Inhibiting Stat3 signaling in the hematopoietic system elicits multicomponent antitumor immunity

By M. Kortylewski, M. Kujawski, Tianhong Wang, Sheng Wei, Shumin M. Zhang, S. Pilon-Thomas, G. Niu, Heidi Kay, J. Mulé, W. Kerr and 3 more. Nature Medicine, 2005

1,098 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/564a2bfe5bd4ffc77dca2ef735665670eb1ef5d6

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Citations in the corpus

Mechanism regulating reactive oxygen species in tumor induced myeloid-derived suppressor cells (2009, methodology): “Ablation of STAT3 using conditional-KO mice or selective inhibitors dramatically reduced the expansion of MDSCs and improved T cell responses in tumor-bearing mice (22, 36).”
Persistently-activated Stat3 maintains constitutive NF-κB activity in tumors (2009, positive): “B16 tumors growing in mice with Stat3 / myeloid cells displayed reduced Stat3 activity (Figure 1A, left), likely due to the interruption of Stat3-mediated crosstalk between tumor cells and tumor stromal myeloid cells (Kortylewski et al., 2005; Kujawski et al., 2008).”
Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer (2009, background): “The Yu and Pardoll lab’s have investigated the basis for the pro-tumorigenic function of STAT3 in immune/inflammatory cells and have found that inhibition of STAT3 within immune cells significantly enhances anti-tumor immune responses (96,97).”
Mechanisms of immune evasion by tumors. (2006, background): “In addition to its role in tumor cells, Stat3 activation in tumor infiltrating hematopoietic elements appears to be a major checkpoint for innate and adaptive antitumor responses (Kortylewski et al., 2005).”
Immunity, Inflammation, and Cancer (2010, background): “Another attractive target is the STAT3 transcription factor and the signaling pathway that leads to its activation (Kortylewski et al., 2005; Yu et al., 2009).”
IL-17 can promote tumor growth through an IL-6–Stat3 signaling pathway (2009, methodology): “The procedure for isolating immune cells from tumors has been described previously (Kortylewski et al., 2005).”
Myeloid-Derived Suppressor Cells: Linking Inflammation and Cancer (2009, background): “In vivo inactivation of genes that govern MDSC accumulation, such as the STAT3 and STAT6 genes (51, 59, 64, 65) and the nonclassical MHC class I CD1d gene (58, 66), also restores T cell activation and promotes tumor regression and/or resistance to metastatic disease.”
Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability. (2009, background): “This transcription factor is constitutively activated both in tumors and in immune cells and plays a role in carcinogenesis, as well as in tumor immune evasion by hampering DC maturation [12,24].”
Cytokine signaling modules in inflammatory responses. (2008, background): “…renders mice sensitive to the pro-inflammatory effects of LPS, whereas established nonhematopoietic tumor lines use Stat3 as a method of suppressing the production of inflammatory markers in order to escape host immune recognition (Kano et al., 2003; Kortylewski et al., 2005; Wang et al., 2004).”