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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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Nuno Baetas da Silva,António Portugal Duartemmatory responses involving the expression of IFN-γ and IL-2 mRNA,. In a subset of patients, diminished T-cell function has also been observed in the peripheral blood, which is mostly associated with reduced production of TH1 type cytokines (e.g., IFN-γ) following stimulation of peripheral-blood T cells with mitogens or anti-CD3 antibody ..
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Ewa Madalińska-Bugaj,Linh Anh Nguyenhe syngeneic normal host, and form progressively growing tumors. It is highly likely—and increasingly recognized—that local tumor cell—host interactions influence the initial steps of tumor formation.
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Pravin Chandrasekaran,R. Muthucumaraswamyrs, including interleukin (IL)-10, transforming growth factor-β (TGF-β), and cyclic adenosine 5′ monophosphate (cAMP)-elevating prostaglandins, contribute to the induction and maintenance of such tolerance, and are variously produced by T lymphocytes themselves and/or by ambient host cells such as macrophages .–..
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Book 2004rder 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.
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Altered Signaling in T Lymphocytes of Patients With Cancert transfer of T lymphocytes, antibodies, or cytokines to tumor-bearing hosts was often successful in the control of tumor growth in animals .,., but frequently failed in man .. By then, the field of tumor immunology had evolved, and principles of tumor immunity had been established.
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Communication Issues in Integrative Oncologysuccess of most anticancer immunization strategies. We also discuss strategies that may help to understand this complex phenomenon, with the ultimate goal of identifying the true algorithm that modulates the immune rejection of cancer.
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CD4+ T-Cell-Mediated Immunity to Cancerogic response modifiers, such as interleukin-2 (IL-2) .. Although it is not the purpose of this chapter to survey all of the potential mechanisms that may underlie the ineffectiveness of such immune effector cells ., one must consider deviation in the functional antitumor CD4+ T “helper” compartment as a major confounding variable.
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The Development and Reversal of T-Cell Tolerance in Cancer Patients Receiving Peptide-Based Vaccinessuccess of most anticancer immunization strategies. We also discuss strategies that may help to understand this complex phenomenon, with the ultimate goal of identifying the true algorithm that modulates the immune rejection of cancer.
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