABSTRACT FROM AUTHOR]
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- 1999
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12. Auditory verbal intervention for the infants with hearing problems.
- Author
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Chang, S., Hwang, H. K., Park, H. Y., Sohn, M., Jang, J. J., Seo, M. H., and Oh, S. H.
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CONFERENCES & conventions ,HEARING impaired ,REHABILITATION ,CHILDREN - Abstract
There has not been much evidence about rehabilitation results for the infants with hearing problems under age 1 even though the 1-3-6 principle of early diagnosis and intervention was accepted worldwide. In this study, we tried to reveal auditory verbal intervention effects for the infants with hearing problems followed by the principle. A total of 50 babies and their caregivers participated. The average hearing thresholds of the babies were worse than 80 dB HL(B) and they were fitted HAs or CIs except 5 babies with no hearing prosthesis. The average age of the participants at the initial assessment was 7.3 months and the average age at the final assessment was 12.6 months. After the initial assessment, their development was closely followed in the 8 developmental areas of sound responses, listening skills, receptive & expressive language, speech development, oral functions, social interactions, and cognitive communication with auditory verbal approach. Their initial developmental rate was 0.55 and the rate had been accelerated up to 1.8, however, after 6 monthintervention, final development rate was 0.76 which had not reached to the normal rate of 1. There were large individual differences as expected, in average, the area of cognitive communication was the most developed area while the area of speech was the least developed area at the end of the intervention. Auditory verbal approach was suitable for the babies as well as their caregivers and could provide valid and timely information about the effects of prostheses they were wearing and the timing of changing devices for the babies. It would be more informative with longer period of the intervention. [ABSTRACT FROM AUTHOR]
- Published
- 2018
13. Heterozygous mice for the transforming growth factor-beta type II receptor gene have increased susceptibility to hepatocellular carcinogenesis.
- Author
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Im YH, Kim HT, Kim IY, Factor VM, Hahm KB, Anzano M, Jang JJ, Flanders K, Haines DC, Thorgeirsson SS, Sizeland A, and Kim SJ
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- Animals, Carcinogens, Diethylnitrosamine, Female, Gene Dosage, Genes, cdc physiology, Genetic Predisposition to Disease, Heterozygote, Liver drug effects, Liver metabolism, Liver physiology, Liver Neoplasms, Experimental chemically induced, Liver Neoplasms, Experimental metabolism, Male, Mice, Mice, Inbred C57BL, Phenobarbital pharmacology, Pregnancy, Protein Serine-Threonine Kinases, RNA, Messenger biosynthesis, RNA, Messenger genetics, Receptor, Transforming Growth Factor-beta Type II, Receptors, Transforming Growth Factor beta biosynthesis, Transforming Growth Factor beta biosynthesis, Transforming Growth Factor beta genetics, Transforming Growth Factor beta1, Cell Transformation, Neoplastic genetics, Liver Neoplasms, Experimental genetics, Receptors, Transforming Growth Factor beta genetics
- Abstract
The transforming growth factor-beta (TGF-beta) receptor complex and its downstream signaling intermediates constitute a tumor suppressor pathway. In many cancers, expression of TGF-beta type II receptor (TbetaR-II) is markedly decreased. In the present study, we show that the hepatocytes isolated from 15-day-old, but not 9-month-old, mice heterozygous for the deletion of the TbetaR-II gene are slightly less sensitive to the growth-inhibitory effect of TGF-beta when compared with wild-type littermates of same age. In addition, the proliferation index of hepatocytes as indicated by bromodeoxyuridine incorporation is mildly increased in the heterozygous mice. These subtle changes in cellular phenotype did not result in either gross or microscopic abnormality of the liver. The treatment of these mice with the chemical carcinogen, diethylnitrosamine, results in a significantly enhanced tumorigenesis in the liver when compared with the wild-type littermates. Our results demonstrate the gene-dosage effect of TbetaR-II and indicate that the reduced expression of TbetaR-II in mice increases susceptibility to tumorigenesis in the liver.
- Published
- 2001
14. Induction of apoptosis in p53-deficient human hepatoma cell line by wild-type p53 gene transduction: inhibition by antioxidant.
- Author
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Lee KH, Kim KC, Jung YJ, Ham YH, Jang JJ, Kwon H, Sung YC, Kim SH, Han SK, and Kim CM
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- Acetylcysteine pharmacology, Carcinoma, Hepatocellular, Cell Survival, Cyclin-Dependent Kinase Inhibitor p21, Cyclin-Dependent Kinases metabolism, Cyclins genetics, DNA Fragmentation, Free Radical Scavengers pharmacology, Glutathione pharmacology, Humans, In Situ Nick-End Labeling, Liver Neoplasms, Retroviridae genetics, Retroviridae metabolism, Tumor Cells, Cultured, Antioxidants pharmacology, Apoptosis drug effects, Cyclins metabolism, Genes, p53, Transduction, Genetic, Tumor Suppressor Protein p53 metabolism
- Abstract
We investigated the role of wild-type (wt)-p53 as an inducer of apoptotic cell death in human hepatoma cell lines. Following the retrovirus-mediated transduction of the wt-p53 gene, Hep3B cells lacking the endogenous p53 expression began to die through apoptosis in 4 h. They showed a maximal apoptotic death at 12 h, whereas HepG2 cells expressing endogenous p53 did not. However, the transduction of the wt-p53 gene elicited growth suppression of both Hep3B and HepG2 cells. P21(WAF1/CIP1), a p53-inducible cell cycle inhibitor, was induced, not only in Hep3B cells undergoing apoptosis, but also in HepG2 cells. The kinetics of the p21(WAF1/CIP1) induction, DNA fragmentation, and growth suppression of the Hep3B cells showed that DNA fragmentation and growth suppression progressed rapidly following p21(WAF1/CIP1) accumulation. N-acetyl-cysteine or glutathione, potent antioxidants, strongly inhibited the DNA fragmentation, but did not reduce the elevated level of p21(WAF1/CIP1). These findings suggested that p21(WAF1/CIP1) was not a critical mediator for the execution of p53-mediated apoptosis, although it contributed to the growth inhibition of cells undergoing apoptosis. Furthermore, p53-mediated apoptosis could be repressed by antioxidants.
- Published
- 2001
15. Fatal submassive hepatic necrosis associated with tyrosine-methionine-aspartate-aspartate-motif mutation of hepatitis B virus after long-term lamivudine therapy.
- Author
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Kim JW, Lee HS, Woo GH, Yoon JH, Jang JJ, Chi JG, and Kim CY
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- Amino Acid Motifs genetics, Antiviral Agents pharmacology, Drug Resistance, Microbial, Fatal Outcome, Hepatitis B, Chronic pathology, Hepatitis B, Chronic physiopathology, Humans, Immunocompetence, Lamivudine pharmacology, Male, Middle Aged, Mutation, Necrosis, Polymorphism, Restriction Fragment Length, Reverse Transcriptase Inhibitors pharmacology, Antiviral Agents therapeutic use, Hepatitis B virus drug effects, Hepatitis B virus genetics, Hepatitis B, Chronic drug therapy, Lamivudine therapeutic use, Reverse Transcriptase Inhibitors therapeutic use
- Abstract
We present a case of infection with lamivudine-resistant mutant hepatitis B virus (HBV) that fatally exacerbated hepatitis following the emergence of HBV with mutations in the tyrosine-methionine-aspartate-aspartate (YMDD) motif in an immunocompetent patient who was receiving long-term lamivudine therapy. Restriction fragment length polymorphism analysis showed that the YMDD-motif mutant was the predominant form of circulating HBV at the time of the fatal exacerbation, and a necropsy specimen of the liver revealed submassive hepatic necrosis without steatosis.
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- 2001
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16. Expression of the G1-S modulators in hepatitis B virus-related hepatocellular carcinoma and dysplastic nodule: association of cyclin D1 and p53 proteins with the progression of hepatocellular carcinoma.
- Author
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Choi YL, Park SH, Jang JJ, and Park CK
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- Adult, Aged, Carcinoma, Hepatocellular chemistry, Carcinoma, Hepatocellular etiology, Cyclin-Dependent Kinase Inhibitor p16 analysis, Female, G1 Phase, Humans, Immunohistochemistry, Liver Neoplasms chemistry, Liver Neoplasms etiology, Male, Microfilament Proteins analysis, Middle Aged, Proliferating Cell Nuclear Antigen analysis, Retinoblastoma Protein analysis, S Phase, Carcinoma, Hepatocellular pathology, Cyclin D1 analysis, Hepatitis B complications, Liver Neoplasms pathology, Muscle Proteins, Precancerous Conditions virology, Tumor Suppressor Protein p53 analysis
- Abstract
Deranged expression of cell cycle modulators has been reported to contribute to the development and progression of hepatocellular carcinoma (HCC). However, their expression patterns remain poorly understood in hepatitis B virus (HBV)-related HCC, which constitutes about 65-70% of HCC in Korea. The aims of this study were to evaluate the expressions of G1-S modulators in HBV-related HCCs and dysplastic nodules (DNs), and to correlate with the histopathologic features of HCCs. Immunohistochemical expressions of cyclin D1, cyclin E, p53, p27, p21, p16, Rb, and PCNA proteins were investigated in 80 HCCs and 22 DNs. Cyclin D1 overexpression showed positive relationships with advanced tumor stage, poor differentiation, larger tumor size, microvascular invasion, intrahepatic meta-stasis, no tumor capsule formation, infiltrative growth, aberrant p53 expression, and high PCNA labeling index (LI) of HCC (p<0.05). Aberrant p53 expression showed positive relationship with poor differentiation of HCC (p<0.01). Expression of cyclin D1 or p53 was not observed in DNs. The p27 LI and p16 LI were lower in HCCs with intrahepatic metastasis (p<0.05). Cyclin D1 overexpression and aberrant p53 expression could be associated with the progression of HBV-related HCC, and might have a less crucial role in the DN-HCC sequence. In addition, elevated expression of p27 and p16 proteins might have inhibitory action to the intrahepatic metastasis of HBV-related HCC.
