Cancer immune evasion is a major stumbling block in designing effective anticancer therapeutic strategies. Although considerable progress has been made in understanding how cancers evade destructive immunity, measures to counteract tumor escape have not kept pace. There are a number of factors that contribute to tumor persistence despite having a normal host immune system. Immune editing is one of the key aspects why tumors evade surveillance causing the tumors to lie dormant in patients for years through "equilibrium" and "senescence" before re-emerging. In addition, tumors exploit several immunological processes such as targeting the regulatory T cell function or their secretions, antigen presentation, modifying the production of immune suppressive mediators, tolerance and immune deviation. Besides these, tumor heterogeneity and metastasis also play a critical role in tumor growth. A number of potential targets like promoting Th1, NK cell, γδ T cell responses, inhibiting Treg functionality, induction of IL-12, use of drugs including phytochemicals have been designed to counter tumor progression with much success. Some natural agents and phytochemicals merit further study. For example, use of certain key polysaccharide components from mushrooms and plants have shown to possess therapeutic impact on tumor-imposed genetic instability, anti-growth signaling, replicative immortality, dysregulated metabolism etc. In this review, we will discuss the advances made toward understanding the basis of cancer immune evasion and summarize the efficacy of various therapeutic measures and targets that have been developed or are being investigated to enhance tumor rejection.

Vinay, D., Ryan, E., Pawelec, G., Talib, W., Stagg, J., Elkord, E., et al. (2015). Immune evasion in cancer: Mechanistic basis and therapeutic strategies. SEMINARS IN CANCER BIOLOGY, 35 Suppl, S185-98-S198 [10.1016/j.semcancer.2015.03.004].

Immune evasion in cancer: Mechanistic basis and therapeutic strategies

CIRIOLO, MARIA ROSA;AQUILANO, KATIA;
2015

Abstract

Cancer immune evasion is a major stumbling block in designing effective anticancer therapeutic strategies. Although considerable progress has been made in understanding how cancers evade destructive immunity, measures to counteract tumor escape have not kept pace. There are a number of factors that contribute to tumor persistence despite having a normal host immune system. Immune editing is one of the key aspects why tumors evade surveillance causing the tumors to lie dormant in patients for years through "equilibrium" and "senescence" before re-emerging. In addition, tumors exploit several immunological processes such as targeting the regulatory T cell function or their secretions, antigen presentation, modifying the production of immune suppressive mediators, tolerance and immune deviation. Besides these, tumor heterogeneity and metastasis also play a critical role in tumor growth. A number of potential targets like promoting Th1, NK cell, γδ T cell responses, inhibiting Treg functionality, induction of IL-12, use of drugs including phytochemicals have been designed to counter tumor progression with much success. Some natural agents and phytochemicals merit further study. For example, use of certain key polysaccharide components from mushrooms and plants have shown to possess therapeutic impact on tumor-imposed genetic instability, anti-growth signaling, replicative immortality, dysregulated metabolism etc. In this review, we will discuss the advances made toward understanding the basis of cancer immune evasion and summarize the efficacy of various therapeutic measures and targets that have been developed or are being investigated to enhance tumor rejection.
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/10
English
Con Impact Factor ISI
Cancer; Immune evasion; T cells; Therapy
Vinay, D., Ryan, E., Pawelec, G., Talib, W., Stagg, J., Elkord, E., et al. (2015). Immune evasion in cancer: Mechanistic basis and therapeutic strategies. SEMINARS IN CANCER BIOLOGY, 35 Suppl, S185-98-S198 [10.1016/j.semcancer.2015.03.004].
Vinay, D; Ryan, E; Pawelec, G; Talib, W; Stagg, J; Elkord, E; Lichtor, T; Decker, W; Whelan, R; Kumara, H; Signori, E; Honoki, K; Georgakilas, A; Amin, A; Helferich, W; Boosani, C; Guha, G; Ciriolo, Mr; Chen, S; Mohammed, S; Azmi, A; Keith, W; Bhakta, D; Halicka, D; Fujii, H; Aquilano, K; Ashraf, S; Nowsheen, S; Yang, X; Choi, B; Kwon, B
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2108/130104
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