Cancer-Associated Fibroblasts Are Activated in Incipient Neoplasia to Orchestrate Tumor-Promoting Inflammation in an NF-kappaB-Dependent Manner.

By Neta Erez, Morgan C. Truitt, P. Olson, S. Arron, D. Hanahan. Cancer Cell, 2010

1,396 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/25a9859a6eca3bcbc48a8174d955c2fcc98db5ac

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Citations in the corpus

Bone marrow-derived myofibroblasts contribute to the mesenchymal stem cell niche and promote tumor growth (2011, neutral): “…of tumor growth and invasion compared to normal or resident fibroblasts, and exhibit a previously reported NF-kB-dependent inflammatory gene expression signature (Erez et al., 2010), which accounts for higher levels of pro-inflammatory cytokines in CAFs (Karnoub et al., 2007; Orimo et al., 2005).”
Macrophage plasticity and polarization: in vivo veritas. (2012, neutral): “macrophage polarization and tumor promotion (94).”
IL-1-induced JAK/STAT signaling is antagonized by TGF-β to shape CAF heterogeneity in pancreatic ductal adenocarcinoma. (2018, background): “We hypothesized that NF-κB signaling might play a role in iCAF formation, as it has been previously identified as a pathway responsible for the induction of an inflammatory profile in CAFs (25,26).”
Tumor-associated stromal cells as key contributors to the tumor microenvironment (2016, background): “[19], TAFs/CAFs in the tumor stroma promoted sustained inflammation via increase of inflammatory cytokines, neoangiogenesis, and macrophage recruitment, enhancing tumor growth.”
Hallmarks of cancer: interactions with the tumor stroma. (2010, background): “[61] N.”
Fibroblast heterogeneity in the cancer wound (2014, background): “…factor (bFGF), and members of the Wnt family (Orimo et al., 2001, 2005; Allinen et al., 2004; Bhowmick et al., 2004; Kalluri and Zeisberg, 2006; Erez et al., 2010; Räsänen and Vaheri, 2010; Chaffer and Weinberg, 2011; Cirri and Chiarugi, 2011), as well as many cytokines, such as CCL7 and…”
Intratumor T helper type 2 cell infiltrate correlates with cancer-associated fibroblast thymic stromal lymphopoietin production and reduced survival in pancreatic cancer (2011, background): “Cancer-related inflammation has been proposed as the seventh hallmark of cancer (Dunn et al., 2004; Grivennikov et al., 2010), and recently proinflammatory CAFs from a transgenic mouse tumor model were shown to orchestrate tumorpromoting inflammation in a NF-B–dependent manner (Erez et al., 2010).”
Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. (2012, background): “CAFs isolated from the initial hyperplastic stage in multistep skin tumorigenesis exhibit activated expression of the pro-inflammatory cytokine IL-6.(152) More important, chemical and physical insults encountered during therapeutic interventions may also cause stress-induced cellular senescence and ”
CD10+GPR77+ Cancer-Associated Fibroblasts Promote Cancer Formation and Chemoresistance by Sustaining Cancer Stemness. (2018, neutral): “…of cytokines, such as CCL18 and IL-1b, in the tumor microenvironment may be responsible for initiating the NF-kB signaling by activating IKK in the CAF subset (Erez et al., 2010; Su et al., 2014), IKK activation is usually not sustainable due to numerous negative feedback loops (Perkins, 2012).”
Carcinoma-associated fibroblasts: orchestrating the composition of malignancy (2016, background): “Indeed, interactions of CAFs with cellular components of the immune system contribute, to a large extent, to the tumor-promoting role of CAFs through immunosuppression and sustained inflammation (Liao et al. 2009; Erez et al. 2010; Quante et al. 2011; Servais and Erez 2013).”