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Titlebook: Chromosomal Translocations and Oncogenic Transcription Factors; Frank J. Rauscher (Associate Professor Chair, Mole Book 1997 The Editor(s)

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發(fā)表于 2025-3-21 18:18:01 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書(shū)目名稱(chēng)Chromosomal Translocations and Oncogenic Transcription Factors
編輯Frank J. Rauscher (Associate Professor Chair, Mole
視頻videohttp://file.papertrans.cn/227/226337/226337.mp4
叢書(shū)名稱(chēng)Current Topics in Microbiology and Immunology
圖書(shū)封面Titlebook: Chromosomal Translocations and Oncogenic Transcription Factors;  Frank J. Rauscher (Associate Professor Chair, Mole Book 1997 The Editor(s)
描述Regulation of gene expression at the level of transcription is one of the major determinants of proper cellular proliferation and differentiation. The key players in these processes are sequence-specific DNA binding transcription factor proteins which coordinate programs of gene expression in the nucleus. The articles in this volume document the myriad of genetic and biochemical alterations sustained by human proto-oncogenic transcription factors which result in diverse neoplastic processes. This volume gives insights into how normal programs of gene expression can be subverted by the action of single transcription factors resulting in a specific tumor type. The book provides inspiration for exploiting these tumor-specific alterations as diagnostic, prognostic tools, or as selective therapeutic targets.
出版日期Book 1997
關(guān)鍵詞DNA; Krebs; cancer; chromosome; gene; gene expression; genetics; molecular genetics; oncogenes; proliferation
版次1
doihttps://doi.org/10.1007/978-3-642-60479-9
isbn_softcover978-3-642-64424-5
isbn_ebook978-3-642-60479-9Series ISSN 0070-217X Series E-ISSN 2196-9965
issn_series 0070-217X
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer-Verlag GmbH, DE
The information of publication is updating

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發(fā)表于 2025-3-21 22:55:52 | 只看該作者
Chromosome Translocation-Mediated Conversion of a Tumor Suppressor Gene into a Dominant Oncogene: F of DNA-binding domain types which are involved in EWS/TLS fusions and, concomitantly, the diversity of the disease processes initiated. This article will expand on this theme by describing a new member of the EWS/TLS family of oncogenes, namely EWS-WT1, which occurs in the solid tumor desmoplastic
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地板
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5#
發(fā)表于 2025-3-22 12:33:33 | 只看該作者
https://doi.org/10.1007/978-3-8350-9400-0tiation of the leukaemic clone rather than by a cytotoxic effect (. et al. 1988; . et al. 1990; . et al. 1990). This has been confirmed using clonal analysis of APL blasts and peripheral blood neutrophils following ATRA therapy (ELLIOTT et al. 1992).
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發(fā)表于 2025-3-22 14:13:48 | 只看該作者
Grundlagen des Strategischen Managements, of DNA-binding domain types which are involved in EWS/TLS fusions and, concomitantly, the diversity of the disease processes initiated. This article will expand on this theme by describing a new member of the EWS/TLS family of oncogenes, namely EWS-WT1, which occurs in the solid tumor desmoplastic
7#
發(fā)表于 2025-3-22 19:54:50 | 只看該作者
Book 1997f single transcription factors resulting in a specific tumor type. The book provides inspiration for exploiting these tumor-specific alterations as diagnostic, prognostic tools, or as selective therapeutic targets.
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發(fā)表于 2025-3-22 23:19:09 | 只看該作者
0070-217X e action of single transcription factors resulting in a specific tumor type. The book provides inspiration for exploiting these tumor-specific alterations as diagnostic, prognostic tools, or as selective therapeutic targets.978-3-642-64424-5978-3-642-60479-9Series ISSN 0070-217X Series E-ISSN 2196-9965
9#
發(fā)表于 2025-3-23 02:14:22 | 只看該作者
Grundlagen des Strategischen Managements,idence suggests that loss of function of TEL may also contribute to pathogenesis of malignancy. In this report, the diverse molecular genetic mechanisms of leukemogenesis mediated by the . gene will be discussed.
10#
發(fā)表于 2025-3-23 09:34:02 | 只看該作者
The , Gene Contributes to the Pathogenesis of Myeloid and Lymphoid Leukemias by Diverse Molecular Gidence suggests that loss of function of TEL may also contribute to pathogenesis of malignancy. In this report, the diverse molecular genetic mechanisms of leukemogenesis mediated by the . gene will be discussed.
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