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- 2001
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17. Nicotine stimulates angiogenesis and promotes tumor growth and atherosclerosis.
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Heeschen C, Jang JJ, Weis M, Pathak A, Kaji S, Hu RS, Tsao PS, Johnson FL, and Cooke JP
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- Animals, Arteriosclerosis pathology, Mice, Mice, Inbred C57BL, Arteriosclerosis complications, Carcinoma, Lewis Lung blood supply, Carcinoma, Lewis Lung pathology, Lung Neoplasms blood supply, Lung Neoplasms pathology, Neovascularization, Pathologic etiology, Nicotine pharmacology
- Abstract
We provide anatomic and functional evidence that nicotine induces angiogenesis. We also show that nicotine accelerates the growth of tumor and atheroma in association with increased neovascularization. Nicotine increased endothelial-cell growth and tube formation in vitro, and accelerated fibrovascular growth in vivo. In a mouse model of hind-limb ischemia, nicotine increased capillary and collateral growth, and enhanced tissue perfusion. In mouse models of lung cancer and atherosclerosis, we found that nicotine enhanced lesion growth in association with an increase in lesion vascularity. These effects of nicotine were mediated through nicotinic acetylcholine receptors at nicotine concentrations that are pathophysiologically relevant. The endothelial production of nitric oxide, prostacyclin and vascular endothelial growth factor might have a role in these effects.
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- 2001
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18. Congenital monoblastic leukemia with 9;11 translocation in monozygotic twins : a case report.
- Author
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Park SY, Jang JJ, Kim CW, Cho HI, and Chi JG
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- Fatal Outcome, Female, Hepatomegaly complications, Hepatomegaly genetics, Hepatomegaly pathology, Humans, Infant, Newborn, Leukemia, Monocytic, Acute complications, Leukemia, Monocytic, Acute genetics, Leukemia, Monocytic, Acute pathology, Liver pathology, Splenomegaly complications, Splenomegaly genetics, Splenomegaly pathology, Chromosomes, Human, Pair 11, Chromosomes, Human, Pair 9, Diseases in Twins genetics, Leukemia, Monocytic, Acute congenital, Translocation, Genetic, Twins, Monozygotic genetics
- Abstract
We report an autopsy case of congenital monoblastic leukemia that developed in monozygotic twins. The twin presented with progressive hepatosplenomegaly at 4 weeks after birth. One twin died of massive bleeding and hypovolemic shock before the treatment started. At autopsy, the liver was diffusely enlarged and showed a diffuse whitish discoloration except for the subcapsular and perivenular areas. Microscopic examination disclosed infiltration of histiocyte-like atypical cells along the sinusoids and portal areas of the liver. Spleen, lymph nodes and choroid plexus were also infiltrated by the tumor cells. However, bone marrow involvement of the tumor was minimal although multifocal. On immunohistochemical staining, these atypical cells were reactive for CD68 (PGM-1) and lysozyme, suggesting that the tumor cells might have been derived from mono- histiocyte. Cytogenetic study revealed 9;11 translocation, which is frequently associated with acute monoblastic leukemia. To the best of our knowledge, this is the first report of congenital monoblastic leukemia of monozygotic twins in Korea.
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- 2001
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19. In vivo antitumor effect of herpes simplex virus thymidine kinase gene therapy in rat hepatocellular carcinoma: feasibility of adenovirus-mediated intra-arterial gene delivery.
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Kwon HC, Kim JH, Kim KC, Lee KH, Lee JH, Lee BH, Lee KH, Jang JJ, Lee CT, Lee H, and Kim CM
- Subjects
- Adenoviridae genetics, Adenoviridae metabolism, Animals, Antiviral Agents therapeutic use, Combined Modality Therapy, Ganciclovir therapeutic use, Genetic Vectors, Humans, Killer Cells, Natural cytology, Liver pathology, Liver physiopathology, Liver Neoplasms, Experimental pathology, Liver Neoplasms, Experimental physiopathology, Macrophages cytology, Male, Rats, Simplexvirus genetics, Thymidine Kinase metabolism, Tumor Cells, Cultured, Gene Transfer Techniques, Genetic Therapy methods, Liver Neoplasms, Experimental therapy, Simplexvirus enzymology, Thymidine Kinase genetics
- Abstract
Transfer of the herpes simplex virus-thymidine kinase gene, followed by the administration of ganciclovir (HSV-tk/GCV), has been a major approach for cancer gene therapy. We investigated the antitumor effect of the HSV-tk/GCV strategy with the rat orthotopic hepatocellular carcinoma (HCC) model and the tumor-selective gene delivery by an adenovirus-mediated gene transfer through the hepatic artery. The complete antitumor effect was demonstrated, after the treatment with GCV in rat HCC established by the implantation of HSV-tk transferred rat HCC cells. The in vivo bystander effect was also observed. The marked infiltration of CD4+ and CD8+ T lymphocytes, macrophages and NK cells were found in the tumor area. After the injection of adenovirus carrying the LacZ gene into the hepatic artery, the selective expression of transgene in the tumor cell was achieved. These findings indicate that the HSV-tk/GCV strategy, using an adenoviral vector, could be a promising avenue for the treatment of hepatocellular carcinoma.
- Published
- 2001
20. Somatic mutations of TRAIL-receptor 1 and TRAIL-receptor 2 genes in non-Hodgkin's lymphoma.
- Author
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Lee SH, Shin MS, Kim HS, Lee HK, Park WS, Kim SY, Lee JH, Han SY, Park JY, Oh RR, Kang CS, Kim KM, Jang JJ, Nam SW, Lee JY, and Yoo NJ
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- Humans, Polymorphism, Genetic, Polymorphism, Single-Stranded Conformational, Receptors, TNF-Related Apoptosis-Inducing Ligand, Lymphoma, Non-Hodgkin genetics, Mutation, Receptors, Tumor Necrosis Factor genetics
- Abstract
Tumor necrosis factor-related apoptosis-inducing ligand-receptor 1 (TRAIL-R1) and tumor necrosis factor-related apoptosis-inducing ligand-receptor 2 (TRAIL-R2) are cell-surface receptors involved in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced cell-death signaling. TRAIL-R1 and TRAIL-R2 genes have recently been mapped to chromosome 8p21-22, which is a frequent site of allelic deletions in many types of human tumors, including non-Hodgkin's lymphoma (NHL). Because TRAIL/TRAIL receptor system plays an important role in lymphocyte homeostasis, we hypothesized that the mutations of TRAIL-R1 and TRAIL-R2 may be involved in the development of NHL and that such mutations may be responsible for the allelic losses of 8p21-22 in NHL. In this study, we analysed the entire coding region of TRAIL-R2 gene and the death domain region of TRAIL-R1 gene for the detection of the somatic mutations in a series of 117 human NHLs using polymerase chain reaction (PCR)-based single strand conformation polymorphism (SSCP) analysis. Overall, eight tumors (6.8%) were found to have two TRAIL-R1 gene mutations or six TRAIL-R2 gene mutations. Interestingly, of the eight mutations, six missense mutations (two TRAIL-R1 and four TRAIL-R2) were detected in the death domains and one nonsense mutation of TRAIL-R2 was detected just before the death domain. Our data suggest that somatic mutations of TRAIL-R1 and TRAIL-R2 genes may play a role in the pathogenesis of some NHLs and that TRAIL-R1 and TRAIL-R2 genes might be the relevant genes to the frequent loss of chromosome 8p21-22 in human NHL.
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- 2001
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21. Overexpression of human telomerase RNA in Helicobacter pylori-infected human gastric mucosa.
- Author
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Hur K, Gazdar AF, Rathi A, Jang JJ, Choi JH, and Kim DY
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- Adult, Formaldehyde, Helicobacter Infections genetics, Humans, In Situ Hybridization, Male, Paraffin Embedding, RNA, Messenger genetics, Telomerase genetics, Testis enzymology, Testis microbiology, Tissue Fixation, Gastric Mucosa enzymology, Gastric Mucosa microbiology, Helicobacter Infections enzymology, Helicobacter pylori, RNA, Messenger biosynthesis, Telomerase biosynthesis
- Abstract
Telomerase, an enzyme associated with cellular immortality and malignancy, plays an important role in cellular immortalization and tumorigenesis. Furthermore, overexpression of the RNA component of the telomerase, called human telomerase RNA (hTR), has been demonstrated in various human cancers as an early event. The pattern of hTR expression following Helicobacter pylori (H. pylori) infection in human gastric mucosa was investigated by a radioactive in situ hybridization (ISH) assay. Paraffin-embedded sections of 50 biopsy specimens taken from the gastric antrum of individual patients infected to different extents with H. pylori, as well as normal gastric mucosa, were studied. In normal gastric mucosa, only weak hTR expression was noted and the expression was limited to basal cells of the gastric glands. However, the degree of hTR expression gradually increased in parallel with the degree of H. pylori infection. The mean scores of gastric mucosa with mild, moderate and severe degrees of H. pylori infection were 2.3, 2.8, and 3.7 times higher than that of normal gastric mucosa, respectively. The results of this study suggested that up-regulation of hTR expression is a frequent and early event associated with H. pylori infection in the gastric mucosa and may play some role in gastric carcinogenesis. Sufficient synthesis of hTR during this early stage may be a prerequisite for telomerase reactivation to occur in gastric cancer.
- Published
- 2000
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22. Angiogenesis is impaired by hypercholesterolemia: role of asymmetric dimethylarginine.
