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Titlebook: Cancer Immunotherapy at the Crossroads; How Tumors Evade Imm James H. Finke,Ronald M. Bukowski Book 2004 Springer Science+Business Media Ne

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發(fā)表于 2025-3-21 16:19:02 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Cancer Immunotherapy at the Crossroads
副標題How Tumors Evade Imm
編輯James H. Finke,Ronald M. Bukowski
視頻videohttp://file.papertrans.cn/222/221140/221140.mp4
概述Includes supplementary material:
叢書名稱Current Clinical Oncology
圖書封面Titlebook: Cancer Immunotherapy at the Crossroads; How Tumors Evade Imm James H. Finke,Ronald M. Bukowski Book 2004 Springer Science+Business Media Ne
描述Leading investigators and clinicians detail the different mechanisms used by tumors to escape and impair the immune system and then spell out possible clinical strategies to prevent or reverse tumor-induced immune dysfunction. The authors review the mechanisms of immune dysfunction and evasion mechanisms in histologically diverse human tumors, focusing on tumor-induced molecular defects in T cells and antigen-presenting cells (dendritic cells and tumors), that may serve as biomarkers for patient prognosis. They discuss the means by which these immune functions may be protected or restored in order to more effectively support the process of tumor rejection in situ. Cutting-edge techniques are outlined with the capacity to monitor the strength and quality of patients‘ immune responses using immunocytometry, MHC-peptide tetramers combined with apoptosis assay, ELISPOT assay, and detection of MHC-TAA peptide complexes on tumor cells.
出版日期Book 2004
關(guān)鍵詞apoptosis; brain tumors; carcinoma; cell; immunotherapy; lymphocytes; lymphoma; renal cell carcinoma; transp
版次1
doihttps://doi.org/10.1007/978-1-59259-743-7
isbn_softcover978-1-4684-9844-8
isbn_ebook978-1-59259-743-7Series ISSN 2364-1134 Series E-ISSN 2364-1142
issn_series 2364-1134
copyrightSpringer Science+Business Media New York 2004
The information of publication is updating

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沙發(fā)
發(fā)表于 2025-3-21 21:59:05 | 只看該作者
978-1-4684-9844-8Springer Science+Business Media New York 2004
板凳
發(fā)表于 2025-3-22 03:43:36 | 只看該作者
地板
發(fā)表于 2025-3-22 04:35:51 | 只看該作者
KangWoo Lee,Jung-Hoon Hwang,Dong-Soo Kwontibility complex (MHC) molecules. However, the TCR : MHC interaction is insufficient to trigger productive activation of T cells. It is now widely recognized that a second signal known as costimulation is required for the productive activation of antigen (Ag)-specific T cells.
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發(fā)表于 2025-3-22 10:16:59 | 只看該作者
Accentuating Tumor Immunity Through Costimulationtibility complex (MHC) molecules. However, the TCR : MHC interaction is insufficient to trigger productive activation of T cells. It is now widely recognized that a second signal known as costimulation is required for the productive activation of antigen (Ag)-specific T cells.
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發(fā)表于 2025-3-22 15:17:59 | 只看該作者
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Current Clinical Oncologyhttp://image.papertrans.cn/c/image/221140.jpg
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發(fā)表于 2025-3-23 04:56:58 | 只看該作者
Aineas Mallios,Ted Lindblom,Stefan Sj?grennate the malignant cells and the chronic infectious agent. This setting is not uncommon in mice or patients with a congenital or acquired immunodeficiencies. However, this problem is also frequently seen in fully immunocompetent individuals, suggesting that malignant cells and certain microorganisms
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發(fā)表于 2025-3-23 07:31:43 | 只看該作者
Kristaps Freimanis,Maija ?enfelded proliferation of different immune cells. Na?ve T cells are unable to directly recognize tumor antigens. They require help from specialized cells known as professional antigen-presenting cells (APCs). APCs first interact with tumors, uptake tumor cells/proteins, process them, and present antigenic
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