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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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Aineas Mallios,Ted Lindblom,Stefan Sjögren responses .. In their purest form, such strategies take the form of adoptively transferred, enriched populations of tumor-reactive CD8+ T cells. These approaches have occasionally been shown to be capable of mediating the regression of lesions in cancer patients .. However, more often, high circula
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Kristaps Freimanis,Maija Šenfeldends on the surface of multiple types of tumor cells has led to the recognition that tumor cells may escape destruction by immune effector cells, and may be actively involved in the killing of Fas-expressing lymphocytes. Thus, the Fas/Fas ligand (Fas/FasL) interaction serves both as a mechanism of cy
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Pravin Chandrasekaran,R. Muthucumaraswamyntigen-presenting cells (APC) such as dendritic cells (DC), and a supportive cytokine milieu. Cytokines present at the immunization site—or in the case of tumors, the tumor site—have been shown to have a marked effect on the magnitude as well as the nature of the response. They play a role in recrui
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Pravin Chandrasekaran,R. Muthucumaraswamyria-laden large intestine .–.. Such chronic tolerance is as important to the immune system as its capacity to destroy pathogens, since it is essential that the host does not reject a growing fetus or loops of bowel that house commensual bacteria. A vast array of physiological immunosuppressive facto
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New Challenges in Banking and Financeions in the apoptotic pathways may determine tumor resistance to current therapeutic strategies. An understanding of the molecular mechanisms involved in the regulation of apoptosis and how tumor cells evade apoptotic death may provide insight into the processes of carcinogenesis and the progression
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Communication Issues in Integrative Oncology insufficient to induce cancer rejection or—although adequate for this task—are most often counteracted by an evolving disease that is capable of escaping them through continuous phenotypic changes. A combination of the two is probably at the basis of the relatively rare observation of tumor regress
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