- Author
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Jang JJ, Ho HK, Kwan HH, Fajardo LF, and Cooke JP
- Subjects
- Angiogenesis Inhibitors antagonists & inhibitors, Angiogenesis Inhibitors blood, Animals, Apolipoproteins E deficiency, Arginine blood, Dose-Response Relationship, Drug, Female, Fibroblast Growth Factor 2 antagonists & inhibitors, Fibroblast Growth Factor 2 pharmacology, Hypercholesterolemia blood, Mice, Mice, Inbred C57BL, Nitric Oxide biosynthesis, Nitric Oxide Synthase blood, Angiogenesis Inhibitors pharmacology, Apolipoproteins E blood, Arginine analogs & derivatives, Arginine pharmacology, Enzyme Inhibitors pharmacology, Hypercholesterolemia physiopathology, Neovascularization, Physiologic drug effects, Nitric Oxide Synthase antagonists & inhibitors
- Abstract
Background: Many angiogenic factors require endothelium-derived nitric oxide (NO) to exert their effects. Recently, an endogenous competitive antagonist of NO synthase has been characterized: asymmetric dimethylarginine (ADMA). Elevated plasma levels of ADMA reduce NO synthesis in hypercholesterolemia. Accordingly, we hypothesized that hypercholesterolemia impairs angiogenesis by an ADMA-dependent mechanism., Methods and Results: Angiogenesis was assessed with the use of a disk angiogenesis system implanted subcutaneously in normal (E(+)) mice or apolipoprotein (apo)E-deficient hypercholesterolemic (E(-)) mice. After 2 weeks, the disks were removed, and the fibrovascular growth area was used as an index of angiogenesis. Basal and fibroblast growth factor-stimulated angiogenesis was impaired in E(-) mice, associated with an elevation in plasma ADMA. Oral administration of L-arginine reversed the impairment of angiogenesis in E(-) mice. By contrast, oral administration of L-nitroarginine (an exogenous antagonist of NO synthase) reduced angiogenesis. When added directly to the disk, ADMA dose-dependently inhibited basal and fibroblast growth factor-induced angiogenesis, an effect that was reversed by oral administration of L-arginine., Conclusions: The derangement of the NO synthase pathway that occurs in hypercholesterolemia is associated with an impairment of angiogenesis. The lipid-induced impairment of angiogenesis can be reversed by oral administration of L-arginine and can be mimicked in normocholesterolemic animals by administration of an NO synthase antagonist. The data are consistent with the hypothesis that ADMA is an endogenous inhibitor of angiogenesis.
- Published
- 2000
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23. Clinicopathologic study of Castleman's disease in Korea.
- Author
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Kim JE, Kim CJ, Park IA, Kim WH, Seo JW, Jang JJ, Kim CW, Park SH, Lee HS, Chi JG, Kim YI, and Ham EK
- Subjects
- Adolescent, Adult, Biomarkers, Castleman Disease classification, Castleman Disease epidemiology, Castleman Disease virology, Dendritic Cells, Follicular pathology, Epstein-Barr Virus Infections epidemiology, Epstein-Barr Virus Infections virology, Female, Germinal Center pathology, Herpesviridae Infections epidemiology, Herpesviridae Infections virology, Herpesvirus 4, Human isolation & purification, Herpesvirus 8, Human isolation & purification, Humans, Hyperplasia, Intercellular Adhesion Molecule-1 analysis, Interleukin-6 analysis, Korea epidemiology, Lymph Nodes chemistry, Lymph Nodes pathology, Lymph Nodes virology, Male, Middle Aged, Neovascularization, Pathologic, Receptors, Complement 3d analysis, Retrospective Studies, Tumor Virus Infections epidemiology, Tumor Virus Infections virology, Castleman Disease pathology
- Abstract
Castleman's disease represents an atypical lymphoproliferative disorder, infrequently associated with various immunologic abnormalities or subsequent development of malignancy such as Kaposi sarcoma, malignant lymphoma and plasmacytoma. Its clinicopathologic features depend on various etiologic factors such as Kaposi sarcoma herpesvirus (KSHV), oversecretion of IL-6, adhesion molecule and follicular dendritic cell dysplasia, etc. To investigate the relationship of Castleman's disease (CD) and the above factors, we reviewed 22 cases of CD. Four cases of KSHV positive CD were detected, all multicentric, plasma cell type, and these cases displayed prominent vascular proliferation, characteristic 'Kaposi-like lesion'. IL-6 and CD54 positive mononuclear cells were scattered in interfollicular areas of KSHV positive cases. Follicular dendritic cell hyperplasia, vascular proliferation, expression of IL-6 and CD54 did not show any significant difference between solitary vs multicentric type, and plasma cell type vs hyaline vascular type. Our study suggests that KSHV positive CD reveals unique pathologic features, and the probable relationship of KSHV and IL-6 and CD54 is discussed.
- Published
- 2000
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24. Somatic mutations of Fas (Apo-1/CD95) gene in cutaneous squamous cell carcinoma arising from a burn scar.
- Author
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Lee SH, Shin MS, Kim HS, Park WS, Kim SY, Jang JJ, Rhim KJ, Jang J, Lee HK, Park JY, Oh RR, Han SY, Lee JH, Lee JY, and Yoo NJ
- Subjects
- Adolescent, Adult, Aged, Alleles, Base Sequence genetics, Carcinoma, Squamous Cell etiology, Carcinoma, Squamous Cell metabolism, Carcinoma, Squamous Cell pathology, Child, Child, Preschool, Female, Humans, Male, Middle Aged, Skin Neoplasms etiology, Skin Neoplasms metabolism, Skin Neoplasms pathology, fas Receptor metabolism, Burns complications, Carcinoma, Squamous Cell genetics, Cicatrix complications, Mutation genetics, Skin Neoplasms genetics, fas Receptor genetics
- Abstract
Fas (Apo-1/CD95) is a cell-surface receptor involved in cell death signaling, and recent reports have suggested that defects within the Fas receptor pathway such as Fas mutation play an important part in the development and progression of human tumors. Burn scar-related squamous cell carcinoma of skin is a unique subtype of cutaneous squamous cell carcinoma, and tends to be more aggressive in nature than conventional squamous cell carcinoma. The molecular mechanisms underlying the development and progression of burn scar-related squamous cell carcinoma, however, are not clear. In this study, we analyzed the entire coding region and all splice sites of the Fas gene for the detection of the somatic mutations in a series of 50 conventional squamous cell carcinomas and 21 burn scar-related squamous cell carcinomas by polymerase chain reaction, single strand conformation polymorphism, and DNA sequencing. We detected mis-sense mutations in three of 21 burn scar-related squamous cell carcinomas (14.3%), whereas no mutation was detected in 50 conventional squamous cell carcinomas. Of the three Fas mutations detected in the burn scar-related squamous cell carcinomas, one was found in Fas ligand-binding domain, another one was identified in the death domain known to be involved in the transduction of an apoptotic signal, and the other one was found in the transmembrane domain. Our data show that some burn scar-related squamous cell carcinomas have Fas gene mutations in important regions for the apoptosis function and suggest that these mutations might be involved in the pathogenesis of burn scar-related squamous cell carcinomas. In addition, our results provide an important clue to understanding the difference between burn scar-related squamous cell carcinoma and conventional squamous cell carcinoma at the molecular level.
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- 2000
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25. Point mutations and deletions of the Bcl10 gene in solid tumors and malignant lymphomas.
- Author
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Lee SH, Shin MS, Kim HS, Park WS, Kim SY, Lee HK, Park JY, Oh RR, Jang JJ, Park KM, Han JY, Kang CS, Lee JY, and Yoo NJ
- Subjects
- B-Cell CLL-Lymphoma 10 Protein, Breast Neoplasms genetics, Carcinoma, Ductal, Breast genetics, Carcinoma, Squamous Cell genetics, Colorectal Neoplasms genetics, Germinoma genetics, Humans, Laryngeal Neoplasms genetics, Lymphoma, B-Cell genetics, Lymphoma, T-Cell genetics, Adaptor Proteins, Signal Transducing, Chromosomes, Human, Pair 1 genetics, Gene Deletion, Neoplasm Proteins genetics, Neoplasms genetics, Point Mutation genetics
- Abstract
The Bcl10 gene, which encodes a protein with proapoptotic activity, recently has been identified on chromosome 1p22. In this study, we analyzed somatic mutations and deletions of the Bcl10 gene in a series of 439 tumor tissues from various histological origins that are known to have frequent loss of heterozygosity at chromosome 1p22. According to the LOH study at intragenic polymorphic sites, deletion of Bcl10 in informative cases was detected in 50% of malignant mesotheliomas, 33% of gastric carcinomas, 23% of breast carcinomas, 20% of hepatocellular carcinomas, 17% of lymphomas, 15% of colorectal carcinomas, 13% of laryngeal carcinomas, and 10% of male germ cell tumors (GCTs). In contrast, we detected Bcl10 mutations in 4 of 120 lymphomas (3.3%) and 2 of 78 GCTs (2.6%), respectively, but no mutation was found in the remaining solid tumors analyzed. Taken together, these data imply that Bcl10 may occasionally be involved in the pathogenesis of lymphoma and GCTs. However, the absence or low frequency of the mutation suggests that either Bcl10 is inactivated by other mechanisms or it is not the only target of chromosome 1p22 deletion in human tumors.
