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Titlebook: Drug Resistance in Leukemia and Lymphoma III; G. J. L. Kaspers,R. Pieters,A. J. P. Veerman Book 1999 The Editor(s) (if applicable) and The

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發(fā)表于 2025-3-21 19:19:15 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Drug Resistance in Leukemia and Lymphoma III
編輯G. J. L. Kaspers,R. Pieters,A. J. P. Veerman
視頻videohttp://file.papertrans.cn/284/283123/283123.mp4
叢書名稱Advances in Experimental Medicine and Biology
圖書封面Titlebook: Drug Resistance in Leukemia and Lymphoma III; G. J. L. Kaspers,R. Pieters,A. J. P. Veerman Book 1999 The Editor(s) (if applicable) and The
描述Cellular drug resistance is a major limitation to the success of chemotherapy of leu- kemia and lymphoma. The importance of this has now been recognized by both clinicians and scientists. It is of utmost importance to bridge the gap between laboratory and clinic in this field of research. This is the main purpose of the series of International Symposia on Drug Resistance in Leukemia and Lymphoma. These are held every three years in Am- sterdam, The Netherlands, since 1992. This book contains the proceedings of the third of these meetings, organised in 1998. The book covers all important aspects of drug resistance in leukemia and lymphoma, both in the form of extensive reviews as in manuscripts describing original data. General mechanisms of resistance are discussed, including the drug resistance related proteins p- glycoprotein, MRP (multi-drug resistance protein) and LRP (lung resistance protein), and the role of glutathione and glutathione-S-transferases. Moreover, more drug type-specific mechanisms of resistance are a topic, such as for glucocorticoids and antifolates. Much in- formation is provided on apoptosis and its regulators, and on the results of cell culture drug resista
出版日期Book 1999
關(guān)鍵詞Antigen; apoptosis; chemotherapy; drug; drug resistance; imaging; interferon; leukemia; lymphoma; pathogenesi
版次1
doihttps://doi.org/10.1007/978-1-4615-4811-9
isbn_softcover978-1-4613-7180-9
isbn_ebook978-1-4615-4811-9Series ISSN 0065-2598 Series E-ISSN 2214-8019
issn_series 0065-2598
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Science+Busines
The information of publication is updating

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https://doi.org/10.1007/978-3-7091-9414-0 strategies are being developed to circumvent drug resistance by inhibiting P-gp, prospective studies concerning the clinical relevance of P-gp in childhood leukemia are warranted. . P-gp was studied in 102 consecutive cases of de novo childhood ALL and in 34 relapsed patients. An immunocytochemical
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https://doi.org/10.1007/978-3-642-83312-0Cyclosporin A (CsA), PSC833 and GF120918. We describe an investigation into the expression, using MRK16 and UIC2, and function of P-gp using daunorubicin with and without modulators by flow cytometric analysis on previously frozen blast cells from 27 patients with primary or secondary AML. We compar
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V?ter, M?nner und kindliche Entwicklungcellular mechanisms underlying this increased expression are completely unknown. Point mutations in the .1 promoter have been found in osteogenic sarcoma (Stein et al., Eur J of Cancer, 30A: 1541–1545, 1994). We therefore analyzed DNA from hematological malignancies for .1 promoter point mutations.
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https://doi.org/10.1007/978-3-322-85040-9ty can also be increased by combining the results of more than one assay. We have used a combination of flow cytometric assays to define MDR positive and negative blasts in 47 AML patients entered into MRC trials. Our primary test is a standardised and reproducible assay for anthracycline accumulati
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