Epithelial-mesenchymal transition status is a remarkable biomarker for the combination treatment with avutometinib and defactinib in KRAS-mutated non-small cell lung cancer.

[1]  M. Jolly,et al.  The exostosin glycosyltransferase 1/STAT3 axis is a driver of breast cancer aggressiveness. , 2024, Proceedings of the National Academy of Sciences of the United States of America.

[2]  H. Ebi,et al.  Scribble mis-localization induces adaptive resistance to KRAS G12C inhibitors through feedback activation of MAPK signaling mediated by YAP-induced MRAS , 2023, Nature Cancer.

[3]  Toshiyuki Sakai "RB-reactivator screening" as a novel cell-based assay for discoveries of molecular targeting agents including the first-in-class MEK inhibitor trametinib (trade name: Mekinist). , 2022, Pharmacology & therapeutics.

[4]  S. Novello,et al.  Single agent VS-6766 or VS-6766 plus defactinib in KRAS-mutant non-small-cell lung cancer: the RAMP-202 phase II trial. , 2022, Future oncology.

[5]  N. Tunariu,et al.  725MO Phase I study of the combination of the dual RAF/MEK inhibitor VS-6766 and the FAK inhibitor defactinib: Results of efficacy in low grade serous ovarian cancer , 2021, Annals of Oncology.

[6]  R. Bernards,et al.  Phase I Study of Afatinib and Selumetinib in Patients with KRAS-Mutated Colorectal, Non-Small Cell Lung, and Pancreatic Cancer. , 2020, The oncologist.

[7]  Yang Zhang,et al.  Abnormally activated OPN/integrin αVβ3/FAK signalling is responsible for EGFR-TKI resistance in EGFR mutant non-small-cell lung cancer , 2020, Journal of Hematology & Oncology.

[8]  Marilyn M. Li,et al.  Phase 2 study of the focal adhesion kinase inhibitor defactinib (VS-6063) in previously treated advanced KRAS mutant non-small cell lung cancer. , 2019, Lung cancer.

[9]  M. Kris,et al.  Characteristics and Outcomes of Patients With Metastatic KRAS‐Mutant Lung Adenocarcinomas: The Lung Cancer Mutation Consortium Experience , 2019, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[10]  Wan-chi Lin,et al.  Autocrine IGF1 Signaling Mediates Pancreatic Tumor Cell Dormancy in the Absence of Oncogenic Drivers. , 2017, Cell reports.

[11]  G. Giaccone,et al.  Selumetinib with and without erlotinib in KRAS mutant and KRAS wild-type advanced nonsmall-cell lung cancer. , 2016, Annals of oncology : official journal of the European Society for Medical Oncology.

[12]  S. Cook,et al.  MEK1 and MEK2 inhibitors and cancer therapy: the long and winding road , 2015, Nature Reviews Cancer.

[13]  D. Planchard,et al.  A randomized phase II study of the MEK1/MEK2 inhibitor trametinib (GSK1120212) compared with docetaxel in KRAS-mutant advanced non-small-cell lung cancer (NSCLC)†. , 2015, Annals of oncology : official journal of the European Society for Medical Oncology.

[14]  Lih‐Chyang Chen,et al.  Emerging Roles of Focal Adhesion Kinase in Cancer , 2015, BioMed research international.

[15]  S. Lim,et al.  Understanding the Roles of FAK in Cancer , 2015, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[16]  M. Horinaka,et al.  The Dual RAF/MEK Inhibitor CH5126766/RO5126766 May Be a Potential Therapy for RAS-Mutated Tumor Cells , 2014, PloS one.

[17]  D. Medici,et al.  Signaling mechanisms of the epithelial-mesenchymal transition , 2014, Science Signaling.

[18]  T. Tan,et al.  Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients , 2014, EMBO molecular medicine.

[19]  S. Lowe,et al.  Disruption of CRAF-mediated MEK activation is required for effective MEK inhibition in KRAS mutant tumors. , 2014, Cancer cell.

[20]  Andreas Schlicker,et al.  Intrinsic resistance to MEK inhibition in KRAS mutant lung and colon cancer through transcriptional induction of ERBB3. , 2014, Cell reports.

[21]  Justin Guinney,et al.  GSVA: gene set variation analysis for microarray and RNA-Seq data , 2013, BMC Bioinformatics.

[22]  D. Bar-Sagi,et al.  RAS oncogenes: weaving a tumorigenic web , 2011, Nature Reviews Cancer.

[23]  J. Thiery,et al.  SnapShot: The Epithelial-Mesenchymal Transition , 2011, Cell.

[24]  P. Atadja,et al.  IGF-1 suppresses Bim expression in multiple myeloma via epigenetic and posttranslational mechanisms. , 2010, Blood.

[25]  A. Magis,et al.  Targeting of the protein interaction site between FAK and IGF-1R. , 2009, Biochemical and biophysical research communications.

[26]  O. Larsson,et al.  Focal adhesion kinase (FAK) activates and stabilizes IGF-1 receptor. , 2009, Biochemical and biophysical research communications.

[27]  Samy Lamouille,et al.  TGF-β-induced epithelial to mesenchymal transition , 2009, Cell Research.

[28]  D. Schlaepfer,et al.  Integrin-regulated FAK-Src signaling in normal and cancer cells. , 2006, Current opinion in cell biology.

[29]  D. Schlaepfer,et al.  The Focal Adhesion Kinase‐‐A Regulator of Cell Migration and Invasion , 2002, IUBMB life.

[30]  S. Hanks,et al.  Focal adhesion protein-tyrosine kinase phosphorylated in response to cell attachment to fibronectin. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[31]  J. Parsons,et al.  pp125FAK a structurally distinctive protein-tyrosine kinase associated with focal adhesions. , 1992, Proceedings of the National Academy of Sciences of the United States of America.