- Published
- 1999
26. Alterations of the DR5/TRAIL receptor 2 gene in non-small cell lung cancers.
- Author
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Lee SH, Shin MS, Kim HS, Lee HK, Park WS, Kim SY, Lee JH, Han SY, Park JY, Oh RR, Jang JJ, Han JY, Lee JY, and Yoo NJ
- Subjects
- Adenocarcinoma genetics, Amino Acid Sequence, Carcinoma, Squamous Cell genetics, Humans, Loss of Heterozygosity, Molecular Sequence Data, Mutation, Missense genetics, Polymerase Chain Reaction, Polymorphism, Single-Stranded Conformational, Receptors, TNF-Related Apoptosis-Inducing Ligand, Carcinoma, Non-Small-Cell Lung genetics, Chromosomes, Human, Pair 8 genetics, Lung Neoplasms genetics, Mutation genetics, Receptors, Tumor Necrosis Factor genetics
- Abstract
Chromosome 8p21-22 is a frequent site of allelic deletions in many types of human tumors, including non-small cell lung cancer (NSCLC). Tumor necrosis factor-related apoptosis-inducing ligand-receptor 2 (TRAIL-R2) is a cell-surface receptor involved in cell death signaling. The TRAIL-R2 gene recently has been mapped to chromosome 8p21-22. To explore the possibility that the TRAIL-R2 gene might be the relevant gene to the frequent deletion of 8p21-22 in NSCLC, we have analyzed the entire coding region and all splice sites of TRAIL-R2 for the detection of the somatic mutations in a series of 104 NSCLCs. Overall, 11 tumors (10.6%) were found to have TRAIL-R2 gene mutations in the death domain known to be involved in the transduction of an apoptotic signal. Our data indicate that somatic mutation of TRAIL-R2 may play a role in the pathogenesis of some NSCLCs and that the TRAIL-R2 gene is one of the genes relevant to the frequent loss of chromosome 8p21-22 in NSCLC.
- Published
- 1999
27. Detection of methylation damage in DNA of gastric cancer tissues using 32P postlabelling assay.
- Author
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Kim DY, Cho MH, Yang HK, Hemminki K, Kim JP, Jang JJ, and Kumar R
- Subjects
- Adenocarcinoma pathology, Adenocarcinoma surgery, Chromatography, High Pressure Liquid, DNA Adducts isolation & purification, DNA, Neoplasm metabolism, Deoxyguanosine analogs & derivatives, Deoxyguanosine analysis, Humans, Phosphorus Radioisotopes, Radioisotope Dilution Technique, Stomach Neoplasms pathology, Stomach Neoplasms surgery, Adenocarcinoma genetics, DNA Damage, DNA Methylation, DNA, Neoplasm genetics, Stomach Neoplasms genetics
- Abstract
Gastric cancer is the most common cancer in Korea. The causes are still unknown but it has been speculated that gastric cancer is associated with consumption of foods rich in nitrates/nitrites or a high dietary intake of salt or pickled food. In the present study, we studied the level of alkylated DNA adducts formed in gastric cancer tissues in comparison with that in normal gastric mucosa. DNA was extracted from surgically removed gastric cancer tissues and patient-matched normal gastric mucosa. The level of N7-methyldeoxyguanosine was measured by 32P-postlabelling assay after high performance liquid chromatography (HPLC) enrichment. We found that the level of N7-methyldeoxyguanosine of gastric cancerous tissues was significantly higher than that of normal gastric mucosa (P=0.01685).
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- 1999
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28. Alterations of Fas (APO-1/CD95) gene in transitional cell carcinomas of urinary bladder.
- Author
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Lee SH, Shin MS, Park WS, Kim SY, Dong SM, Pi JH, Lee HK, Kim HS, Jang JJ, Kim CS, Kim SH, Lee JY, and Yoo NJ
- Subjects
- Amino Acid Substitution, Antigens, CD genetics, Carcinoma, Transitional Cell immunology, Carcinoma, Transitional Cell pathology, Carcinoma, Transitional Cell surgery, DNA Primers, Exons, Fas Ligand Protein, Frameshift Mutation, Humans, Membrane Glycoproteins genetics, Mutation, Missense, Neoplasm Staging, Polymerase Chain Reaction, Urinary Bladder Neoplasms immunology, Urinary Bladder Neoplasms pathology, Urinary Bladder Neoplasms surgery, Carcinoma, Transitional Cell genetics, Loss of Heterozygosity, Point Mutation, Polymorphism, Single-Stranded Conformational, Urinary Bladder Neoplasms genetics, fas Receptor genetics
- Abstract
Fas (Apo-1/CD95) is a cell-surface receptor involved in cell death signaling. The key role of the Fas system in negative growth regulation has been studied mostly within the immune system, and somatic mutations of Fas in cancer patients have been described solely in lymphoid-lineage malignancies. We analyzed somatic mutations and loss of heterozygosity of Fas gene in 43 transitional cell carcinomas of urinary bladder. Overall, 12 tumors (28%) were found to have Fas mutations, including 11 missense mutations and 1 frameshift mutation. Ten of the 12 mutations were located in the death domain known to be involved in the transduction of an apoptotic signal, and 8 of these 10 mutations showed an identical G to A transition at bp 993, indicating a potential hotspot in bladder cancers. Three of eight (38%) informative tumors carrying Fas mutations showed LOH at polymorphic sites in the promoter region. This is the first report on the Fas gene mutations in nonlymphoid malignancies, and our data suggest that alterations of the Fas gene might lead to the loss of its apoptotic function and contribute to the pathogenesis of some bladder cancers.
- Published
- 1999
29. 2-(Allylthio)pyrazine inhibition of aflatoxin B1-induced hepatocarcinogenesis in rats.
- Author
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Ha TG, Jang JJ, Kim SG, and Kim ND
- Subjects
- Aflatoxin B1 metabolism, Animals, Carcinogenicity Tests, DNA Adducts drug effects, DNA Adducts urine, DNA, Neoplasm metabolism, Glutathione Transferase metabolism, Hepatectomy, Immunoenzyme Techniques, Liver drug effects, Liver enzymology, Liver pathology, Liver Neoplasms, Experimental chemically induced, Liver Neoplasms, Experimental enzymology, Male, Phenobarbital pharmacology, Precancerous Conditions enzymology, Precancerous Conditions pathology, RNA metabolism, Rats, Rats, Sprague-Dawley, Aflatoxin B1 toxicity, Enzyme Inhibitors pharmacology, Liver Neoplasms, Experimental prevention & control, Pyrazines pharmacology
- Abstract
2-(Allylthio)pyrazine (2-AP), a synthetic pyrazine derivative with an allylsulfur moiety, has hepatoprotective effects against toxicants. Effect of 2-AP on hepatic tumorigenesis in association with glutathione S-transferase (GST) induction was examined in rats exposed to aflatoxin B1 (AFB1). Both AFB1-DNA adduct formation in the liver and urinary elimination of 8,9-dihydro-8-(N7-guanyl)-9-hydroxy-aflatoxin B1 (AFB1-N7-guanine) adduct were also determined. Male Sprague Dawley rats were treated with 2-AP at the daily oral doses of 10, 25 and 50 mg/kg for 16 consecutive days, during which four repeated doses of AFB1 (1.0 mg/kg) were given to the animals. Rats were then subjected to two-thirds of hepatectomy, followed by administration of phenobarbital (PB). Focal areas of hepatocellular alteration were identified after 44 days and preneoplastic foci expressing the placental form of glutathione S-transferase P (GST-P) were quantified by immunostaining of liver sections. 2-AP reduced the volume of liver occupied by GST-P foci by 65-96%. Under these experimental conditions, 2-AP treatment resulted in significant elevations in GST activity in the liver. Levels of radiolabeled AFB1 covalently bound to hepatic DNA, RNA and proteins were significantly reduced in rats treated with 2-AP for 5 days. 2-AP pretreatment also caused a 45% reduction in the urinary elimination of AFB1-N7-guanine adduct over the 24-h postdosing period. The present findings demonstrated that 2-AP exhibited protective effects against AFB1-induced hepatocarcinogenesis in rats with a marked decrease in the level of AFB1-DNA adduct. Reduction of hepatic DNA adducts might result from elevations of activity of GST, which catalyzes detoxification of the carcinogen.
- Published
- 1999
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30. A pathologic study of abdominal lymphangiomas.
- Author
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Chung JH, Suh YL, Park IA, Jang JJ, Chi JG, Kim YI, and Kim WH
- Subjects
- Abdominal Neoplasms metabolism, Abdominal Neoplasms physiopathology, Adult, Child, Child, Preschool, Factor VIII biosynthesis, Female, Humans, Lymphangioma metabolism, Lymphangioma physiopathology, Male, Middle Aged, Platelet Endothelial Cell Adhesion Molecule-1 biosynthesis, Retrospective Studies, Abdominal Neoplasms pathology, Lymphangioma pathology
- Abstract
Abdominal lymphangiomas are uncommon angiomatous tumor occurring mainly in childhood. This is a retrospective clinicopathologic study of 17 cases of abdominal lymphangioma. The patients included are five children and 12 adults, with a mean age at initial presentation of 30.7 years (age ranges 3-63). The locations of the tumors were mesentery (5), retroperitoneum (4), colon (3), omentum (3), mesocolon (1) and gallbladder (1). Infiltrative growth was more common pattern than entirely circumscribed pattern. Masses were mostly multilocular cysts and contained chyle or serous fluid. On immunohistochemical staining, 16 cases were reactive for either CD31 or factor VIII-related antigen. These fact would suggest that intra-abdominal lymphangiomas simulate the immunohistochemical features of collecting lymphatics. Follow up was possible in 12 cases for 3-50 months (mean 19 months) and only one patient showed local recurrence. Although abdominal lymphangiomas are rare in adulthood and correct preoperative diagnosis is difficult, awareness of such a possibility in adulthood will contribute to make a correct preoperative diagnosis.
- Published
- 1999
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31. Correlation of changes in natural killer cell activity and glutathione S-transferase placental form positive hepatocytes in diethylnitrosamine-induced rat hepatocarcinogenesis.
