The three Es of cancer immunoediting.
By G. Dunn, Lloyd J. Old, Robert Schreiber. Annual Review of Immunology, 2004
2,997 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/4d6b787d361b508ea3cdeaf46fee546e7a64cfde
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Citations in the corpus
- Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer (2009, background): “Genetic or pharmacological inhibition or intervention with these cytokines in various models of cancer either increases or decreases tumor growth and also affects tumormultiplicity [29,45,87–91].”
- Immunosuppressive strategies that are mediated by tumor cells. (2007, background): “The renaissance of tumor immunosurveillance in the new concept of “immunoediting” holds the idea that the immune system not only protects the host against tumor development, but can also promote tumor growth by selecting for tumor escape variants with reduced immunogenicity (3).”
- Targeting Tim-3 and PD-1 pathways to reverse T cell exhaustion and restore anti-tumor immunity (2010, background): “In support of cancer immunosurveillance is the fact that both immunodeficient or immunosuppressed patients and experimental animals are more susceptible to tumor development (for reviews see Dunn et al., 2004; Zitvogel et al., 2006; Swann and Smyth, 2007).”
- NK cells and cancer immunosurveillance (2008, background): “Interestingly, mice deficient for both RAG2 and STAT1 have been reported to spontaneously develop adenocarcinoma at higher rates as compared with mice deficient only for RAG2, implicating NK cells in tumour immunosurveillance (Shankaran et al., 2001; Dunn et al., 2004; Swann and Smyth, 2007).”
- Combining radiotherapy and cancer immunotherapy: a paradigm shift. (2013, background): “As mentioned before, tumors express a large number of neoantigens (16), but the antigens that are strongly immunogenic are usually already lost at the time of clinical presentation of the disease, “edited” out when tumors escape immune control (3,14,15).”
- The complexity of NF-κB signaling in inflammation and cancer (2013, background): “This immune defense against cancer cells, however, is normally not tight enough to eliminate all the aberrant cells, resulting in a shift to an equilibrium phase, which is often followed by an “escape” phase of the cancer cells, in which they outperform the immune system [79].”
- Cancer Exome Analysis Reveals a T Cell Dependent Mechanism of Cancer Immunoediting (2012, positive): “This mechanism most likely also produces other types of escape tumours, such as those that develop inactivating mutations in antigen presentation genes (for example, those encoding MHC class I proteins), which are frequently observed in clinically apparent human cancer”