9 results on '"Störkel, S."'
Search Results
2. Cytogenetic analysis of epithelial renal‐cell tumors: Relationship with a new histopathological classification
- Author
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van den Berg, E., primary, van der Hout, A. H., additional, Oosterhuis, J. W., additional, Störkel, S., additional, Dijkhuizen, T., additional, Dam, A., additional, Zweers, H. M. M., additional, Mensink, H. J. A., additional, Buys, C. H. C. M., additional, and de Jong, B., additional
- Published
- 1993
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3. Loss of heterozygosity at the short arm of chromosome 3 in renal‐cell cancer correlates with the cytological tumour type
- Author
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Van Hout, A. H. Der, primary, Van Berg, E. Den, additional, Van Vlies, P. Der, additional, Dijkhuizen, T., additional, Störkel, S., additional, Oosterhuis, J. W., additional, De Jong, B., additional, and Buys, C. H. C. M., additional
- Published
- 1993
- Full Text
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4. Renal oncocytoma with t(5;12;11), der(1)t(1;8) and add(19): true oncocytoma or chromophobe adenoma?
- Author
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Dijkhuizen, T., Berg, E. van den, Störkel, S., Vries, B. de, Veen, A.Y. van der, Wilbrink, M., Kessel, A. Geurts van, and Jong, B. de
- Abstract
Renal oncocytomas reveal a considerable (cyto)genetic heterogeneity. At least 2 genetic subsets are currently recognized, characterized by (1) translocations involving breakpoint 11q13 and (2) the combined loss of chromosomes 1 and X/Y. We present a case of oncocytoma revealing a 3-way translocation involving breakpoint 11q13, a der (1)t(1;8) and an add(19). The der(1) resulted in loss of chromosome 1 sequences. Using fluorescence in situ hybridization, the 11q13 breakpoint of the present case proved to be slightly different from the one observed previously in 3 cases of renal oncocytoma. Whether the 11q13 breakpoint observed in our case resides in or near another gene remains to be elucidated. Int. J. Cancer 73:521524, 1997. © 1997 Wiley-Liss, Inc.
- Published
- 1997
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5. MHC class I antigen processing pathway defects, ras mutations and disease stage in colorectal carcinoma.
- Author
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Atkins D, Breuckmann A, Schmahl GE, Binner P, Ferrone S, Krummenauer F, Störkel S, and Seliger B
- Subjects
- ATP Binding Cassette Transporter, Subfamily B, Member 2, ATP Binding Cassette Transporter, Subfamily B, Member 3, ATP-Binding Cassette Transporters genetics, Adenocarcinoma metabolism, Adenocarcinoma pathology, Adult, Aged, Aged, 80 and over, Carcinoma in Situ metabolism, Carcinoma in Situ pathology, Cell Division, Colorectal Neoplasms metabolism, Colorectal Neoplasms pathology, Cysteine Endopeptidases genetics, Female, Gene Expression Regulation, Neoplastic, Histocompatibility Antigens Class I metabolism, Humans, Ki-67 Antigen metabolism, Lymphatic Metastasis, Male, Middle Aged, Neoplasm Staging, Proteasome Endopeptidase Complex, Proto-Oncogene Mas, Adenocarcinoma genetics, Antigen Presentation genetics, Carcinoma in Situ genetics, Colorectal Neoplasms genetics, Genes, ras genetics, Histocompatibility Antigens Class I genetics, Multienzyme Complexes, Mutation genetics
- Abstract
Colorectal tumorigenesis has been associated with the progressive acquisition of a variety of genetic alterations. These include mutations of the Ki-ras proto-oncogene in codons 12 and 13, which account for 85% of genetic changes in colorectal cancer. In murine in vitro models of oncogenic transformation, an association between ras-mediated transformation and downregulation of different components of the MHC class I antigen processing machinery (APM) has been described. In order to investigate whether this association also exists in human tumors, 10 cases of high-grade intraepithelial neoplasia (HIN), as well as primary tumors and autologous lymph node metastases from 42 patients with colorectal carcinoma, were monitored by allele-specific restriction analysis for Ki-ras mutations. In parallel, APM component expression and tumor cell proliferation were analyzed by immunohistochemistry. In comparison to autologous colorectal mucosa, TAP1, LMP2 and tapasin loss was found in 68%, 67% and 80% of HIN, respectively. In contrast, impaired TAP1, LMP2 and tapasin expression was found in 42%, 42% and 63% of primary adenocarcinomas of stage III disease and in 63%, 47% and 79% of the matched lymph node metastases, respectively. More than 60% of colorectal tumor lesions with TAP1, LMP2 and/or tapasin defects displayed Ki-ras mutations. The frequency of TAP1, LMP2 and tapasin loss varied between 33% of primary adenocarcinomas, 40% of HIN to approximately 67% of metastases. These data suggest that i) APM component deficiencies occur more frequently in Ki-ras-mutated colorectal carcinoma lesions and ii) APM abnormalities in conjunction with Ki-ras mutations appear to be associated with disease stage. These findings support the hypothesis that Ki-ras mutations may contribute to immune escape mechanisms of tumors by downregulating the MHC class I APM component expression., (Copyright 2003 Wiley-Liss, Inc.)