- Author
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Lee YS, Choe GY, Kim YI, Park SH, Park IA, Lee MJ, and Jang JJ
- Subjects
- Animals, Body Weight, Female, Liver cytology, Organ Size, Placenta, Rats, Rats, Sprague-Dawley, Carcinogens pharmacology, Diethylnitrosamine pharmacology, Glutathione Transferase metabolism, Killer Cells, Natural immunology, Liver enzymology, Liver Neoplasms physiopathology
- Abstract
To evaluate the induction of preneoplastic hepatic foci in relation to natural killer cell (NK) activity, we sequentially analyzed glutathione S-transferase placental form positive (GST-P+) hepatocytes and NK activity during diethylnitrosamine (DEN) and phenobarbital (PB)-induced hepatocarcinogenesis in Sprague-Dawley rats. Previous studies have shown that NK activity can modulate the carcinogenic process induced by chemical carcinogens. Newborn females were initially given a single intraperitoneal injection of 15 mg DEN/kg and three weeks later, they were treated with 500 ppm phenobarbital (PB). From week 3, PB was administered in drinking water for 9 weeks. Interim and terminal sacrifices were performed at weeks 12, 15 and 30. GST-P+ hepatocytes increased with age in DEN-treated rats, especially in the population of more than two GST-P+ hepatocytes. The NK activity of DEN-treated rats did not significantly differ from that of control rats until week 12, but it progressively decreased from week 15 to 30. These results indicate that changes of NK activity inversely correlated with the induction of preneoplastic hepatic foci. This strong correlation of decreased NK activity with enhanced induction of GST-P+ foci suggests that NK activity is important in the early progression of hepatocarcinogenesis in rats.
- Published
- 1999
- Full Text
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32. Mechanisms related to [18F]fluorodeoxyglucose uptake of human colon cancers transplanted in nude mice.
- Author
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Chung JK, Lee YJ, Kim C, Choi SR, Kim M, Lee K, Jeong JM, Lee DS, Jang JJ, and Lee MC
- Subjects
- Animals, Blotting, Northern, Blotting, Western, Colonic Neoplasms diagnostic imaging, Hexokinase analysis, Humans, Immunohistochemistry, Male, Mice, Mice, Nude, Monosaccharide Transport Proteins analysis, Monosaccharide Transport Proteins genetics, Neoplasm Transplantation, Polymerase Chain Reaction, RNA, Messenger analysis, Radionuclide Imaging, Transplantation, Heterologous, Tumor Cells, Cultured, Colonic Neoplasms metabolism, Fluorodeoxyglucose F18 pharmacokinetics, Radiopharmaceuticals pharmacokinetics
- Abstract
Unlabelled: [18F]Fluorodeoxyglucose ([18F]FDG), a glucose analogue, has been widely used for tumor imaging. To investigate the mechanisms related to [18F]FDG uptake by tumors, an experiment involving nude mice was performed., Methods: Human colon cancer cell lines SNU-C2A, SNU-C4 and SNU-C5 were transplanted to nude mice. Using immunohistochemical staining and Western blot, the expression of glucose transporter (Glut) isoforms (Glut-1 through -5) in xenografted tumors was analyzed. For the analysis of messenger ribonucleic acid (mRNA) expression, reverse-transcription polymerase chain reaction and Northern blot were used and the enzyme activity of hexokinase in cancer tissues was measured by continuous spectrophotometric rate determination., Results: [18F]FDG uptake in SNU-C4 and SNU-C5 cells was higher than in normal colon cells. Among these cells and xenografted tumors, SNU-C5 showed the highest level of [18F]FDG uptake, followed by SNU-C4 and SNU-C2A. An immunostaining experiment showed intense staining of Glut-1 in SNU-C5 tumors but somewhat faint staining in SNU-C4. SNU-C5 tumors also showed positive staining with Glut-3, although this was not the case with SNU-C2A and SNU-C4. Western blot analysis showed the expression of Glut-1 and Glut-3 in all tumors. Experiments involving Northern blot analysis and reverse-transcription polymerase chain reaction confirmed the overexpression of Glut-1 mRNA in all tumors, with the highest level in SNU-C5. The level of Glut-3 mRNA was also elevated in SNU-C5 tumors but not in SNU-C2A and SNU-C4. The enzyme activity of hexokinase did not vary among different tumors., Conclusion: Gluts, especially Glut-1, are responsible for [18F]FDG uptake in a nude mouse model of colon cancer rather than hexokinase activity. Increased numbers of glucose transporters at the plasma membrane of cancer cells is attributed to an increased level of transcripts of glucose transporter genes and may be a cause of increased [18F]FDG uptake, at least in colon cancer tumors.
- Published
- 1999
33. Somatic mutations in the kinase domain of the Met/hepatocyte growth factor receptor gene in childhood hepatocellular carcinomas.
- Author
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Park WS, Dong SM, Kim SY, Na EY, Shin MS, Pi JH, Kim BJ, Bae JH, Hong YK, Lee KS, Lee SH, Yoo NJ, Jang JJ, Pack S, Zhuang Z, Schmidt L, Zbar B, and Lee JY
- Subjects
- Adolescent, Adult, Aged, Carcinoma, Hepatocellular etiology, Child, Female, Hepatitis B complications, Humans, Liver Neoplasms etiology, Male, Middle Aged, Carcinoma, Hepatocellular genetics, Liver Neoplasms genetics, Mutation, Proto-Oncogene Proteins c-met genetics
- Abstract
The MET protooncogene encodes a transmembrane tyrosine kinase identified as the receptor of a polypeptide known as hepatocyte growth factor/scatter factor. We performed PCR-based single-strand conformational polymorphism and sequencing analysis of the tyrosine kinase domain of the MET gene (exon 15-19) in 75 primary liver cancers. Three missense mutations were detected exclusively in 10 childhood hepatocellular carcinomas (HCCs), while no mutations were detected in 16 adult HCCs, 21 cholangiocarcinomas, or 28 hepatoblastomas. The extremely short incubation period from hepatitis B virus infection to the genesis of childhood HCC as compared with the adult HCC suggests that there may be an additional mechanism that accelerates the carcinogenesis of childhood HCC. Our results indicate that mutations of the tyrosine kinase domain of the MET gene may be involved in the acceleration of the carcinogenesis in childhood HCC.
- Published
- 1999
34. Engagement of CD99 induces apoptosis through a calcineurin-independent pathway in Ewing's sarcoma cells.
- Author
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Sohn HW, Choi EY, Kim SH, Lee IS, Chung DH, Sung UA, Hwang DH, Cho SS, Jun BH, Jang JJ, Chi JG, and Park SH
- Subjects
- 12E7 Antigen, Antibodies, Monoclonal pharmacology, Antigens, CD immunology, Calcineurin, Calcium physiology, Caspase Inhibitors, Caspases physiology, Cell Adhesion Molecules immunology, Cell Differentiation, Cyclosporine pharmacology, Dactinomycin pharmacology, Fluorescent Antibody Technique, Indirect, Humans, Membrane Potentials, Microscopy, Confocal, Microscopy, Electron, Neuroblastoma pathology, Neuroectodermal Tumors, Primitive pathology, Tacrolimus pharmacology, Tumor Cells, Cultured, Antigens, CD physiology, Apoptosis, Cell Adhesion Molecules physiology, Sarcoma, Ewing pathology
- Abstract
Programmed cell death (PCD) is a prominent feature of the development of the immune and nervous systems. In both systems, widespread PCD occurs in primitive progenitor cells during development. In this study, we demonstrated that Ewing's sarcoma (ES) cells, undifferentiated neural precursors, underwent apoptosis upon engagement of CD99 with anti-CD99 monoclonal antibody. Apoptosis via CD99 occurred only in the undifferentiated state of ES cells, but not in differentiated ES cells. CD99-induced apoptosis in ES cells appeared to require de novo synthesis of RNA and protein as well as caspase activation. Cyclosporin A, known to be a potent inhibitor of both calcineurin activation and mitochondrial permeability transition pore opening, inhibited CD99-mediated apoptosis, whereas FK-506, a specific calcineurin inhibitor, did not, indicating the induction of CD99-mediated apoptosis through a calcineurin-independent pathway. Furthermore, the dying cells displayed the reduction of mitochondrial transmembrane potential (delta psi m). These results suggest that CD99 engagement induce CsA-inhibitable mitochondrial permeability transition pore opening, followed by a reduction of delta psi m and caspase activation, thereby leading to apoptosis. Based on these results, we suggest the possible involvement of CD99 in the apoptotic processes that occur during nervous system development and also its application in immunotherapeutic trials for ES cases.
- Published
- 1998
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35. Frequent somatic mutations in serine/threonine kinase 11/Peutz-Jeghers syndrome gene in left-sided colon cancer.
- Author
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Dong SM, Kim KM, Kim SY, Shin MS, Na EY, Lee SH, Park WS, Yoo NJ, Jang JJ, Yoon CY, Kim JW, Kim SY, Yang YM, Kim SH, Kim CS, and Lee JY
- Subjects
- AMP-Activated Protein Kinase Kinases, Base Sequence, Chromosomes, Human, Pair 19, Genes, Tumor Suppressor, Humans, Loss of Heterozygosity, Molecular Sequence Data, Colonic Neoplasms genetics, Mutation, Peutz-Jeghers Syndrome genetics, Protein Serine-Threonine Kinases genetics
- Abstract
We analyzed somatic mutation and loss of heterozygosity (LOH) in the serine/threonine kinase 11 (STK11)/Peutz-Jeghers syndrome gene in 49 colorectal tumors in three different stages of a dysplasia-carcinoma sequence. We detected LOH in 10 of 19 (52.6%) informative colorectal cancers at loci D19S886 and/or D19S883, but no LOH was observed in 25 informative adenomas. We detected a total of 9 somatic mutations [7 of 13 (53.8%) left-sided colon cancers and 2 of 7 (28.6%) left-sided adenomas with high-grade dysplasia], but no mutations were detected in right-sided colon tumors. Of the nine mutations, one was a frameshift mutation (the same mutation detected in Peutz-Jeghers syndrome family previously), and the other eight were missense mutations. This results indicate that STK11 is a tumor suppressor gene and that genetic changes of STK11 play an important role in left-sided colon cancer carcinogenesis.
