ALK Resistance Mutations in ALK-Positive Lung Cancer

Authors: Justin F. Gainor, Leila Dardaei, Satoshi Yoda, Luc Friboulet, Ignaty Leshchiner, Ryohei Katayama, Ibiayi Dagogo-Jack, Shirish Gadgeel, Katherine Schultz, Manrose Singh, Emily Chin, Melissa Parks, Dana Lee, Richard H. DiCecca, Elizabeth Lockerman, Tiffany Huynh, Jennifer Logan, Lauren L. Ritterhouse, Long P. Le, Ashok Muniappan, Subba Digumarthy, Colleen Channick, Colleen Keyes, Gad Getz, Dora Dias-Santagata, Rebecca S. Heist, Jochen Lennerz, Lecia V. Sequist, Cyril H. Benes, A. John Iafrate, Mari Mino-Kenudson, Jeffrey A. Engelman, and Alice T. Shaw

[1]  Y. Yatabe,et al.  Transformation to SCLC after Treatment with the ALK Inhibitor Alectinib. , 2016, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[2]  Benjamin Solomon,et al.  Safety and efficacy of lorlatinib (PF-06463922) from the dose-escalation component of a study in patients with advanced ALK+ or ROS1+ non-small cell lung cancer (NSCLC). , 2016 .

[3]  H. Lee,et al.  A Case of ALK-Rearranged Adenocarcinoma with Small Cell Carcinoma-Like Transformation and Resistance to Crizotinib. , 2016, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[4]  Michael Thomas,et al.  Intracranial and whole-body response of ceritinib in ALK inhibitor-naïve and previously ALK inhibitor-treated patients with ALK-rearranged non-small-cell lung cancer (NSCLC): updated results from the phase 1, multicentre, open-label ASCEND-1 trial , 2016, The Lancet. Oncology.

[5]  Yi-Song Wang,et al.  EMT is associated with, but does not drive resistance to ALK inhibitors among EML4‐ALK non‐small cell lung cancer , 2016, Molecular Oncology.

[6]  K. Kiura,et al.  Non-Small Cell Lung Cancer Cells Acquire Resistance to the ALK Inhibitor Alectinib by Activating Alternative Receptor Tyrosine Kinases. , 2016, Cancer research.

[7]  R. Govindan,et al.  Alectinib in Crizotinib-Refractory ALK-Rearranged Non-Small-Cell Lung Cancer: A Phase II Global Study. , 2016, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[8]  M. Socinski,et al.  Alectinib in ALK-positive, crizotinib-resistant, non-small-cell lung cancer: a single-group, multicentre, phase 2 trial. , 2016, The Lancet. Oncology.

[9]  G. Getz,et al.  Resensitization to Crizotinib by the Lorlatinib ALK Resistance Mutation L1198F. , 2016, The New England journal of medicine.

[10]  A. Iafrate,et al.  P-glycoprotein Mediates Ceritinib Resistance in Anaplastic Lymphoma Kinase-rearranged Non-small Cell Lung Cancer , 2015, EBioMedicine.

[11]  S. Miyamoto,et al.  Transformation to small-cell lung cancer as a mechanism of acquired resistance to crizotinib and alectinib. , 2015, Japanese journal of clinical oncology.

[12]  S. Ou,et al.  ALK F1174V mutation confers sensitivity while ALK I1171 mutation confers resistance to alectinib. The importance of serial biopsy post progression. , 2016, Lung cancer.

[13]  L. Borsu,et al.  Acquired Resistance of EGFR-Mutant Lung Cancer to a T790M-Specific EGFR Inhibitor: Emergence of a Third Mutation (C797S) in the EGFR Tyrosine Kinase Domain. , 2015, JAMA oncology.

[14]  S. Asthana,et al.  RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK–positive lung cancer , 2015, Nature Medicine.

[15]  Shibing Deng,et al.  PF-06463922, an ALK/ROS1 Inhibitor, Overcomes Resistance to First and Second Generation ALK Inhibitors in Preclinical Models. , 2015, Cancer cell.

[16]  Y. Ichinose,et al.  Identification of a Novel ALK G1123S Mutation in a Patient with ALK-rearranged Non-small-cell Lung Cancer Exhibiting Resistance to Ceritinib. , 2015, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[17]  T. Clackson,et al.  Safety and efficacy of brigatinib (AP26113) in advanced malignancies, including ALK+ non–small cell lung cancer (NSCLC). , 2015 .

[18]  L. Sequist,et al.  The Allelic Context of the C797S Mutation Acquired upon Treatment with Third-Generation EGFR Inhibitors Impacts Sensitivity to Subsequent Treatment Strategies , 2015, Clinical Cancer Research.

[19]  S. Ou,et al.  I1171 missense mutation (particularly I1171N) is a common resistance mutation in ALK-positive NSCLC patients who have progressive disease while on alectinib and is sensitive to ceritinib. , 2015, Lung cancer.

