Stat3/Socs3 activation by IL-6 transsignaling promotes progression of pancreatic intraepithelial neoplasia and development of pancreatic cancer.
By M. Lesina, Magdalena U. Kurkowski, K. Ludes, S. Rose‐John, M. Treiber, G. Klöppel, A. Yoshimura, W. Reindl, B. Sipos, Shizuo Akira and 2 more. Cancer Cell, 2011
849 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/627bf81a3bae58f828328b9733d3d52ec85bdd64
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In Oncology
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In Surgery
Citations in the corpus
- IL-1-induced JAK/STAT signaling is antagonized by TGF-β to shape CAF heterogeneity in pancreatic ductal adenocarcinoma. (2018, background): “The secretory phenotype of iCAFs suggest a role for this CAF subtype in promoting tumor progression, chemoresistance and other cancer-associated systemic effects, such as cachexia and immune suppression (6,9,11,21-24,38,45,46).”
- IL-6 Trans-Signaling via the Soluble IL-6 Receptor: Importance for the Pro-Inflammatory Activities of IL-6 (2012, background): “Pancreatic Cancer Pancreatic cancer caused by expression of oncogenic G12D K-ras [105]”
- Tumor-derived granulocyte-macrophage colony stimulating factor regulates myeloid inflammation and T cell immunity in pancreatic cancer (2012, background): “Indeed, our data are consistent with those of previous studies demonstrating IL-6 production primarily by stromal cells, not the tumor, in mouse models (Lesina et al., 2011) as well as human PDA (Bellone et al., 2006; Lesina et al., 2011).”
- Human Gut Microbiota and Gastrointestinal Cancer (2018, background): “pylori infections can promote pancreatic cancer progression by upregulating the expression of anti-apoptotic and pro-proliferative proteins, including Bcl-xL, MCL-1, survivin, c-myc, and cyclin D1 [173,186,187].”
- Vitamin D Receptor-Mediated Stromal Reprogramming Suppresses Pancreatitis and Enhances Pancreatic Cancer Therapy (2014, neutral): “Notably, cytokine induction in the stroma has been shown to promote pancreatic cancer initiation and progression in a paracrine manner (Fukuda et al., 2011; Lesina et al., 2011).”
- Therapeutic strategies for the clinical blockade of IL-6/gp130 signaling. (2011, methodology): “Using sgp130 as a molecular tool, various in vivo studies have now documented roles of IL-6 trans-signaling in experimental models of arthritis, colitis, infection, allergy, and inflammation-induced cancer (71, 75, 76, 78–84).”
- Interleukin-6 Family Cytokines. (2018, background): “Intestinal inflammation (Atreya et al. 2000; Mitsuyama et al. 2006) Pancreatic cancer (Lesina et al. 2011) Ovarian hyperstimulation (Wei et al. 2013) Rheumatoid arthritis (Nowell et al. 2003, 2009; Richards et al. 2006) Acute inflammation (Chalaris et al. 2007; Rabe et al. 2008) Lupus erythematosus…”
- Coordinated regulation of myeloid cells by tumours (2012, background): “STAT3, in turn, induces anti-apoptotic and pro-proliferative genes, fuelling tumour initiation, promotion and progressio”
- Oncogenic Kras-induced GM-CSF production promotes the development of pancreatic neoplasia (2012, background): “a protumorigenic inflammatory microenvironment (Fukuda et al., 2011; Lesina et al., 2011) further underscores the crucial contribution of non-cell-autonomous mechanisms to pancreatic tumor initiation and progression.”
- IL-6 in inflammation, autoimmunity and cancer (2020, background): “Mutated K-RAS activates NF-κ B in a mouse model of lung cancer (315), and the K-RAS-induced activation of NF-κ B is required for pancreatic cancer development (316), which depends on IL-6 trans-signaling-mediated STAT3 activation (317).”