- Published
- 1998
36. Association of Helicobacter pylori infection with gastric adenocarcinoma.
- Author
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Lee BM, Jang JJ, Kim JS, You YC, Chun SA, Kim HS, Han HM, Ahn MY, and Byun SH
- Subjects
- Adenocarcinoma microbiology, Adult, Aged, Clinical Enzyme Tests, Comorbidity, Helicobacter Infections diagnosis, Helicobacter pylori enzymology, Humans, Korea epidemiology, Male, Middle Aged, Stomach enzymology, Stomach microbiology, Stomach Neoplasms microbiology, Urease analysis, Adenocarcinoma epidemiology, Helicobacter Infections epidemiology, Helicobacter pylori isolation & purification, Stomach Diseases microbiology, Stomach Neoplasms epidemiology
- Abstract
Gastric adenocarcinoma is the most prevalent cancer in South Korea, and Helicobacter pylori (H. pylori) infection is also common. This study was performed to examine the association between H. pylori infection and gastric cancer, taking into account various other factors. To investigate the association between gastric adenocarcinoma and H. pylori infection, determined by urease-positive reaction in the CLO test, a total of 175 paired specimens (175 tumor and 175 tissues adjacent to tumor) of stomach cancer patients and a total of 113 control specimens were obtained. The positive H. pylori infection rates were 78.9% (138/175) among the patients in specimens of tumor or tissues adjacent to the tumor and 41.6% (47/113) among controls in the CLO test. A positive correlation between H. pylori infection and gastric cancer was observed (age-adjusted odds ratio, 7.0; MH chi2=34.5 with P<0.0005). These data suggest that stomach cancer patients in Korea have high infection rates of H. pylori regardless of site specificity, and this infection might be causally associated with stomach cancer.
- Published
- 1998
- Full Text
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37. A distinct region of chromosome 19p13.3 associated with the sporadic form of adenoma malignum of the uterine cervix.
- Author
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Lee JY, Dong SM, Kim HS, Kim SY, Na EY, Shin MS, Lee SH, Park WS, Kim KM, Lee YS, Jang JJ, and Yoo NJ
- Subjects
- Adenocarcinoma genetics, Cell Separation, Chromosome Mapping, Female, Humans, Loss of Heterozygosity, Sequence Deletion, Adenoma genetics, Chromosomes, Human, Pair 19, Genes, Tumor Suppressor, Peutz-Jeghers Syndrome genetics, Uterine Cervical Neoplasms genetics
- Abstract
Adenoma malignum (AM) is known to be one of the malignant tumors that is commonly associated with Peutz-Jeghers syndrome. Recently, the genetic locus of Peutz-Jeghers syndrome was mapped to the telomeric region of chromosome 19p. We analyzed nine sporadic cases of AM with high-density loss of heterozygosity to study the region of chromosome 19p13.2-13.3 using eight microsatellite markers. Our deletion mapping data revealed a distinct region with 100% loss of heterozygosity frequency at marker D19S216. This result indicates that a putative tumor suppressor gene for AM is located at D19S216 on chromosomal band 19p13.3 and plays an important role in AM tumorigenesis.
- Published
- 1998
38. Loss of heterozygosity and somatic mutations of the VHL tumor suppressor gene in sporadic cerebellar hemangioblastomas.
- Author
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Lee JY, Dong SM, Park WS, Yoo NJ, Kim CS, Jang JJ, Chi JG, Zbar B, Lubensky IA, Linehan WM, Vortmeyer AO, and Zhuang Z
- Subjects
- Adolescent, Adult, Aged, Aged, 80 and over, Cell Transformation, Neoplastic genetics, Cerebellar Neoplasms pathology, DNA, Neoplasm genetics, Female, Hemangioblastoma pathology, Humans, Loss of Heterozygosity, Male, Middle Aged, Stromal Cells chemistry, Stromal Cells pathology, Von Hippel-Lindau Tumor Suppressor Protein, Cerebellar Neoplasms genetics, Genes, Tumor Suppressor, Hemangioblastoma genetics, Ligases, Proteins genetics, Tumor Suppressor Proteins, Ubiquitin-Protein Ligases
- Abstract
Cerebellar hemangioblastoma is a benign central nervous system neoplasm with characteristic proliferation of vascular and stromal cells. There is increasing evidence that the stromal cell population may represent the neoplastic component of hemangioblastoma, whereas the vascular component may be composed of reactive, nonneoplastic cells. Therefore, successful genetic testing for loss of heterozygosity requires selective analysis of target cell populations. Here, tissue microdissection was used to selectively analyze the stromal cell component of 20 archival sporadic cerebellar hemangioblastomas for loss of heterozygosity at the Von-Hippel Lindau (VHL) gene and somatic VHL gene mutations. Allelic deletions at the VHL gene locus were detected in the stromal cell component with one or more markers (D3S1038, D3S1110, and/or 104/105) in 10 of 19 (52.6%) informative cases. In all cases, heterozygosity at the VHL gene locus was retained in the vascular component. In two cases, aberrant bands in exon 2 of the VHL gene were demonstrated in the stromal cells by PCR-based single-strand conformation polymorphism analysis, and somatic missense mutations were successfully characterized in two of the sporadic hemangioblastomas by direct sequencing. The results suggest that allelic losses and mutations of the VHL tumor suppressor gene play a role in sporadic cerebellar hemangioblastoma tumorigenesis. Furthermore, because the genetic changes were detected in selectively procured stromal cell areas, the data provide strong evidence that the stromal cell represents a neoplastic component of hemangioblastoma.
- Published
- 1998
39. Blockade of nitric oxide synthesis reduces myocardial oxygen consumption in vivo.
- Author
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Sherman AJ, Davis CA 3rd, Klocke FJ, Harris KR, Srinivasan G, Yaacoub AS, Quinn DA, Ahlin KA, and Jang JJ
- Subjects
- Animals, Blood Pressure drug effects, Carbon Dioxide blood, Coronary Circulation drug effects, Dogs, Heart physiology, Heart Rate drug effects, Myocardial Contraction drug effects, Nitric Oxide physiology, Oxygen blood, Ventricular Function, Left drug effects, Enzyme Inhibitors pharmacology, Heart drug effects, Hemodynamics drug effects, Myocardium metabolism, NG-Nitroarginine Methyl Ester pharmacology, Nitric Oxide Synthase antagonists & inhibitors, Nitroarginine pharmacology, Oxygen Consumption drug effects
- Abstract
Background: Although cardiac myocytes and coronary vascular endothelium are known to express a constitutive form of NO synthase, the in vivo effects of tonic endogenous production of NO on myocardial O2 consumption and contractile performance remain unclear., Methods and Results: The effects of blockade of NO synthase were determined in intact dogs. Myocardial O2 consumption decreased systematically over a wide range of hemodynamic demand after the systemic administration of N omega-nitro-L-arginine methyl ester (L-NAME) or N omega-nitro-L-arginine. Decreases after doses of 1 and 10 mg/kg L-NAME averaged 23 +/- 3.8% and 34 +/- 7.2% at a heart rate of 90 bpm in open-chest animals. Similar reductions occurred after the administration of L-NAME and N omega-nitro-L-arginine in chronically instrumented animals and were unaffected by beta-adrenergic blockade. Intracoronary infusion of L-NAME in chronically instrumented animals reduced both myocardial O2 consumption and regional segment shortening, even at a dose that did not increase systemic arterial pressure., Conclusions: The blockade of NO synthesis reduces myocardial O2 consumption in vivo. The decrease in O2 consumption is accompanied by a decrease in segment shortening. It involves a direct myocardial action of NO, is unaffected by beta-blockade, and is consistent with in vitro studies indicating that low levels of NO augment contractile performance by inhibition of a cGMP-dependent phosphodiesterase.
- Published
- 1997
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40. Overexpression of tissue inhibitors of metalloproteinase-1 and -2 in the stroma of gastric cancer.
- Author
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Hong SI, Park IC, Hong WS, Son YS, Lee SH, Lee JI, Choi DW, Moon NM, Choe TB, and Jang JJ
- Subjects
- Blotting, Northern, Glycoproteins genetics, Humans, Proteins genetics, RNA, Messenger biosynthesis, Tissue Inhibitor of Metalloproteinase-2, Tissue Inhibitor of Metalloproteinases, Adenocarcinoma enzymology, Glycoproteins biosynthesis, Protein Biosynthesis, Stomach Neoplasms enzymology
- Abstract
The fundamental event of cancer invasion and metastasis is the complicated interaction of cancer cells with host cells, in which event, a number of proteases and their inhibitors are involved. Matrix metalloproteinases are the potent proteases in degrading the basement membrane and extra cellular matrix and are inhibited by specific endogeneous inhibitors, tissue inhibitors of metalloproteinases-1(TIMP-1) and TIMP-2. The expression of mRNA for TIMP-1 and -2 was investigated by Northern blot analysis in specimens taken from 27 patients with primary gastric adenocarcinoma; 25 samples from the primary site, six from the metastatic lymph nodes and two from the peritoneal fluids. The expression for TIMP-1 and -2 was compared in primary gastric cancer tissues, metastatic lymph nodes and normal gastric mucosae. TIMP-1 mRNA was overexpressed in 24 (96%) out of 25 primary cancer tissues compared with the paired normal mucosae, while TIMP-2 was in 10 (40%). In six specimens of metastatic lymph nodes, TIMP-1 and -2 were overexpressed in 6 (100%) and 4 (67%) specimens, respectively. Of two specimens prepared from the peritoneal fluids, all specimens overexpressed TIMP-1 compared with the those of primary cancer tissues, while one (50%) specimen overexpressed TIMP-2. Immunohistochemical staining was done to investigate the localization of TIMP-1 and -2, demonstrating that the immunoreactivity for TIMP-1 and -2 was clearly detected in the cytoplasm of the stromal cells. These results suggest that both TIMP-1 and -2 are overexpressed by stromal cells in most of primary and some metastatic gastric cancer tissues and that TIMP-1 and TIMP-2, produced by stromal cells, may play an important role in inhibiting the proteolytic activity of matrix metalloproteinases originated from cancer cells, in gastric cancer.
