We are analyzing https://link.springer.com/article/10.1007/s00262-003-0469-5.

Title:
Tumour escape: antitumour effectors too much of a good thing? | Cancer Immunology, Immunotherapy
Description:
Although even “spontaneous” tumours are immunogenic and are commonly infiltrated by tumour antigen-specific T cells (at least in melanoma), most tumours are not completely rejected by the host, and cancer progresses. There is a growing realisation that many responses defined as antitumour effector mechanisms act as double-edged swords and under different conditions either become ineffective or even protumorigenic. Examples are interleukin 2 (also proapoptotic for activated T cells), interferon γ (by induction of ligands for T and NK cell inhibitory receptors), angiogenesis inhibition (by hypoxia-mediated induction of growth factors promoting metastasis), and macrophage free radical-mediated cytotoxicity (by inhibiting T cells). Immune selection pressure itself, resulting in outgrowth of resistant tumour variants could also be viewed in this light. On the other hand, knowledge of the many tumour escape pathways offers the theoretical possibility of reconstituting antitumour immunity. Tumour escape from immunosurveillance represents the last series of hurdles to be overcome in formulating truly effective cancer immunotherapy, but given the immense plasticity of the tumour cell, and the complex balance between pro- and antitumour activity of the very same effector pathways, this remains a major challenge.
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google, scholar, pubmed, cas, cancer, article, tumour, immunol, cell, cells, interleukin, human, expression, immune, patients, lymphocytes, carcinoma, melanoma, growth, res, immunother, tumours, int, escape, med, fas, pawelec, immunotherapy, role, clin, blood, exp, ligand, class, molecules, serum, apoptosis, receptors, immunity, biol, receptor, levels, cytokine, metastatic, mice, antitumour, antigenspecific, hla, invest, progression,

Topics {✒️}

month download article/chapter t-cell receptor zeta-chain long-term renal transplants ifn-gamma-deficient mice immunodominant epstein-barr virus immunologically-deficient nude mice tumour growth factor-beta inhibit cell-mediated immunity monocyte-derived dendritic cells human t-cells starved macrophage suppressor activity small-cell lung cancer tumour necrosis factor-alpha decreased antigen-specific responsiveness squamous cell carcinomas promote tumour evasion mhc class ii effective anticancer vaccines melanoma/melanocyte epitope mart1 high-affinity il-4 receptors hla-dr-restricted manner cell receptor-cd3 complex cd94/nkg2a-dependent mechanism inferior failure-free survival antigen-specific cd8+ cytotoxic janssen-van rhijn cm melanoma-antigen-specific anergy antibody-dependent immune memory t-cell tolerance article cancer immunology antigen-processing machinery defects de-novo breast cancer autologous dendritic cells hla class-ii human dendritic cells chronic lymphocytic leukemia inhibits tumour-specific full article pdf unique tumour antigen tumour-induced death resistant tumour variants lymphocyte apoptosis induced th2 cell differentiation lung cancers growing t-cell activation active specific immunotherapy b-cell lymphomas cell-tumour cell regulates hla class-1 lymphocyte-mediated lysis

Questions {❓}

Chappell DB, Restifo NP (1998) T cell-tumour cell: a fatal interaction?
Effros R, Pawelec G (1997) Replicative senescence of T lymphocytes: does the Hayflick Limit lead to immune exhaustion?
Mellor AL, Munn DH (1999) Tryptophan catabolism and T-cell tolerance: immunosuppression by starvation?
Mouawad R, Khayat D, Merle S, Antoine EC, Gil-Delgado M, Soubrane C (1999) Is there any relationship between interleukin-6/ interleukin-6 receptor modulation and endogenous interleukin-6 release in metastatic malignant melanoma patients treated by biochemotherapy?
Pawelec G (1999) Tumour escape from the immune response: the last hurdle for successful immunotherapy of cancer?
Trapani JA (2002) Tumour-mediated apoptosis of cancer-specific T lymphocytes--reversing the “kiss of death”?
Tumour escape: antitumour effectors too much of a good thing?
Tumour escape: antitumour effectors too much of a good thing?

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         description:Although even “spontaneous” tumours are immunogenic and are commonly infiltrated by tumour antigen-specific T cells (at least in melanoma), most tumours are not completely rejected by the host, and cancer progresses. There is a growing realisation that many responses defined as antitumour effector mechanisms act as double-edged swords and under different conditions either become ineffective or even protumorigenic. Examples are interleukin 2 (also proapoptotic for activated T cells), interferon γ (by induction of ligands for T and NK cell inhibitory receptors), angiogenesis inhibition (by hypoxia-mediated induction of growth factors promoting metastasis), and macrophage free radical-mediated cytotoxicity (by inhibiting T cells). Immune selection pressure itself, resulting in outgrowth of resistant tumour variants could also be viewed in this light. On the other hand, knowledge of the many tumour escape pathways offers the theoretical possibility of reconstituting antitumour immunity. Tumour escape from immunosurveillance represents the last series of hurdles to be overcome in formulating truly effective cancer immunotherapy, but given the immense plasticity of the tumour cell, and the complex balance between pro- and antitumour activity of the very same effector pathways, this remains a major challenge.
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      description:Although even “spontaneous” tumours are immunogenic and are commonly infiltrated by tumour antigen-specific T cells (at least in melanoma), most tumours are not completely rejected by the host, and cancer progresses. There is a growing realisation that many responses defined as antitumour effector mechanisms act as double-edged swords and under different conditions either become ineffective or even protumorigenic. Examples are interleukin 2 (also proapoptotic for activated T cells), interferon γ (by induction of ligands for T and NK cell inhibitory receptors), angiogenesis inhibition (by hypoxia-mediated induction of growth factors promoting metastasis), and macrophage free radical-mediated cytotoxicity (by inhibiting T cells). Immune selection pressure itself, resulting in outgrowth of resistant tumour variants could also be viewed in this light. On the other hand, knowledge of the many tumour escape pathways offers the theoretical possibility of reconstituting antitumour immunity. Tumour escape from immunosurveillance represents the last series of hurdles to be overcome in formulating truly effective cancer immunotherapy, but given the immense plasticity of the tumour cell, and the complex balance between pro- and antitumour activity of the very same effector pathways, this remains a major challenge.
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