- Published
- 2004
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6. HER-2/neu is expressed in human renal cell carcinoma at heterogeneous levels independently of tumor grading and staging and can be recognized by HLA-A2.1-restricted cytotoxic T lymphocytes.
- Author
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Seliger B, Rongcun Y, Atkins D, Hammers S, Huber C, Störkel S, and Kiessling R
- Subjects
- Antigens, Neoplasm biosynthesis, Antigens, Neoplasm genetics, Carcinoma, Renal Cell genetics, Carcinoma, Renal Cell metabolism, Carcinoma, Renal Cell pathology, Cytotoxicity, Immunologic, Dendritic Cells immunology, Epitopes immunology, Humans, Kidney Neoplasms genetics, Kidney Neoplasms metabolism, Kidney Neoplasms pathology, Neoplasm Proteins biosynthesis, Neoplasm Proteins genetics, Neoplasm Staging, Peptide Fragments immunology, RNA, Messenger biosynthesis, RNA, Neoplasm biosynthesis, Receptor, ErbB-2 biosynthesis, Antigens, Neoplasm immunology, Carcinoma, Renal Cell immunology, Genes, erbB-2, HLA-A2 Antigen immunology, Kidney Neoplasms immunology, Neoplasm Proteins immunology, Receptor, ErbB-2 immunology, T-Lymphocytes, Cytotoxic immunology
- Abstract
The HER-2/neu oncoprotein, a 185 kDa membrane-associated tyrosine kinase with extensive homology to the epidermal growth factor receptor (EGF-R), is overexpressed in breast and ovarian carcinomas. Its overexpression is closely associated with poor prognosis in the course of disease. Here we demonstrate HER-2/neu overexpression in both established cell lines and biopsy material obtained from renal epithelial tumors. Immunohistochemical analysis of human kidney tumor lesions using 2 HER-2/neu-specific antibodies revealed HER-2/neu expression in more than 40% of primary epithelial renal tumors and more than 30% of primary renal cell carcinoma (RCC) specimens. A distinctive HER-2/neu expression pattern was found in different subtypes of kidney tumors with the highest frequency in chromophilic and chromophobic RCC, but neither associated with disease stage nor tumor grade. Eight of 10 RCC cell lines expressed significant levels of HER-2/neu mRNA and protein, but at a lower level compared with HER-2/neu overexpressing ovarian carcinoma cells. To evaluate the immune response against HER-2/neu expressing HLA-A2-positive (HLA-A2(+)) RCC cells, allogeneic HLA-A2-restricted cytotoxic T-lymphocyte (CTL) lines generated by pulsing dendritic cells with 3 different HER-2/neu-derived peptides, (HER-2(9.369), HER-2(9.435) and HER-2(9.689), were utilized in chromium-release assays. Specific lysis of HER-2/neu expressing HLA-A2(+) RCC cell lines was mediated by CTL lines specific for each of these 3 HER-2/neu-derived epitopes. The fine specificity of 2 CTL clones was defined to the epitopes HER-2(9.435) and HER-2(9.689). Their specificity was then confirmed by cold target inhibition assays. In addition, CTL-mediated lysis was enhanced by pulsing tumor cells with exogenous HER-2/neu-specific peptides. Our data suggest that (i) HER-2/neu is heterogeneously expressed in different subtypes of RCC, (ii) HER-2/neu is naturally processed by RCC and (iii) HER-2/neu epitopes presented by RCC can be recognized by HLA-A2-restricted, HER-2/neu-specific CTL., (Copyright 2000 Wiley-Liss, Inc.)
