Epithelial to mesenchymal transition is a determinant of sensitivity of non-small-cell lung carcinoma cell lines and xenografts to epidermal growth factor receptor inhibition.

By S. Thomson, E. Buck, F. Petti, Graeme Griffin, E. Brown, Nishal Ramnarine, K. Iwata, N. Gibson, J. Haley. Cancer Research, 2005

650 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/127763e5787e9768e65f3b23d757e412a073a102

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In Molecular Biology

1. R. Weinberg
2. M. Nieto
3. Jing Yang
4. J. P. Thiery
5. J. Tsai
6. R. Huang
7. Anurag Singh
8. J. Settleman

In Oncology

1. R. Weinberg
2. M. Nieto
3. Jing Yang
4. J. P. Thiery
5. R. Huang
6. J. Tsai
7. Anurag Singh
8. J. Settleman

In Pulmonary and Respiratory Medicine

1. R. Weinberg
2. J. P. Thiery
3. M. Nieto
4. R. Huang
5. Erik Sahai
6. S. Lippman
7. Jormay Lim

Citations in the corpus

• A gene expression signature associated with "K-Ras addiction" reveals regulators of EMT and tumor cell survival. (2009, background): “Moreover, insensitivity to EGFR inhibitors in lung and liver cancers has been associated with EMT, further supporting a link between EMT and loss of oncogene addiction (Fuchs et al., 2008; Thomson et al., 2005).”
• An epithelial-mesenchymal transition (EMT) gene signature predicts resistance to EGFR and PI3K inhibitors and identifies Axl as a therapeutic target for overcoming EGFR inhibitor resistance (2012, positive): “These markers were selected on the basis of their previously established role as markers of EMT in lung cancer, as well as other epithelial tumors (15, 16, 24).”
• Identification of selective inhibitors of cancer stem cells by high-throughput screening (2009, background): “Drug treatment of cancer cell populations leads to a concomitant enrichment for CSCs (Levina et al., 2008) and for cells that have undergone an EMT (Eyler and Rich, 2008; Thomson et al., 2005; Yang et al., 2006; Yauch et al., 2005).”
• Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “For example, Erlotinib is currently used in advanced stage metastatic pancreatic tumours even though cells appear to have an increased sensitivity only in the epithelial early-stage disease [212].”
• A mechanically active heterotypic E-cadherin/N-cadherin adhesion enables fibroblasts to drive cancer cell invasion (2017, background): “Three classes of duration time were defined: longer than 60 min (>60), between 30 to 60 min (30-60) and less than 30 min (<30).”
• Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression (2010, background): “In addition to inducing a tumor-initiating cell phenotype, regulators of EMT also influence cell survival, specifically after treatment with chemotherapeutic agents [87, 88], as well as prevent oncogene-induced senescence [89], both properties associated with tumor progression.”
• Up-regulation of miR-200 and let-7 by natural agents leads to the reversal of epithelial-mesenchymal transition in gemcitabine-resistant pancreatic cancer cells (2009, positive): “Further studies have shown that EMT marker proteins including E-cadherin and vimentin could serve as a determinant of epidermal growth factor receptor activity in non–small cell lung cancer cells and that E-cadherin expression was a novel biomarker predicting clinical positive activity of the epider”
• Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, background): “Using several human NSCLC lines, Thomson et al. (2005) demonstrated that cell lines expressing epithelial markers were more sensitive to epidermal growth factor receptor (EGFR) inhibition, whereas cells lines presenting mesenchymal markers were more resistant to treatment.”
• Epithelial-mesenchymal transitions in development and disease. (2009, background): “Interestingly, there is a clear correlation between the EMT status of each cell line and the degree of response (Frederick et al., 2007; Thomson et al., 2005; Yauch et al., 2005).”
• The epithelial–mesenchymal transition: new insights in signaling, development, and disease (2006, neutral): “John Haley (OSI Pharmaceuticals, Melville, NY) presented data showing that the sensitivity of nonsmall cell lung cancer cell lines to erlotinib, which is an EGFR-targeted monoclonal antibody, did not correlate with EGFR levels, but rather depended on their EMT status, with those having undergone EMT”