Interferons, immunity and cancer immunoediting

By G. Dunn, Catherine M. Koebel, Robert Schreiber. Nature reviews. Immunology, 2006

1,573 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/584ed995fc93bbe75edce4702db5882815eaa035

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Citations in the corpus

Long-term survival for patients with non-small-cell lung cancer with intratumoral lymphoid structures. (2008, background): “The density of tumorinfiltrating lymphocytes (TILs) with cytotoxic and memory phenotypes is highly predictive of good clinical outcome.(8-14) However, although prognosis is related to the homing of effector immune cells, it is still unclear where the activation of the specific immune response takes ”
Type I interferon is selectively required by dendritic cells for immune rejection of tumors (2011, neutral): “There is strong experimental support for all three phases of cancer immuno editing, elimination, equilibrium, and escape, and many of the key cellular mediators and immune effector molecules involved in host protection from tumor development have been identified (Dunn et al., 2006; Smyth et al., 20”
IL-17 can promote tumor growth through an IL-6–Stat3 signaling pathway (2009, background): “The immune system can act as an extrinsic suppressor of tumors, and the importance of Th1, characterized by IFN- and type 1 IFNs, in inhibiting tumor incidence and growth has been established (Kaplan et al., 1998; Dunn et al., 2006).”
Cancer to bone: a fatal attraction (2011, neutral): “Although T lymphocytes have a key role in influencing general tumour growt”
New insights into cancer immunoediting and its three component phases — elimination, equilibrium and escape (2014, neutral): “Whereas one body of work has clearly established the capacity of chronic inflammation to initiate and promote cancer [1], a second set of studies from other laboratories, including our own, has revealed that an intact immune system can prevent/ control and shape/promote cancer by a process we call ‘”
Indoleamine 2,3-dioxygenase and tumor-induced tolerance. (2007, background): “Alternatively, IDO is known to be inducible in many tumor cell lines by IFN-γ and other inflammatory mediators (37); therefore, IDO might be secondarily induced in tumor cells or in host stromal cells in response to inflammatory cytokines from the initial host response against the tumor (76).”
Immunity, Inflammation, and Cancer (2010, neutral): “According to the immunosurveillance hypothesis, NK cells and CTLs engage in tumor killing (via perforin, granzyme B, TRAIL or FasL dependent mechanisms), whereas Th1 (by virtue of IFNγ production) and in some instances Th17 cells (via production of IL-17A) provide important help that boosts cytotoxi”
CD4+ T Cells Regulate Pulmonary Metastasis of Mammary Carcinomas by Enhancing Protumor Properties of Macrophages (2009, background): “…profiling from breast-cancer-associated stroma revealed a gene signature predictive of good prognostic outcome (>98%, 5 year survival) that was functionally enriched for elements of a T H 1-type immune response, including genes suggestive of CTL and NK cell activity (Finak et al., 2008 ).”