Download Cancer Immunotherapy at the Crossroads: How Tumors Evade by James H. Finke (Editor), Ronald M. Bukowski (Editor) PDF

By James H. Finke (Editor), Ronald M. Bukowski (Editor)

Prime investigators and clinicians aspect the several mechanisms utilized by tumors to flee and impair the immune method after which spell out attainable medical options to avoid or opposite tumor-induced immune disorder. The authors evaluate the mechanisms of immune disorder and evasion mechanisms in histologically various human tumors, concentrating on tumor-induced molecular defects in T cells and antigen-presenting cells (dendritic cells and tumors), which could function biomarkers for sufferer analysis. They speak about the ability wherein those immune features will be safe or restored with the intention to extra successfully aid the method of tumor rejection in situ. state of the art ideas are defined with the ability to observe the energy and caliber of sufferers' immune responses utilizing immunocytometry, MHC-peptide tetramers mixed with apoptosis assay, ELISPOT assay, and detection of MHC-TAA peptide complexes on tumor cells.

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Additional resources for Cancer Immunotherapy at the Crossroads: How Tumors Evade Immunity and What Can Be Done (Current Clinical Oncology)

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Morel S, Levy F, Burlet-Schiltz O, Brasseur F, Probst-Kepper M, Peitrequin AL, et al. Processing of some antigens by the standard proteasome but not by the immunoproteasome results in poor presentation by dendritic cells. Immunity 2000;12:107–117. 97. Sun Y, Sijts AJ, Song M, Janek K, Nussbaum AK, Kral S, et al. Expression of the proteasome activator PA28 rescues the presentation of a cytotoxic T lymphocyte epitope on melanoma cells. Cancer Res 2002;62:2875–2882. 98. Porgador A, Yewdell JW, Deng Y, Bennink JR, Germain RN.

Although two mutational events are required for total HLA class I antigen loss, TAP downregulation appears to be primarily caused by abnormalities in regulatory mechanisms. In only two cases, mutations in the Tap1 gene have been observed. These mutations have led to altered function of the TAP1 protein itself or a lack of protein translation. An amino acid substi- 16 Part I / Basic Mechanisms of Immune Evasion tution was identified at position 659 (R659Q) near the ATP-binding site of Tap1 in a human SCLC cell line (70).

Chapter 1 / HLA Peptide-Complex Defects 21 3. HLA CLASS I ALLOSPECIFICITY-TAA-DERIVED PEPTIDE COMPLEXES ON TUMOR CELLS As already discussed, a crucial role in the interactions between HLA class I antigen-restricted, TAA-specific CTLs and tumor cells is played by HLA class I antigen-TAA-derived peptide complexes. Therefore, it is important to ask whether the level of a HLA class I allospecificity on the cell membrane can be used as a measure of the respective HLA class I allospecificity-peptide complex.

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