Mutations in the EGFR kinase domain mediate STAT3 activation via IL-6 production in human lung adenocarcinomas.

By S. Gao, Kevin G Mark, K. Leslie, William Pao, N. Motoi, W. Gerald, W. Travis, W. Bornmann, D. Veach, B. Clarkson and 1 more. Journal of Clinical Investigation, 2007

675 citations recorded by the source corpus.

Subfields: Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/3a7a0c766721ff7df036b113a9483d2f6695a90d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Oncology

1. M. Karin
2. A. Mantovani
3. A. Sica
4. T. Hirano
5. P. Allavena
6. S. Grivennikov
7. F. Greten
8. C. Garlanda

In Pulmonary and Respiratory Medicine

1. J. Engelman
2. N. Hynes
3. Gwen Macdonald
4. P. Jänne
5. R. Weinberg
6. D. Hanahan
7. Jin-Yuan Shih

Citations in the corpus

• ErbB receptors and signaling pathways in cancer. (2009, background): “activation is indirect and mediated by enhanced IL-6 production in tumor cells [27] (Figure 3).”
• Targeting interleukin-6 in inflammatory autoimmune diseases and cancers. (2014, background): “tion of EGFR activity leads to partially blocked transcription of IL-6 and decreased IL-6 production (Gao et al., 2007).”
• IL-6 in inflammation, autoimmunity and cancer (2020, background): “Similarly, activated mutant EGFR in lung cancer induces IL-6 gene expression to activate constitutive IL-6–STAT3 signaling in a paracrine and autocrine manner (257).”
• IL-6 and STAT3 are required for survival of intestinal epithelial cells and development of colitis associated cancer (2009, background): “…associated with underlying chronic inflammation, IL-6 produced by epithelial and cancer cells may still contribute to tumorigenesis in models without an obvious inflammatory component (Ancrile et al., 2007; Gao et al., 2007; Grivennikov and Karin, 2008; Hodge et al., 2005; Sansone et al., 2007).”
• Adaptive resistance to therapeutic PD-1 blockade is associated with upregulation of alternative immune checkpoints (2016, background): “…also no significant differences in PD-L1 expression levels in TAM and tumour cells (CD45 (cid:2) EpCAM þ ) and levels of the cytokines IL-6 in bronchoalveolar lavage fluids (BALFs), that can promote tumour growth 18,19 , between untreated (U) and PD-1 treatment-resistant mice (R) (Supplementary Fig.”
• Immunity, Inflammation, and Cancer (2010, neutral): “In most cases, tumor promoting cytokines act in a paracrine manner, yet several types of cancer cells produce their own cytokines, including IL-6, to achieve the same effect (Gao et al., 2007).”
• gp130-mediated Stat3 activation in enterocytes regulates cell survival and cell-cycle progression during colitis-associated tumorigenesis. (2009, background): “Recent circumstantial evidence has further promoted the concept that the IL-6/gp130/Stat3 signaling axis may also provide an autocrine and paracrine amplification loop in lung adenocarcinoma (Gao et al., 2007), multiple myeloma (CatlettFalcone et al.”
• Inflammation: The Common Pathway of Stress-Related Diseases (2017, background): “Additionally, in some cancers (e.g., colon, renal cell, lung and breast) secretion of these same cytokines by tumor cells helps drive and sustain pro-tumorigenic inflammatory loops (Angelo et al., 2002; Gao et al., 2007).”
• Pyruvate Kinase M2 Regulates Gene Transcription by Acting as A Protein Kinase (2012, neutral): “Stat3 is a transcription activator that is activated in response to inflammatory cytokines, such as IL-6 (Gao et al., 2007; Watson and Neoh, 2008).”