Resistance to TRK inhibition mediated by convergent MAP kinase pathway activation
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Amanda R. Kulick | M. Ladanyi | M. Berger | A. Drilon | B. Tuch | E. Stanchina | R. Somwar | B. Houck-Loomis | P. Razavi | R. Yaeger | A. Schram | J. Hechtman | R. Ptashkin | H. Won | D. Hyman | S. D. Selcuklu | E. de Stanchina | M. Scaltriti | E. Toska | S. Misale | M. Mattar | E. Cocco | K. Ebata | J. Patel | A. Samoila | R. Lanman | R. Nagy | Maurizio Scaltriti | Sophie G. Shifman | J. Cownie | S. Guzman | Amanda Kulick | Eneda Toska
[1] Patrick J. Paddison,et al. A kinase-deficient NTRK2 splice variant predominates in glioma and amplifies several oncogenic signaling pathways , 2020, Nature Communications.
[2] Liangsong Zhu,et al. ZHX2 drives cell growth and migration via activating MEK/ERK signal and induces Sunitinib resistance by regulating the autophagy in clear cell Renal Cell Carcinoma , 2020, Cell Death & Disease.
[3] F. Santini,et al. TRK Inhibitors in Non-Small Cell Lung Cancer , 2020, Current Treatment Options in Oncology.
[4] R. Mehra,et al. New Targets in Lung Cancer (Excluding EGFR, ALK, ROS1) , 2020, Current Oncology Reports.
[5] C. Arteaga,et al. Overcoming Endocrine Resistance in Breast Cancer. , 2020, Cancer cell.
[6] B. Taylor,et al. Author Correction: HER kinase inhibition in patients with HER2- and HER3-mutant cancers , 2019, Nature.
[7] B. Taylor,et al. EGFR and MET Amplifications Determine Response to HER2 Inhibition in ERBB2-Amplified Esophagogastric Cancer. , 2018, Cancer discovery.
[8] J. Krauss,et al. Efficacy and safety of entrectinib in patients with NTRK fusion-positive tumours: Pooled analysis of STARTRK-2, STARTRK-1, and ALKA-372-001. , 2018, Annals of oncology : official journal of the European Society for Medical Oncology.
[9] A. Drilon,et al. NTRK fusion-positive cancers and TRK inhibitor therapy , 2018, Nature Reviews Clinical Oncology.
[10] J. Krauss,et al. Efficacy and safety of entrectinib in patients with NTRK fusion-positive (NTRK-fp) Tumors: Pooled analysis of STARTRK-2, STARTRK-1 and ALKA-372-001. , 2018, Annals of oncology : official journal of the European Society for Medical Oncology.
[11] J. Roth,et al. Landscape of EGFR-Dependent and -Independent Resistance Mechanisms to Osimertinib and Continuation Therapy Beyond Progression in EGFR-Mutant NSCLC , 2018, Clinical Cancer Research.
[12] A. Drilon,et al. Repotrectinib (TPX-0005) Is a Next-Generation ROS1/TRK/ALK Inhibitor That Potently Inhibits ROS1/TRK/ALK Solvent- Front Mutations. , 2018, Cancer discovery.
[13] A. Drilon,et al. Activity of larotrectinib in patients with TRK fusion GI malignancies. , 2018, Annals of oncology : official journal of the European Society for Medical Oncology.
[14] Jessica L. Davis,et al. Larotrectinib for paediatric solid tumours harbouring NTRK gene fusions: phase 1 results from a multicentre, open-label, phase 1/2 study. , 2018, The Lancet. Oncology.
[15] Funda Meric-Bernstam,et al. Efficacy of Larotrectinib in TRK Fusion–Positive Cancers in Adults and Children , 2018, The New England journal of medicine.
[16] Ying Cheng,et al. Osimertinib in Untreated EGFR-Mutated Advanced Non–Small-Cell Lung Cancer , 2018 .
[17] M. Cabanillas. Faculty of 1000 evaluation for Safety and Antitumor Activity of the Multitargeted Pan-TRK, ROS1, and ALK Inhibitor Entrectinib: Combined Results from Two Phase I Trials (ALKA-372-001 and STARTRK-1). , 2018 .
[18] B. Taylor,et al. HER kinase inhibition in patients with HER2- and HER3-mutant cancers , 2018, Nature.
[19] Lu Wang,et al. Mechanisms of Acquired Resistance to BRAF V600E Inhibition in Colon Cancers Converge on RAF Dimerization and Are Sensitive to Its Inhibition. , 2017, Cancer research.