- Published
- 1996
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41. Primary malignant lymphomas of the stomach. Pathological and clinical analyses of 38 resected cases.
- Author
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Kang YK, Kim CW, Kim WH, Jang JJ, Park SH, and Kim YI
- Subjects
- Adult, Aged, Aged, 80 and over, Female, Humans, Lymphoma metabolism, Lymphoma therapy, Male, Middle Aged, Stomach Neoplasms metabolism, Stomach Neoplasms therapy, Survival Analysis, Lymphoma pathology, Stomach Neoplasms pathology
- Abstract
The stomach is the most frequent site of extranodal lymphoma and primary gastric lymphoma might be distinguished from the nodal lymphoma by its different pathogenesis and prognosis. Based on the Isaacson's classification, clinico-pathologic reviews of 38 resected primary gastric lymphomas were done. Immunohistochemical stainings for PCNA, B and T cell markers, bcl-2 and p53 were performed. Eighteen were of low grade and 20 were of high grade. There were significant differences between low and high graders in the aspect of the size, depth of lesion, gross type, immunophenotype, staining intensity for PCNA, expressions of bcl-2 and p53. The overall 2-year survival rate was 85.3%. Factors with prognostic significance on survival by univariate analyses included immunophenotype, histologic grading and PCNA staining pattern. After multivariate analyses, immunophenotype proved to be a significant factor. We think that the histologic grading by Isaacson's classification and the immunohistochemical stainings performed were useful in pathologic and/or clinical aspects. The excellent survival rate in this study was partly due to the selection of resectable cases. However, earlier diagnosis and appropriate treatment might have contributed to the improved prognosis of gastric lymphoma in recent years.
- Published
- 1996
- Full Text
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42. Concentration and distribution of tumor associated antigens TAG-72 and CEA in stomach cancer.
- Author
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Chung JK, Lee MC, Chung HK, Lim SM, Jang JJ, and Koh CS
- Subjects
- Adenocarcinoma diagnostic imaging, Adenocarcinoma surgery, Adenocarcinoma, Mucinous diagnostic imaging, Adenocarcinoma, Mucinous pathology, Adenocarcinoma, Mucinous surgery, Antibodies, Monoclonal, Autoradiography, Carcinoma diagnostic imaging, Carcinoma surgery, Humans, Intestines pathology, Iodine Radioisotopes, Least-Squares Analysis, Metaplasia, Radionuclide Imaging, Stomach Neoplasms diagnostic imaging, Stomach Neoplasms surgery, Adenocarcinoma pathology, Antigens, Neoplasm analysis, Carcinoembryonic Antigen analysis, Carcinoma pathology, Glycoproteins analysis, Stomach Neoplasms pathology
- Abstract
We measured the concentration and distribution of tumor associated antigens, TAG-72 and CEA, in stomach cancer by in vitro quantitative autoradiography (IV-QAR). Frozen sections of 33 specimens were incubated with varying concentrations of 125I-labeled CEA-79.1 and B72.3 antibodies specific for carcinoembryonic antigen (CEA) and tumor-associated glycoprotein-72 (TAG-72), respectively. Computer analysis of specific antibody binding gave maximal binding values which were equal to the concentrations of the antigen or epitope. TAG-72 was detected in 25 specimens, at a concentration ranging from 8.4 to 562.9 pmol/g. CEA was detected in 32 of the 33 specimens and its concentration ranged from 8.8 to 525.3 pmol/g. The distribution of TAG-72 by IV-QAR coincided with that of the tumor cells in 41.4% of the pathologic lesions. The distribution of CEA coincided with the tumor cells in 80.5% of pathologic lesions, nearly twice the TAG-72. The concentration of TAG-72 was significantly higher in mucinous adenocarcinoma and mucin containing adenocarcinomas than other types of adenocarcinomas. There was no significant difference in the concentration of CEA among the pathologic types of stomach cancer. In summary, stomach cancer exhibited wide variations in TAG-72 and CEA expression. CEA expression was more frequent and homogeneous than TAG-72.
- Published
- 1995
- Full Text
- View/download PDF
43. Over-expression of p53 protein in squamous cell carcinoma of the skin.
- Author
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Rhim KJ, Hong SI, Hong WS, Lee DS, Park IC, Lee SY, and Jang JJ
- Subjects
- Adult, Aged, Female, Genes, p53, Humans, Male, Middle Aged, Mutation, Carcinoma, Squamous Cell chemistry, Skin Neoplasms chemistry, Tumor Suppressor Protein p53 analysis
- Abstract
p53 gene mutations have been known to be highly related to the particular stage of transformation in various types of human cancers. This study was conducted to investigate the p53 mutations at the protein level by an immunohistochemical method using anti-p53 antibody, NCL-p53-DO-7. Twenty-five cancer specimens were obtained surgically from patients with squamous cell cancer of the skin at the Korea Cancer Center Hospital. The cancers were classified according to the possible etiology into two groups, burn scar originated and UV-related cancers. Overexpression of p53 protein was detected in ten (40%) out of 25 cases tested: six (40%) of 15 cases associated with burn scar and four (40%) of ten cases related to UV exposure. In all normal skin cells in specimens, p53 protein was not stained at all. The stages and histological grades were evaluated for their relationship with the overexpression of p53 protein. No significant difference was found between the overexpression of p53 protein and the stages or histological grades. These results demonstrating that 40% of skin cancers were positive for p53 overexpression suggest that the alterations of the p53 gene may play a role and the exact role of p53 gene in the development of squamous cell carcinoma of the skin will be studied.
- Published
- 1995
- Full Text
- View/download PDF
44. Adult T-cell leukemia/lymphoma in a Korean--a case report.
- Author
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Lee SS, Hong SI, Lee DS, Kang YK, Kim CW, and Jang JJ
- Subjects
- Antineoplastic Combined Chemotherapy Protocols therapeutic use, Cyclophosphamide administration & dosage, DNA, Viral blood, Doxorubicin administration & dosage, Etoposide administration & dosage, Human T-lymphotropic virus 1 isolation & purification, Humans, Immunophenotyping, Korea epidemiology, Lymph Nodes pathology, Male, Middle Aged, Neoplastic Stem Cells chemistry, Neoplastic Stem Cells pathology, Prednisone administration & dosage, Proviruses isolation & purification, Vincristine administration & dosage, Leukemia-Lymphoma, Adult T-Cell drug therapy, Leukemia-Lymphoma, Adult T-Cell epidemiology, Leukemia-Lymphoma, Adult T-Cell pathology, Leukemia-Lymphoma, Adult T-Cell virology
- Abstract
The clinicopathologic features of a Korean patient with adult T-cell leukemia/lymphoma(ATLL) are presented. A 51-year-old man, who has lived in Korea since birth, had multiple cutaneous nodules and multiple lymphadenopathy for the previous two months. A histopathologic study of the lymph node and skin lesion revealed T-cell non-Hodgkin's lymphoma of pleomorphic type, medium and large cell type. Peripheral blood examination showed leukemic features with 30% of abnormal lymphoid cells. HTLV-I proviral DNA pX region was detected in the DNA from peripheral blood mononuclear cells(PBMC) and the specific gag, pol, and env HTLV-I sequences were detected in the lymph node using polymerase chain reaction technique. Human T-cell leukemia/lymphoma type I(HTLV-I) antibodies were present in the serum. An immunophenotypic study of the lymph node revealed CD4 positive and CD8 negative helper/inducer T cell type surface markers. This case is the acute type, i.e. prototypic ATLL. He was treated with an intensive chemotherapy including cyclophosphamide, etoposide, doxorubicin, vincristine, and prednisone. Despite initial transient improvement, the tumor progressed after three cycles of the regimen and became refractory to further chemotherapy. These clinicopathologic findings, including the immunophenotypic analysis, established with certainty the diagnosis of HTLV-I-induced adult T-cell leukemia/lymphoma.
- Published
- 1994
- Full Text
- View/download PDF
45. Aberrant expression of p53 gene product in malignant melanoma.
- Author
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Rhim KJ, Hong SI, Hong WS, Lee SY, Lee DS, and Jang JJ
- Subjects
- Adult, Aged, Aged, 80 and over, Female, Genes, p53, Humans, Immunohistochemistry, Male, Melanoma genetics, Middle Aged, Sex Factors, Melanoma metabolism, Tumor Suppressor Protein p53 analysis
- Abstract
According to the current concept of carcinogenesis, the alterations of p53 tumor suppressor gene have been the most frequently detected in both human cancer cell lines and cancer tissues freshly isolated. This study was conducted to investigate the p53 gene alteration in malignant melanoma. Nineteen tumor tissues were obtained from 19 patients with malignant melanoma and examined for the expression of p53 protein by immunohistochemical staining with mouse monoclonal anti-p53 antibody, NCL-p53-DO-7. Twelve out of 19 cases (63%) showed positive reactions for p53 protein: 26, 21 and 16% of which had low, intermediate and high reactivity, respectively. p53 alteration more frequently expressed in female (10/12) than male patients (2/7) with malignant melanoma (p < 0.05). The incidence of expression of p53 protein was compared according to the stages and the sites of tissue obtained. The positive rate for p53 protein was not significantly different between the stages. The positive rates for p53 protein were five out of five (100%), one out of two (50%) and six out of twelve (50%) in tissues obtained from the metastatic, lymph node, and primary sites, respectively. The difference in the positive rates, however, is not statistically significant. These results suggest that p53 gene is a frequent target for mutation in the development of malignant melanoma.
