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1,174 results on '"Dörken B"'

1. Assessment of free light chains in the cerebrospinal fluid of patients with lymphomatous meningitis – a pilot study

Author

Scholz C, Dörken B, Daniel PT, Pezzutto A, Müller C, and Hildebrandt B

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Lymphomatous meningitis (LM) represents a severe complication of malignant lymphomas. While clinical suspicion is raised by symptoms ranging from mild disturbances of sensation to severe pain or impaired consciousness, the definite diagnosis of LM is often difficult to obtain. Since B-cell lymphomas are clonally restricted to express either kappa or lambda immunoglobulin light chain, we hypothesised that analysis of free light chain (FLC) ratios might facilitate the diagnosis of LM. Methods Kappa and lambda FLC were measured using a novel nephelometric assay in cerebrospinal fluid (CSF) and serum from 17 patients. 5/17 suffered from LM as demonstrated by cytology, immunocytology, and/or imaging procedures. Results Measurement of FLC concentrations in CSF was achieved for all 17 patients. FLC levels in CSF were lower than serum FLC levels in samples for the same patient obtained at the same time (p < 0.01). CSF and serum FLC concentrations correlated weakly in all patients irrespective of LM status. Significantly more patients with cytopathologically and immunohistochemically proven LM displayed abnormal kappa/lambda FLC ratios in CSF compared to individuals with no LM (p < 0.01). Conclusion This is the first report demonstrating that a significant proportion of LM patients display an abnormal kappa/lambda FLC ratio in the CSF.

Published
2007
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2. EGR2 mutations define a new clinically aggressive subgroup of chronic lymphocytic leukemia

Author

Young, E, Noerenberg, D, Mansouri, L, Ljungström, V, Frick, M, Sutton, L-A, Blakemore, SJ, Galan-Sousa, J, Plevova, K, Baliakas, P, Rossi, D, Clifford, R, Roos-Weil, D, Navrkalova, V, Dörken, B, Schmitt, CA, Smedby, KE, Juliusson, G, Giacopelli, B, Blachly, JS, Belessi, C, Panagiotidis, P, Chiorazzi, N, Davi, F, Langerak, AW, Oscier, D, Schuh, A, Gaidano, G, Ghia, P, Xu, W, Fan, L, Bernard, OA, Nguyen-Khac, F, Rassenti, L, Li, J, Kipps, TJ, Stamatopoulos, K, Pospisilova, S, Zenz, T, Oakes, CC, Strefford, JC, Rosenquist, R, and Damm, F

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Oncology and Carcinogenesis, Cancer, Hematology, Rare Diseases, Lymphoma, Clinical Research, Genetics, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Adult, Aged, Early Growth Response Protein 2, Female, Genes, p53, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Male, Middle Aged, Mutation, Proportional Hazards Models, Clinical Sciences, Immunology, Cardiovascular medicine and haematology, Clinical sciences, Oncology and carcinogenesis
Abstract

Recurrent mutations within EGR2 were recently reported in advanced-stage chronic lymphocytic leukemia (CLL) patients and associated with a worse outcome. To study their prognostic impact, 2403 CLL patients were examined for mutations in the EGR2 hotspot region including a screening (n=1283) and two validation cohorts (UK CLL4 trial patients, n=366; CLL Research Consortium (CRC) patients, n=490). Targeted deep-sequencing of 27 known/postulated CLL driver genes was also performed in 38 EGR2-mutated patients to assess concurrent mutations. EGR2 mutations were detected in 91/2403 (3.8%) investigated cases, and associated with younger age at diagnosis, advanced clinical stage, high CD38 expression and unmutated IGHV genes. EGR2-mutated patients frequently carried ATM lesions (42%), TP53 aberrations (18%) and NOTCH1/FBXW7 mutations (16%). EGR2 mutations independently predicted shorter time-to-first-treatment (TTFT) and overall survival (OS) in the screening cohort; they were confirmed associated with reduced TTFT and OS in the CRC cohort and independently predicted short OS from randomization in the UK CLL4 cohort. A particularly dismal outcome was observed among EGR2-mutated patients who also carried TP53 aberrations. In summary, EGR2 mutations were independently associated with an unfavorable prognosis, comparable to CLL patients carrying TP53 aberrations, suggesting that EGR2-mutated patients represent a new patient subgroup with very poor outcome.

Published
2017

3. Combined administration of imatinib mesylate and ionizing radiation leads to increased radiosensitivity in the human glioblastoma cell line RuSi RS1.

Author

Holdhoff, M, Kreuzer, KA, Appelt, C, Scholz, R, Jordan, A, Hildebrandt, B, Schmidt, CA, Van Etten, RA, Dörken, B, and Le Coutre, P

Subjects
Oncology & Carcinogenesis, Oncology and Carcinogenesis
Abstract

1564 Background: The selective tyrosine kinase inhibitor imatinib mesylate (Gleevec) effectively inhibits the activity of the abl, PDGF receptor (PDGFR) and c-kit tyrosine kinases. Because of the specific target profile of this orally available and generally well tolerated drug, imatinib is under intensive investigation for the potential treatment of other diseases. Malignant gliomas frequently show a high expression of PDGF receptor which is involved in tumorigenesis by formation of an autocrine loop. A role in DNA repair carried out through c-abl and c-kit was previously described both for c-abl and c-kit. In this study we address the potential use of imatinib mesylate and concomitant ionizing radiation (IR) to improve the radiosensitivity of the glioblastoma cell line RuSi RS1.Cells of the primary glioblastoma cell line RuSi RS1, as well as of the colon cancer cell line WiDr and of BT20, a human breast cancer cell line, were incubated with different concentrations of imatinib mesylate 30 minutes prior to irradiation (doses between 0 and 16 Gy). Western blots were done comparing the different expression of c-abl, PDGFR alpha and beta, and c-kit in the different cell lines. Immunoprecipitation was performed to assess inhibition of the different kinases by imatinib mesylate.Under combined treatment with imatinib and IR a significant shift of the IC50 (dose needed to reduce the survival fraction by 50%) was detected in RuSi RS1 compared to IR alone. This effect was not seen in WiDr or BT20. RuSi RS1 showed an overexpression of PDGFR beta. Inhibition of tyrosine kinase phosphorylation by imatinib could be shown for PDGFR beta and c-abl (the IP failed for c-kit).Concomitant administration of imatinib mesylate and ionizing radiation increases the radiosensitivity of the glioblastoma cell line RuSi RS1. This effect might partly be due to disruption of an autocrine loop of the PDGF/PDGFR system. Inhibition of DNA repair mechanisms in which the tyrosine kinase activity of c-abl and c-kit is involved might be important causes of this observed phenomenon as well. No significant financial relationships to disclose.

Published
2004

20. Intermediate Dose Cytarabine and Idarubicin for Salvage Therapy of Acute Myeloid Leukemia

Author

Schott, G., Grüneisen, A., Fülle, H. H., Sperling, C., Notter, M., Kerschgens, C., Krahl, D., Blau, W., Pasold, R., Neubauer, A., Klinkenstein, C., Schwartz, S., Arnold, R., Hellriegel, K.-P., Huhn, D., Thiel, E., Dörken, B., Ludwig, W.-D., Hiddemann, W., editor, Büchner, T., editor, Wörmann, B., editor, Ritter, J., editor, Creutzig, U., editor, Keating, M., editor, and Plunkett, W., editor

Published
1998
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