[20] B. Taylor,et al. A Next-Generation TRK Kinase Inhibitor Overcomes Acquired Resistance to Prior TRK Kinase Inhibition in Patients with TRK Fusion-Positive Solid Tumors. , 2017, Cancer discovery.
[21] A. Drilon,et al. Fusions in solid tumours: diagnostic strategies, targeted therapy, and acquired resistance , 2017, Nature Reviews Clinical Oncology.
[22] Rafal Dziadziuszko,et al. Alectinib versus Crizotinib in Untreated ALK‐Positive Non–Small‐Cell Lung Cancer , 2017, The New England journal of medicine.
[23] Donavan T. Cheng,et al. Mutational Landscape of Metastatic Cancer Revealed from Prospective Clinical Sequencing of 10,000 Patients , 2017, Nature Medicine.
[24] A. Drilon,et al. Safety and Antitumor Activity of the Multitargeted Pan-TRK, ROS1, and ALK Inhibitor Entrectinib: Combined Results from Two Phase I Trials (ALKA-372-001 and STARTRK-1). , 2017, Cancer discovery.
[25] A. Bardelli,et al. MET-Driven Resistance to Dual EGFR and BRAF Blockade May Be Overcome by Switching from EGFR to MET Inhibition in BRAF-Mutated Colorectal Cancer. , 2016, Cancer discovery.
[26] Jeffrey W. Clark,et al. Acquired Resistance to Crizotinib in NSCLC with MET Exon 14 Skipping , 2016, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.
[27] Grant W. Brown,et al. HELB Is a Feedback Inhibitor of DNA End Resection. , 2016, Molecular cell.
[28] Mari Mino-Kenudson,et al. Tumor Heterogeneity and Lesion-Specific Response to Targeted Therapy in Colorectal Cancer. , 2016, Cancer discovery.
[29] Gang Li,et al. Acquired Resistance to the TRK Inhibitor Entrectinib in Colorectal Cancer. , 2015, Cancer discovery.
[30] N. Socci,et al. Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity , 2015, Nature Biotechnology.
[31] S. Cook,et al. MEK1 and MEK2 inhibitors and cancer therapy: the long and winding road , 2015, Nature Reviews Cancer.
[32] M. Nowak,et al. Vertical suppression of the EGFR pathway prevents onset of resistance in colorectal cancers , 2015, Nature Communications.
[33] F. Nicolantonio,et al. Erratum: Clonal evolution and resistance to EGFR blockade in the blood of colorectal cancer patients , 2015, Nature Medicine.
[34] John C. Hunter,et al. Biochemical and Structural Analysis of Common Cancer-Associated KRAS Mutations , 2015, Molecular Cancer Research.
[35] Beatriz Bellosillo,et al. Clonal evolution and resistance to EGFR blockade in the blood of colorectal cancer patients , 2015, Nature Medicine.
[36] Donavan T. Cheng,et al. Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets (MSK-IMPACT): A Hybridization Capture-Based Next-Generation Sequencing Clinical Assay for Solid Tumor Molecular Oncology. , 2015, The Journal of molecular diagnostics : JMD.
[37] J. Utikal,et al. Combined BRAF and MEK inhibition versus BRAF inhibition alone in melanoma. , 2014, The New England journal of medicine.
[38] Richard F. Kefford,et al. Preexisting MEK1P124 Mutations Diminish Response to BRAF Inhibitors in Metastatic Melanoma Patients , 2014, Clinical Cancer Research.
[39] Andrea Bertotti,et al. Amplification of the MET receptor drives resistance to anti-EGFR therapies in colorectal cancer. , 2013, Cancer discovery.
[40] K. Flaherty,et al. Activity of the oral MEK inhibitor trametinib in patients with advanced melanoma: a phase 1 dose-escalation trial. , 2012, The Lancet. Oncology.
[41] Enzo Medico,et al. Emergence of KRAS mutations and acquired resistance to anti-EGFR therapy in colorectal cancer , 2012, Nature.
[42] Jie Qi,et al. Multiple mutations and bypass mechanisms can contribute to development of acquired resistance to MET inhibitors. , 2011, Cancer research.
[43] Luca Toschi,et al. Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC. , 2010, Cancer cell.
[44] N. Socci,et al. Accelerating Discovery of Functional Mutant Alleles in Cancer. , 2018, Cancer discovery.
[45] R. Doebele,et al. TRKing down an old oncogene in a new era of targeted therapy. , 2015, Cancer discovery.
[46] C. Hancock. The long and winding road , 2005, Nature Reviews Drug Discovery.
[47] M. Barbacid,et al. A human oncogene formed by the fusion of truncated tropomyosin and protein tyrosine kinase sequences , 1986, Nature.