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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review

Tumor Escape

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Disease relevance of Tumor Escape


High impact information on Tumor Escape

  • Our findings demonstrate that although even advanced stages of epithelial malignancy remain dependent upon continued Wnt signaling for maintenance and growth, loss of p53 facilitates tumor escape and the acquisition of oncogene independence [5].
  • The FAS receptor-ligand system plays a key role in regulating apoptotic cell death, and corruption of this signaling pathway has been shown to participate in tumor-immune escape and carcinogenesis [6].
  • Therefore, our data indicate that CD95-dependent apoptosis constitutes a more prominent mechanism for tumor clearance than has so far been anticipated and that blockade of this pathway can result in tumor escape even when the perforin pathway is operational [7].
  • Thus, expansion of peripheral immune repertoire to Melan-A/Mart-1 takes place in some metastatic patients and leads to enhanced CTL induction after antigen-presenting cell-mediated selection, but, in most metastatic lesions, it does not overcome tumor escape from immune surveillance [8].
  • A tumor escape variant that has lost one major histocompatibility complex class I restriction element induces specific CD8+ T cells to an antigen that no longer serves as a target [9].

Biological context of Tumor Escape

  • This suggests that tumor escape from immune surveillance may have occurred in vivo as a sequential result of (a) antigen loss, and (b) downregulation of the peptide-transporter protein TAP-1 expression by this patient's tumor over a 6-yr period from 1987 to 1993 [10].
  • These altered HLA class I phenotypes and non-ubiquitous expression of NK receptor ligands constitute the major tumor escape mechanism facing tumor-specific CTL and/or NK cell mediated responses [11].
  • The presented results suggest that RCAS1 might play an important role in tumor escape from host immunological surveillance and carry weight in the down regulation of the maternal immune response, thereby maintaining pregnancy [12].

Anatomical context of Tumor Escape


Associations of Tumor Escape with chemical compounds


Gene context of Tumor Escape

  • These findings identify mucin secretion as a novel mechanism of tumor escape from immune surveillance and provide the basis for the generation of potentially tolerogenic DC [21].
  • The identification of T cell epitopes presented by alternative HLA-B and -C alleles may provide a means to counteract the tumor escape mechanism based on the selection of tumor cells no longer susceptible to HLA-A-restricted T cell recognition [22].
  • On the basis of numerous studies, HLA-G is also expressed in malignant tumors and involved in tumor immune escape [23].
  • The selection of tumor variants with altered expression of classical and nonclassical MHC class I molecules: implications for tumor immune escape [24].
  • AIM: To explore the role and significance of costimulatory molecules B7H1,B7H2 and ICOS within tissues of human gastric carcinoma and the possible mechanisms in tumor escape [25].