- Published
- 1994
- Full Text
- View/download PDF
46. Tumor concentration and distribution of carcinoembryonic antigen measured by in vitro quantitative autoradiography.
- Author
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Chung JK, Jang JJ, Lee DS, Lee MC, and Koh CS
- Subjects
- Adenocarcinoma immunology, Antibodies, Monoclonal, Binding Sites, Breast Neoplasms immunology, Carcinoma, Squamous Cell immunology, Gastrointestinal Neoplasms immunology, Humans, Kinetics, Lung Neoplasms immunology, Autoradiography methods, Carcinoembryonic Antigen analysis, Neoplasms immunology
- Abstract
Unlabelled: One of the most critical factors in successful immunoscintigraphy and radioimmunotherapy is the local concentration and distribution of the target antigen. The purpose of this study was to evaluate the concentration and distribution of carcinoembryonic antigen (CEA) in various carcinomas., Methods: In vitro quantitative autoradiography was performed in carcinomas of the stomach (32 cases), colon (20 cases), breast (29 cases) and lung (26 cases). Frozen tumor sections were incubated with varying concentrations of 125I-labeled monoclonal antibody (Mab) CEA-79.1 (IgG2a), which is specific for CEA. Digitized autoradiographic images from these sections were compared to adjacent H & E and immunoperoxidase-stained sections. Computer analysis of specific antibody binding quantitated the maximal value (Bmax), which is equal to the concentrations of CEA., Results: Stomach cancer expressed CEA in 31 cases (97%). All colon cancer specimens exhibited CEA and breast cancer expressed CEA in 24 cases (83%). In adenocarcinoma of the lung, CEA was measured in all specimens. The concentration of CEA did not vary significantly among the pathologic types or among the various degrees of differentiation in each carcinoma. CEA was expressed homogeneously in adenocarcinomas of the colon and lung. However, CEA exhibited a heterogeneous distribution in a significant number of breast cancer (42%) and bronchogenic squamous-cell carcinoma (78%) specimens., Conclusions: CEA was expressed in most cases of stomach, colon, breast and lung carcinomas. These carcinomas, however, exhibited wide variation in the concentration and distribution of CEA expression. The concentration and distribution of CEA in a particular tumor type should be considered before undertaking tumor targeting methods.
- Published
- 1994
47. Development of altered hepatocyte foci by separate and combined treatments with radiation and diethylnitrosamine in neonatal rats.
- Author
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Kim SH, Lee YS, Lee MS, Kim TH, and Jang JJ
- Subjects
- Animals, Body Weight, Female, Gamma Rays adverse effects, Liver pathology, Liver Neoplasms epidemiology, Liver Neoplasms pathology, Neoplasms, Radiation-Induced epidemiology, Neoplasms, Radiation-Induced pathology, Neutrons adverse effects, Organ Size, Placenta drug effects, Placenta radiation effects, Pregnancy, Radiation Dosage, Rats, Rats, Sprague-Dawley, Time Factors, Diethylnitrosamine adverse effects, Glutathione Transferase drug effects, Glutathione Transferase radiation effects, Liver drug effects, Liver radiation effects, Liver Neoplasms etiology, Neoplasms, Radiation-Induced etiology, Phenobarbital adverse effects
- Abstract
To establish an in vivo radiation carcinogenesis model using glutathione S-transferase placental form positive (GST-P+) hepatic foci, newborn rats were irradiated once by 0.5 Gy and 2 Gy of gamma ray or 0.15 Gy and 0.6 Gy of neutron with or without 0.05% phenobarbital (PB). When the rats were sacrificed at the 12th or 21st week, the incidence of GST-P+ foci induction by radiation alone was very low. The neutron was more sensitive than the gamma ray at week 12 and the reverse phenomenon was observed in the groups at week 21. PB combination showed an increased incidence of GST-P+ foci in gamma ray irradiated groups. The neutron irradiation combined with PB did not show any significant difference compared with the corresponding PB untreated groups. We also investigated the combined effect of diethylnitrosamine (DEN) and 0.75 Gy of gamma ray irradiation. Intraperitoneal injection of 0.15 mumol/g body weight of DEN at 1 hour after gamma ray irradiation showed significantly increased the number and area of GST-P+ foci compared with those of DEN alone or DEN at 1 hour before gamma radiation (P < 0.001). From these data, after more defined experiments, an in vivo radiation carcinogenesis model will be established by radiation alone or a combination of radiation and carcinogens.
- Published
- 1994
- Full Text
- View/download PDF
48. Biphasic modifying effect of indole-3-carbinol on diethylnitrosamine-induced preneoplastic glutathione S-transferase placental form-positive liver cell foci in Sprague-Dawley rats.
- Author
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Kim DJ, Lee KK, Han BS, Ahn B, Bae JH, and Jang JJ
- Subjects
- Animals, Biomarkers, Tumor analysis, Body Weight drug effects, Diethylnitrosamine, Enzyme Induction, Female, Glutathione Transferase drug effects, In Vitro Techniques, Isoenzymes drug effects, Liver anatomy & histology, Liver drug effects, Liver Neoplasms, Experimental chemically induced, Male, Organ Size drug effects, Placenta enzymology, Precancerous Conditions chemically induced, Rats, Rats, Sprague-Dawley, Anticarcinogenic Agents therapeutic use, Biomarkers, Tumor biosynthesis, Glutathione Transferase biosynthesis, Indoles therapeutic use, Isoenzymes biosynthesis, Liver Neoplasms, Experimental enzymology, Liver Neoplasms, Experimental prevention & control, Precancerous Conditions enzymology, Precancerous Conditions prevention & control
- Abstract
The biphasic modifying effects of indole-3-carbinol (I3C), a naturally occurring constituent of edible cruciferous vegetables, on the development of glutathione S-transferase placental form (GST-P)-positive liver cell foci were investigated by using a medium-term liver bioassay system and a newborn rat hepatocarcinogenesis system. In Experiment 1, a total of 65 male Sprague-Dawley (SD) rats were divided into 5 groups. Animals were given a single intraperitoneal (i.p.) injection of 200 mg/kg diethylnitrosamine (DEN) dissolved in saline for groups 1, 2, and 3 or a single i.p. injection of saline for groups 4 and 5. Group 1 was given the diet containing 0.25% I3C for 2 weeks prior to DEN initiation and then basal diet for 8 weeks. Group 2 was given basal diet for 4 weeks prior to and after DEN initiation and then the diet containing 0.25% I3C for 6 weeks. The rats of group 3 were placed on basal diet during the experiment. Animals of groups 4 and 5 were treated in the same manner as those of groups 1 and 2 except for injection with saline instead of DEN solution. All rats were subjected to two-thirds partial hepatectomy at week 3 and were killed at week 8 after DEN or saline injection. In Experiment 2, a total of 45 female SD rats were dosed with DEN (100 mg/kg, i.p.) or saline at 24 h after birth. After weaning at week 3, the rats were fed diet containing 0.25% I3C for 9 weeks and then were killed at week 12. In Experiment 1, preinitiation exposure to 0.25% I3C caused a significant decrease in numbers of GST-P-positive liver cell foci (P < 0.05), while postinitiation exposure to 0.25% I3C caused significant increases in both number (No./cm2) and area (mm2/cm2) of GST-P-positive liver cell foci (P < 0.05 or 0.01). In Experiment 2, the relative liver weight in the DEN + I3C group was significantly increased (P < 0.001). The numbers and areas of GST-P-positive liver cell foci in the DEN + I3C group were significantly increased as compared to the values of the DEN-alone group (P < 0.001). These results clearly demonstrated that I3C exerts a promoting effect on the postinitiation stage as well as an inhibitory effect on the preinitiation stage in the medium-term liver bioassay.
- Published
- 1994
- Full Text
- View/download PDF
49. Thymic carcinoid tumor combined with thymoma--neuroendocrine differentiation in thymoma?
- Author
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Cho KJ, Ha CW, Koh JS, Zo JI, and Jang JJ
- Subjects
- Humans, Male, Middle Aged, Carcinoid Tumor pathology, Neoplasms, Multiple Primary pathology, Thymoma pathology, Thymus Neoplasms pathology
- Abstract
A carcinoid tumor of the thymus combined with thymoma in a 62-year-old man is described. The mediastinal tumor had been present for 13 years and was associated with pure red cell aplasia. Carcinoid tumor occupied the central two-thirds of the tumor, consisting of nests and trabeculae of monotonous round cells, which ultrastructurally showed many intracytoplasmic dense-core granules. Typical spindle cell type thymoma surrounded the carcinoid area. Clinico-pathologic findings of this unique case suggested that the carcinoid tumor developed within a preexisting thymoma, illustrating a possibility of neuroendocrine differentiation of thymic epithelial cells.
- Published
- 1993
- Full Text
- View/download PDF
50. Pathological responses to preoperative high-dose methotrexate chemotherapy in osteosarcoma--experience in Korea cancer hospital.
- Author
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Lee SY, Jeon DG, Kim SS, Jang JJ, and Cho KJ
- Subjects
- Adolescent, Adult, Bone Neoplasms pathology, Bone Neoplasms surgery, Child, Combined Modality Therapy, Female, Humans, Male, Methotrexate administration & dosage, Osteosarcoma pathology, Osteosarcoma surgery, Bone Neoplasms drug therapy, Methotrexate therapeutic use, Osteosarcoma drug therapy
- Abstract
During the last decade, many clinical investigators at various cancer centers have reported the efficacy of various chemotherapeutic agents in the treatment of osteosarcoma. The regimens using high-dose methotrexate (HDMTX) with citrovorum factor rescue are now considered to be one of the most effective treatments of choice. From December 1989 to May 1991, sixteen patients with Enneking's stage (Enneking et al., 1980) IIB osteosarcoma of the extremities were treated with a high-dose methotrexate regimen. After two cycles of preoperative chemotherapy, an operation was performed; either limb salvage or amputation. The resected lesions were examined pathologically and classified according to Huvos' criteria. On pathological examination, 8 (50%) cases showed Grade IV; 1 (6.25%) Grade III; 4 (25%) Grade II; and 3 (18.75%) Grade I. The types of surgery performed were tumor prosthesis replacement (11); wide resection with or without reconstruction (2); resection and arthrodesis (1); and amputation (2).
- Published
- 1993
- Full Text
- View/download PDF
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