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MHC Class I Antigens In Malignant Cells : Immune Escape And Response To Immunotherapy / by Natalia Aptsiauri, Angel Miguel Garcia-Lora, Teresa Cabrera

By: Aptsiauri, Natalia
Contributor(s): Garcia-Lora, Angel Miguel | Cabrera, Teresa
Material type: materialTypeLabelE-bookSeries: SpringerBriefs in Cancer Research; 66Publisher: New York : Springer International Publishing, 2013Description: 1 recurso en línea (VIII, 51 p.) 17 il., 14 il. col..ISBN: 9781461465430.Subject: Cáncer -- Aspectos inmunológicosOnline resources: Acceso a este recurso digital (usuarios Universidad Europea de Madrid)Digital Resources Summary: Abnormal expression of MHC class I molecules in malignant cells is a frequent occurrenceÂ{u4A21}t ranges from total loss of all class I antigens to partial loss of MHC specific haplotypes or alleles. Different mechanisms are described to be responsible for these alterations, requiring different therapeutic approaches.Â{u1823}complete characterization of these molecular defects is important for improvement of the strategies for the selection and follow-up of patients undergoing T-cell based cancer immunotherapy. Â{u0CA5}cise identification of the mechanism leading to MHC class I defects Â{u7A6C}l help to develop new personalized patient-tailored treatment protocols.Â{u4A25}re is significant new researchÂ{uFBA0}the prevalence of various patterns of MHC class I defects and the underlying molecular mechanisms in different types of cancer. In contrast, few data isÂ{u1DA1}ilable on the changes in MHC class I expression during the course of cancer immunotherapy, but the authors have recently made discoveries thatÂ{u3A2F}wÂ{u4A25}Â{u0CAF}gression or regression of a tumor lesion in cancer patients undergoing immunotherapy depends on the molecular mechanism responsible for the MHC class I alteration and not on the type of immunotherapy used. According to this notion, the nature of the preexisting MHC class I lesion in the cancer cell has a crucial impact onÂ{u4974}ermining the final outcome of cancer immunotherapy.Â{u4A29}s SpringerBrief will presentÂ{u8BF7} MHC class 1 is expressed, explain its role in tumor progression, and its role in resistance to immunotherapy. Â{u0000}
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Item type Current library Collection Call number Copy number Status Date due Barcode Item holds
LIBRO-E NO PRÉSTAMO LIBRO-E NO PRÉSTAMO Madrid Digital Acceso Electrónico (UEM) Ciencias de la Salud RC268.3 A687 2013 EB (Browse shelf(Opens below)) .i11545148 Acceso electrónico eBOOK .i11545148
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Abnormal expression of MHC class I molecules in malignant cells is a frequent occurrenceÂ{u4A21}t ranges from total loss of all class I antigens to partial loss of MHC specific haplotypes or alleles. Different mechanisms are described to be responsible for these alterations, requiring different therapeutic approaches.Â{u1823}complete characterization of these molecular defects is important for improvement of the strategies for the selection and follow-up of patients undergoing T-cell based cancer immunotherapy. Â{u0CA5}cise identification of the mechanism leading to MHC class I defects Â{u7A6C}l help to develop new personalized patient-tailored treatment protocols.Â{u4A25}re is significant new researchÂ{uFBA0}the prevalence of various patterns of MHC class I defects and the underlying molecular mechanisms in different types of cancer. In contrast, few data isÂ{u1DA1}ilable on the changes in MHC class I expression during the course of cancer immunotherapy, but the authors have recently made discoveries thatÂ{u3A2F}wÂ{u4A25}Â{u0CAF}gression or regression of a tumor lesion in cancer patients undergoing immunotherapy depends on the molecular mechanism responsible for the MHC class I alteration and not on the type of immunotherapy used. According to this notion, the nature of the preexisting MHC class I lesion in the cancer cell has a crucial impact onÂ{u4974}ermining the final outcome of cancer immunotherapy.Â{u4A29}s SpringerBrief will presentÂ{u8BF7} MHC class 1 is expressed, explain its role in tumor progression, and its role in resistance to immunotherapy. Â{u0000}

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