Analytical, diagnostic and therapeutic context of Tumor Escape


  1. Inhibition of alpha(v)beta3 integrin survival signaling enhances antiangiogenic and antitumor effects of radiotherapy. Abdollahi, A., Griggs, D.W., Zieher, H., Roth, A., Lipson, K.E., Saffrich, R., Gröne, H.J., Hallahan, D.E., Reisfeld, R.A., Debus, J., Niethammer, A.G., Huber, P.E. Clin. Cancer Res. (2005) [Pubmed]
  2. Presence and specificity of tumor associated lymphocytes from ascites fluid in prostate cancer. Ozenci, V., Miller, A.M., Palmborg, A., Egevad, L., Jaremko, G.A., Kälkner, K.M., Pisa, P. Prostate (2005) [Pubmed]
  3. Inhibition of dendropoiesis by tumor derived and purified prostate specific antigen. Aalamian, M., Tourkova, I.L., Chatta, G.S., Lilja, H., Huland, E., Huland, H., Shurin, G.V., Shurin, M.R. J. Urol. (2003) [Pubmed]
  4. The Fas/Fas-ligand system: a mechanism for immune evasion in human breast carcinomas. Gutierrez, L.S., Eliza, M., Niven-Fairchild, T., Naftolin, F., Mor, G. Breast Cancer Res. Treat. (1999) [Pubmed]
  5. Impact of p53 loss on reversal and recurrence of conditional Wnt-induced tumorigenesis. Gunther, E.J., Moody, S.E., Belka, G.K., Hahn, K.T., Innocent, N., Dugan, K.D., Cardiff, R.D., Chodosh, L.A. Genes Dev. (2003) [Pubmed]
  6. FASL -844C polymorphism is associated with increased activation-induced T cell death and risk of cervical cancer. Sun, T., Zhou, Y., Li, H., Han, X., Shi, Y., Wang, L., Miao, X., Tan, W., Zhao, D., Zhang, X., Guo, Y., Lin, D. J. Exp. Med. (2005) [Pubmed]
  7. Immune escape of tumors in vivo by expression of cellular FLICE-inhibitory protein. Medema, J.P., de Jong, J., van Hall, T., Melief, C.J., Offringa, R. J. Exp. Med. (1999) [Pubmed]
  8. An expanded peripheral T cell population to a cytotoxic T lymphocyte (CTL)-defined, melanocyte-specific antigen in metastatic melanoma patients impacts on generation of peptide-specific CTLs but does not overcome tumor escape from immune surveillance in metastatic lesions. Anichini, A., Molla, A., Mortarini, R., Tragni, G., Bersani, I., Di Nicola, M., Gianni, A.M., Pilotti, S., Dunbar, R., Cerundolo, V., Parmiani, G. J. Exp. Med. (1999) [Pubmed]
  9. A tumor escape variant that has lost one major histocompatibility complex class I restriction element induces specific CD8+ T cells to an antigen that no longer serves as a target. Seung, S., Urban, J.L., Schreiber, H. J. Exp. Med. (1993) [Pubmed]
  10. Tumor escape from immune recognition: lethal recurrent melanoma in a patient associated with downregulation of the peptide transporter protein TAP-1 and loss of expression of the immunodominant MART-1/Melan-A antigen. Maeurer, M.J., Gollin, S.M., Martin, D., Swaney, W., Bryant, J., Castelli, C., Robbins, P., Parmiani, G., Storkus, W.J., Lotze, M.T. J. Clin. Invest. (1996) [Pubmed]
  11. Strategies to endow cytotoxic T lymphocytes or natural killer cells with antibody activity against carcinoembryonic antigen. Kuroki, M., Kuroki, M., Shibaguchi, H., Badran, A., Hachimine, K., Zhang, J., Kinugasa, T. Tumour Biol. (2004) [Pubmed]
  12. Comparative analysis of RCAS1 level in neoplasms and placenta. Wicherek, L., Dutsch, M., Mak, P., Klimek, M., Skladzien, J., Dubin, A. Acta Biochim. Pol. (2003) [Pubmed]
  13. Human urinary bladder transitional cell carcinomas acquire the functional Fas ligand during tumor progression. Chopin, D., Barei-Moniri, R., Maillé, P., Le Frère-Belda, M.A., Muscatelli-Groux, B., Merendino, N., Lecerf, L., Stoppacciaro, A., Velotti, F. Am. J. Pathol. (2003) [Pubmed]
  14. Tumor escape from killing: role of killer inhibitory receptors and acquisition of tumor resistance to cell death. Chouaib, S., Thiery, J., Gati, A., Guerra, N., El Behi, M., Dorothée, G., Mami-Chouaib, F., Bellet, D., Caignard, A. Tissue Antigens (2002) [Pubmed]
  15. Altered MHC class I antigens in tumors. Algarra, I., Collado, A., Garrido, F. Int. J. Clin. Lab. Res. (1997) [Pubmed]
  16. Serum requirements for in vivo modulation of thymus-leukemia antigens on mouse leukemia cells and thymocytes. Stackpole, C.W. J. Natl. Cancer Inst. (1979) [Pubmed]
  17. Androgens repress the expression of the angiogenesis inhibitor thrombospondin-1 in normal and neoplastic prostate. Colombel, M., Filleur, S., Fournier, P., Merle, C., Guglielmi, J., Courtin, A., Degeorges, A., Serre, C.M., Bouvier, R., Clézardin, P., Cabon, F. Cancer Res. (2005) [Pubmed]
  18. Pattern of hormone receptor status of secondary contralateral breast cancers in patients receiving adjuvant tamoxifen. Bachleitner-Hofmann, T., Pichler-Gebhard, B., Rudas, M., Gnant, M., Taucher, S., Kandioler, D., Janschek, E., Dubsky, P., Roka, S., Sporn, E., Jakesz, R. Clin. Cancer Res. (2002) [Pubmed]
  19. Salvage therapy for hepatocellular carcinoma with thalidomide. Wang, T.E., Kao, C.R., Lin, S.C., Chang, W.H., Chu, C.H., Lin, J., Hsieh, R.K. World J. Gastroenterol. (2004) [Pubmed]
  20. Eosinophil granulocytes account for indoleamine 2,3-dioxygenase-mediated immune escape in human non-small cell lung cancer. Astigiano, S., Morandi, B., Costa, R., Mastracci, L., D'Agostino, A., Ratto, G.B., Melioli, G., Frumento, G. Neoplasia (2005) [Pubmed]
  21. Tumor-derived MUC1 mucins interact with differentiating monocytes and induce IL-10highIL-12low regulatory dendritic cell. Monti, P., Leone, B.E., Zerbi, A., Balzano, G., Cainarca, S., Sordi, V., Pontillo, M., Mercalli, A., Di Carlo, V., Allavena, P., Piemonti, L. J. Immunol. (2004) [Pubmed]
  22. Novel HLA-Cw8-restricted T cell epitopes derived from tyrosinase-related protein-2 and gp100 melanoma antigens. Castelli, C., Tarsini, P., Mazzocchi, A., Rini, F., Rivoltini, L., Ravagnani, F., Gallino, F., Belli, F., Parmiani, G. J. Immunol. (1999) [Pubmed]
  23. HLA-G gene activation in tumor cells involves cis-acting epigenetic changes. Mouillot, G., Marcou, C., Rousseau, P., Rouas-Freiss, N., Carosella, E.D., Moreau, P. Int. J. Cancer (2005) [Pubmed]
  24. The selection of tumor variants with altered expression of classical and nonclassical MHC class I molecules: implications for tumor immune escape. Algarra, I., García-Lora, A., Cabrera, T., Ruiz-Cabello, F., Garrido, F. Cancer Immunol. Immunother. (2004) [Pubmed]
  25. In situ expression and significance of B7 costimulatory molecules within tissues of human gastric carcinoma. Chen, X.L., Cao, X.D., Kang, A.J., Wang, K.M., Su, B.S., Wang, Y.L. World J. Gastroenterol. (2003) [Pubmed]
  26. Suppression of tumor metastasis by blockade of transforming growth factor beta signaling in bone marrow cells through a retroviral-mediated gene therapy in mice. Shah, A.H., Tabayoyong, W.B., Kundu, S.D., Kim, S.J., Van Parijs, L., Liu, V.C., Kwon, E., Greenberg, N.M., Lee, C. Cancer Res. (2002) [Pubmed]
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