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Original Articles
- Prognostic Value of CD44v6 Isoform in Infiltrating Ductal Carcinoma of Breast.
- Seung Cheol Lee, Yoon Kyung Sohn, Jung Sik Kwak, Woon Bok Jhung, Jung Wan Kim
- Korean J Pathol. 1997;31(7):635-643.
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Abstract
PDF - CD44 is a family of transmembrane glycoproteins involved in cell-cell and cell-matrix interactions. Expression of CD44 isofonns (splice variants) has been shown to be associated with poor prognosis in several human cancers. We evaluated the expression patterns of the CD44 isofortn (CD 44 splice variant v6) in infiltrating ductal carcinoma of the breast by immunohistochemical and RT-PCR method. Paraffin embedded blocks from seventy-five cases of mastectomized samples were analyzed immunohistochemically using monoclonoal antibody against CD44v6. CD44v6 was detected in fifty-seven cases (76%) of the tumor samples. Adjacent normal myoepithelial cells and ductal epithelial cells revealed focal positive reaction to CD44v6. Thirtytwo cases (80.0%) with lymph nodal metastasis revealed overexpression of CD44v6 monoclonal antibody, but twenty-five cases (71.4%) without nodal metastasis also showed positive reaction to CD44v6 monoclonal antibody, and there is no statistically significant value. Other prognostic factors of infiltrating ductal carcinoma, such as tumor size, histologic grade and hormonal receptors did not show any significant correlation with CD44v6 expression. The RT-PCR studies for 9 cases of infiltrating ductal carcinoma showed the same band patterns both in the normal and tumor tissues. From the above results, it is concluded that the expression of CD44v6 is not a valuable prognostic marker of infiltrating ductal carcinoma of breast.
- Immunohistochemical Analysis of Transforming Growth Factor (TGF)-beta1 and TGF-beta Receptor II and Quantitative Analysis of TGF-beta1 mRNA during Multistep Hepatocarcinogenesis Induced by Diethylnitrosamine in Sprague-Dawley Rats.
- Mee Yon Cho, Ju Han Lee, Yong Koo Kang, Nam Hee Won
- Korean J Pathol. 1999;33(11):1009-1023.
- 1,697 View
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Abstract
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- Transforming growth factor (TGF)-beta1 plays an important role in hepatocarcinogenesis and has been described as a useful tumor marker and one of the poor prognostic indicators in patients with hepatocellular carcinoma (HCC). To investigate the role and cellular localization of TGF-beta1 during multistep hepatocarcinogenesis we performed a quantitative analysis of TGF-beta1 mRNA and immunohistochemical expression of TGF-beta1 and TGF-beta receptor II (TGF-betarII) in female Sprague-Dawley rats. The experimental groups included neoplastic lesions produced by Solt-Farber's protocol, regenerating liver after partial hepatectomy, and normal control. Quantitative change of TGF-beta1 mRNA was analysed by competitive reverse-transcription polymerase chain reaction (RT-PCR). TGF-beta1 protein and TGF-betarII expression were evaluated by immunohistochemical stain. The discrete tumor nodules were detected on 14th day and then increased in number and size. Three HCCs were induced on 8th or 9th month. RT-PCR demonstrated TGF-beta1 mRNA band in all examples of the normal and regenerating liver, nodules and HCCs. Competitive RT-PCR displayed higher TGF-beta1 mRNA in nodules, HCCs and regenerating liver than in normal controls. Hepatocytes from control and regenerating livers showed weak immunoreactivity for TGF-beta1. In contrast, the cytoplasm of hepatocytes of nodules in 7th, 8th and 9th month and HCCs were intensely stained for TGF-beta1. Some sinusoidal cells showed immunoreactivity for TGF-beta1 in all experimental groups. In early phase of carcinogenesis, the cytoplasm of hepatocytes in liver of 12h, 1d and 3d showed transiently increased immunoreactivity for TGF-beta1 and The immunoreactivity decreased thereafter. TGF-beta1 mRNA was also detected in the neoplastic hepatocytes by in-situ hybridization. Although TGF-betarII expression was correlated with TGF-beta1 immunoreactivity during early phase of carcinogenesis, hepatocytes in most nodules in 7th, 8th, 9th month and carcinomas showed decreased or little immunoreactivity for TGF-betarII. Based on the above results, it is concluded that TGF-beta1 expression increases not only in precancerous nodules but also in HCCs and its increase seems to be correlated with decrease or loss of TGF-betarII expression although its mechanism remains unclear. Hepatocytes may be a major cellular source of TGF-beta1 during hepatocarcinogenesis.
- Expression Pattern of DNA Mismatch Repair Genes in Tumors of Microsatellite Mutator Phenotype.
- Jung Jin Kim, Myung Jin Baek, Nam Gyun Kim, Yun Hee Kim, Ji Eun Kim, Hoguen Kim, Chanil Park
- Korean J Pathol. 2000;34(9):609-614.
- 1,640 View
- 11 Download
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Abstract
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- Microsatellite mutator phenotype (MMP) tumors were reported in a subset of gastrointestinal carcinomas. The molecular pathogenesis of MMP tumors shows defects in the DNA mismatch repair genes, and also many germline and somatic mutations were reported in the MMP tumors. However, the detection of genetic defects in the MMP tumors is very difficult, mainly because many genes are included in the DNA mismatch repair genes. This study was undertaken to determine the best strategy for detecting defects in the DNA mismatch repair genes in gastrointestinal carcinomas. One of the effective ways for detecting defects in DNA mismatch repair genes is to screen the MMP tumors and evaluate the products of DNA mismatch repair genes by performing the multiplex RT-PCR method. We have screened the MMP tumors by using 5 microsatellite markers in the 12 cancer cell lines, 120 colon carcinomas and 99 gastric carcinomas and found 6 MMP cell lines, 10 MMP colon cancers, and 9 MMP gastric carcinomas. In addition, we evaluated 6 DNA mismatch repair gene products (hMSH2, hMSH3, hMSH6, hMLH1, hPMS1 and hPMS2) by multiplex RT-PCR analysis and found decreased expression of the DNA mismatch repair genes in 5 (hMSH6 in DLD-1 and HCT-15; hMSH2 in LoVo; hMLH1 and hMSH3 in HCT-116; hMLH1 in SNU-638) out of 6 MMP cell lines. We also found a decreased expression of hMLH1 in 3 out of 10 MMP colon carcinomas, and in 6 out of 9 MMP gastric carcinomas. Our results indicate that the expression analysis of the DNA mismatch repair genes by multiplex RT-PCR method can reduce the number of genes subjected to mutational analysis and is convenient for screening the responsible DNA mismatch repair genes.
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