[20]  S. Digumarthy,et al.  Heterogeneity Underlies the Emergence of EGFRT790 Wild-Type Clones Following Treatment of T790M-Positive Cancers with a Third-Generation EGFR Inhibitor. , 2015, Cancer discovery.

[21]  Pei Su,et al.  EML4-ALK induces epithelial-mesenchymal transition consistent with cancer stem cell properties in H1299 non-small cell lung cancer cells. , 2015, Biochemical and biophysical research communications.

[22]  J. Engelman,et al.  Progression-Free and Overall Survival in ALK-Positive NSCLC Patients Treated with Sequential Crizotinib and Ceritinib , 2015, Clinical Cancer Research.

[23]  Sridhar Ramaswamy,et al.  Patient-derived models of acquired resistance can identify effective drug combinations for cancer , 2014, Science.

[24]  F. Cappuzzo,et al.  First-line crizotinib versus chemotherapy in ALK-positive lung cancer. , 2014, The New England journal of medicine.

[25]  Y. Ichinose,et al.  Secondary mutations at I1171 in the ALK gene confer resistance to both Crizotinib and Alectinib. , 2014, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[26]  A. Iafrate,et al.  Anchored multiplex PCR for targeted next-generation sequencing , 2014, Nature Medicine.

[27]  A. Iafrate,et al.  Two Novel ALK Mutations Mediate Acquired Resistance to the Next-Generation ALK Inhibitor Alectinib , 2014, Clinical Cancer Research.

[28]  William Pao,et al.  Rationale for co-targeting IGF-1R and ALK in ALK fusion positive lung cancer , 2014, Nature Medicine.

[29]  D. Hsiang,et al.  Next-generation sequencing reveals a Novel NSCLC ALK F1174V mutation and confirms ALK G1202R mutation confers high-level resistance to alectinib (CH5424802/RO5424802) in ALK-rearranged NSCLC patients who progressed on crizotinib. , 2014, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[30]  Makoto Nishio,et al.  The ALK inhibitor ceritinib overcomes crizotinib resistance in non-small cell lung cancer. , 2014, Cancer discovery.

[31]  Samy Lamouille,et al.  Molecular mechanisms of epithelial–mesenchymal transition , 2014, Nature Reviews Molecular Cell Biology.

[32]  A. Shaw,et al.  Emerging paradigms in the development of resistance to tyrosine kinase inhibitors in lung cancer. , 2013, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[33]  Michael Thomas,et al.  Crizotinib versus chemotherapy in advanced ALK-positive lung cancer. , 2013, The New England journal of medicine.

[34]  C. Peschel,et al.  Sequential Inhibitor Therapy in CML: In Vitro Simulation Elucidates the Pattern of Resistance Mutations after Second- and Third-Line Treatment , 2013, Clinical Cancer Research.

[35]  A. Iafrate,et al.  Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers , 2012, Science Translational Medicine.

[36]  Tatiana G. Kutateladze,et al.  Mechanisms of Resistance to Crizotinib in Patients with ALK Gene Rearranged Non–Small Cell Lung Cancer , 2012, Clinical Cancer Research.

[37]  T. Clackson,et al.  Crizotinib-Resistant Mutants of EML4-ALK Identified Through an Accelerated Mutagenesis Screen , 2011, Chemical biology & drug design.

[38]  Hiroshi Sakamoto,et al.  CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. , 2011, Cancer cell.

[39]  S. Digumarthy,et al.  Genotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors , 2011, Science Translational Medicine.

[40]  D. Sgroi,et al.  A Unique Spectrum of Somatic PIK3CA (p110α) Mutations Within Primary Endometrial Carcinomas , 2011, Clinical Cancer Research.

[41]  Jeffrey W. Clark,et al.  Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer. , 2010, The New England journal of medicine.

[42]  B. Druker,et al.  MET receptor sequence variants R970C and T992I lack transforming capacity. , 2010, Cancer research.

[43]  David N Louis,et al.  Rapid targeted mutational analysis of human tumours: a clinical platform to guide personalized cancer medicine , 2010, EMBO molecular medicine.

[44]  T. Clackson,et al.  Abstract LB-298: AP26113, a potent ALK inhibitor, overcomes mutations in EML4-ALK that confer resistance to PF-02341066 (PF1066) , 2010 .

[45]  V. Preedy,et al.  European Organization for Research and Treatment of Cancer , 2010 .

[46]  S. Digumarthy,et al.  Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[47]  L. Schwartz,et al.  New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1). , 2009, European journal of cancer.

[48]  C. Sawyers,et al.  Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency. , 2007, The Journal of clinical investigation.

[49]  H. Aburatani,et al.  Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer , 2007, Nature.

[50]  M. Christian,et al.  [New guidelines to evaluate the response to treatment in solid tumors]. , 2000, Bulletin du cancer.

[51]  M Van Glabbeke,et al.  New guidelines to evaluate the response to treatment in solid tumors. European Organization for Research and Treatment of Cancer, National Cancer Institute of the United States, National Cancer Institute of Canada. , 2000, Journal of the National Cancer Institute.