- Published
- 2000
7. Genetics as a diagnostic tool in sarcomatoid renal-cell cancer.
- Author
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Dijkhuizen T, Van Den Berg E, Van Den Berg A, Van De Veen A, Dam A, Faber H, Buys CH, Störkel S, and De Jong B
- Subjects
- Carcinoma, Renal Cell genetics, Carcinosarcoma genetics, Humans, Karyotyping, Kidney Neoplasms genetics, Male, Middle Aged, Biomarkers, Tumor genetics, Carcinoma, Renal Cell diagnosis, Carcinosarcoma diagnosis, Chromosome Aberrations, Chromosomes, Human, Kidney Neoplasms diagnosis, Tumor Suppressor Protein p53 genetics
- Abstract
Renal-cell cancer comprises a heterogeneous group of tumors, which currently can be sub-divided into morphologically distinct entities, each characterized by a specific combination of genetic changes. Sarcomatoid transformation might occur in any of the sub-types, resulting in tumors consisting of both carcinomatous and sarcomatous components. The specific diagnosis of these neoplasms, as to tumor sub-type, is usually made on the histologic properties of the carcinomatous tissue present. However, this might not reflect the true nature of the sarcomatous component. Since the genetic changes associated with the development of the different sub-types of renal-cell cancer are well established, this knowledge might serve as a tool in diagnosing sarcomatoid tumors. Assessing the genetic constitution of the latter may lead to correct diagnosis. It may also provide valuable information about the genetic changes associated with sarcomatoid transformation. Hence we performed a genetic characterization of a case of sarcomatoid renal-cell cancer, histologically diagnosed as being of the chromophilic type. The observed genetic changes included loss of 3p, 6q, 8p, 9, 13, 14 and 17p, and gain of 5, 12 and 20, as well as a mutation in the coding region of the p53 gene. This combination of genetic changes points to clear-cell rather than chromophilic origin of the sarcomatoid tumor investigated, indicating that the genetic constitution of sarcomatoid tumors may be a more reliable indicator of tumor sub-type than histologic appearance.
- Published
- 1997
- Full Text
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8. Chromosomal findings and p53-mutation analysis in chromophilic renal-cell carcinomas.
- Author
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Dijkhuizen T, Van den Berg E, Van den Berg A, Störkel S, De Jong B, Seitz G, and Henn W
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- Adult, Aged, Chromosomes, Human, Pair 17, Female, Gene Deletion, Humans, Male, Middle Aged, Mutation, Polymorphism, Single-Stranded Conformational, Sex Characteristics, Translocation, Genetic, Trisomy, X Chromosome, Y Chromosome, Carcinoma, Renal Cell genetics, Chromosome Aberrations, DNA Mutational Analysis, Genes, p53, Kidney Neoplasms genetics
- Abstract
The chromosomal pattern of 31 specimens of chromophilic renal-cell cancer (RCC), selected according to the criteria mentioned in the classification of Thoenes and Störkel, is presented. A high male preponderance was found (8.7:1). Cytogenetic analysis revealed a typical pattern of numeric alterations specific for this sub-type in the majority of cases (i.e., --Y,+7, +12, +16, +17, and/or +20), which is different from the chromosomal patterns found in other sub-types of RCC. Gain of chromosome 20, as well as loss of the extra copy of chromosome 17 or loss of 17p, was found to be related to the higher-grade chromophilic carcinomas. None of the 14 cases examined by SSCP analysis revealed mutations of the p53 gene, indicating that other genes at 17(p) might be important in the progression of this sub-type of RCC.
- Published
- 1996
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9. Cellular immune response to human renal-cell carcinomas: definition of a common antigen recognized by HLA-A2-restricted cytotoxic T-lymphocyte (CTL) clones.
- Author
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Bernhard H, Karbach J, Wölfel T, Busch P, Störkel S, Stöckle M, Wölfel C, Seliger B, Huber C, and Meyer zum Büschenfelde KH
- Subjects
- Antibodies, Monoclonal immunology, Cross Reactions immunology, Histocompatibility Antigens Class I immunology, Humans, Immunity, Cellular immunology, Kidney immunology, Lymphocyte Culture Test, Mixed, Melanoma immunology, Tumor Cells, Cultured, Antigens, Differentiation immunology, Antigens, Neoplasm immunology, Carcinoma, Renal Cell immunology, HLA-A2 Antigen immunology, Kidney Neoplasms immunology, T-Lymphocytes, Cytotoxic immunology
- Abstract
Cytotoxic T lymphocyte (CTL) clones directed against autologous renal-cell carcinoma (RCC) cell lines were generated by mixed lymphocyte/tumor-cell culture (MLTC) using peripheral blood lymphocytes (PBL). A CD8+, CD4- CTL clone MZ1257-CTL 5/30 with high cytolytic activity for the autologous tumor cell line MZ1257-RCC was established. No lysis of the autologous EBV-transformed B lymphocytes (EBV-B) or K562 cells was observed. A panel of HLA-A2-matched allogeneic RCC lines was recognized by CTL 5/30. Further specificity analysis showed a cross-reactivity with HLA-A2-matched allogeneic tumor cells of various origins, especially melanoma. CTL 5/30 was also cross-reactive with several HLA-A2-positive allogeneic normal kidney cells in culture. The restriction element identified for CTL 5/30 was HLA-A2, as shown by blocking of cytotoxicity using an anti-HLA-A2 monoclonal antibody (MAb) and by resistance of an HLA-A2-negative melanoma variant SK29-MEL. 1.22 against lysis by CTL 5/30. In this report we demonstrate HLA-A2-restricted recognition of a T-cell-defined antigen on autologous renal-cancer cells. This antigen is also expressed and recognized in association with HLA-A2 on normal kidney cells in culture and other HLA-A2-positive tumor cells. It may therefore be a normal differentiation antigen to which tolerance is incomplete in the renal-cell cancer system investigated.
- Published
- 1994
- Full Text
- View/download PDF
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