Epithelial-mesenchymal transition status is a remarkable biomarker for the combination treatment with avutometinib and defactinib in KRAS-mutated non-small cell lung cancer.
暂无分享,去创建一个
H. Ono | T. Yaoi | A. Yoshimura | Mano Horinaka | Tadaaki Yamada | Koichi Takayama | Kyoko Itoh | Toshiyuki Sakai
[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.