The function and therapeutic targeting of anaplastic lymphoma kinase (ALK) in non-small cell lung cancer (NSCLC)

[1]  T. Hielscher,et al.  cMyc and ERK activity are associated with resistance to ALK inhibitory treatment in glioblastoma , 2019, Journal of Neuro-Oncology.

[2]  H. Nehoff,et al.  ALK and IGF-1R as independent targets in crizotinib resistant lung cancer , 2017, Scientific Reports.

[3]  Qingsong Liu,et al.  Discovery of N-(5-((5-chloro-4-((2-(isopropylsulfonyl)phenyl)amino)pyrimidin-2-yl)amino)-4-methoxy-2-(4-methyl-1,4-diazepan-1-yl)phenyl)acrylamide (CHMFL-ALK/EGFR-050) as a potent ALK/EGFR dual kinase inhibitor capable of overcoming a variety of ALK/EGFR associated drug resistant mutants in NSCLC. , 2017, European journal of medicinal chemistry.

[4]  P. Brousset,et al.  Detection of known and novel ALK fusion transcripts in lung cancer patients using next-generation sequencing approaches , 2017, Scientific Reports.

[5]  Jie Yang,et al.  Efficacy of alectinib in central nervous system metastases in crizotinib-resistant ALK-positive non-small-cell lung cancer: Comparison of RECIST 1.1 and RANO-HGG criteria. , 2017, European journal of cancer.

[6]  H. Prosch,et al.  Complete remission of intrathecal metastases with lorlatinib therapy in a heavily pretreated ALK-positive lung cancer patient , 2017, Anti-cancer drugs.

[7]  Jeffrey W. Scott,et al.  ASCEND‐8: A Randomized Phase 1 Study of Ceritinib, 450 mg or 600 mg, Taken with a Low‐Fat Meal versus 750 mg in Fasted State in Patients with Anaplastic Lymphoma Kinase (ALK)‐Rearranged Metastatic Non–Small Cell Lung Cancer (NSCLC) , 2017, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[8]  Kentaro Inamura,et al.  Lung Cancer: Understanding Its Molecular Pathology and the 2015 WHO Classification , 2017, Front. Oncol..

[9]  M. Lesperance,et al.  Performance of a RT-PCR Assay in Comparison to FISH and Immunohistochemistry for the Detection of ALK in Non-Small Cell Lung Cancer , 2017, Cancers.

[10]  E. Giovannetti,et al.  Spotlight on ceritinib in the treatment of ALK+ NSCLC: design, development and place in therapy , 2017, Drug design, development and therapy.

[11]  A. Jimeno,et al.  EGFR Mediates Responses to Small-Molecule Drugs Targeting Oncogenic Fusion Kinases. , 2017, Cancer research.

[12]  J. Xia,et al.  Pooled safety analyses of ALK-TKI inhibitor in ALK-positive NSCLC , 2017, BMC Cancer.

[13]  Rafal Dziadziuszko,et al.  Alectinib versus Crizotinib in Untreated ALK‐Positive Non–Small‐Cell Lung Cancer , 2017, The New England journal of medicine.

[14]  Edward S. Kim,et al.  Brigatinib in Patients With Crizotinib-Refractory Anaplastic Lymphoma Kinase-Positive Non-Small-Cell Lung Cancer: A Randomized, Multicenter Phase II Trial. , 2017, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[15]  A. Dingemans,et al.  Heat shock protein antagonists in early stage clinical trials for NSCLC , 2017, Expert opinion on investigational drugs.

[16]  A. Shaw,et al.  Targeting ALK: Precision Medicine Takes on Drug Resistance. , 2017, Cancer discovery.

[17]  R. Govindan,et al.  Phase I Results from a Study of Crizotinib in Combination with Erlotinib in Patients with Advanced Nonsquamous Non–Small Cell Lung Cancer , 2017, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[18]  N. Hanna,et al.  Systemic Therapy for Stage IV Non-Small-Cell Lung Cancer: American Society of Clinical Oncology Clinical Practice Guideline Update Summary. , 2017, Journal of oncology practice.

[19]  Brigatinib Approved, but Treatment Role Uncertain. , 2017, Cancer discovery.

[20]  Lauren L. Ritterhouse,et al.  Molecular Mechanisms of Resistance to First- and Second-Generation ALK Inhibitors in ALK-Rearranged Lung Cancer. , 2016, Cancer discovery.

[21]  T. Clackson,et al.  The Potent ALK Inhibitor Brigatinib (AP26113) Overcomes Mechanisms of Resistance to First- and Second-Generation ALK Inhibitors in Preclinical Models , 2016, Clinical Cancer Research.

[22]  Richard Z. Liu,et al.  Coupling an EML4-ALK–centric interactome with RNA interference identifies sensitizers to ALK inhibitors , 2016, Science Signaling.

[23]  K. Kerr,et al.  Precision medicine in NSCLC and pathology: how does ALK fit in the pathway? , 2016, Annals of oncology : official journal of the European Society for Medical Oncology.

[24]  Serafino Pantano,et al.  Genetic landscape of ALK+ non-small cell lung cancer (NSCLC) patients (pts) and response to ceritinib in ASCEND-1. , 2016 .

[25]  G. Giaccone,et al.  Combined Pan‐HER and ALK/ROS1/MET Inhibition with Dacomitinib and Crizotinib in Advanced Non–Small Cell Lung Cancer: Results of a Phase I Study , 2016, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[26]  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.

[27]  Shaomeng Wang,et al.  Elucidation of Resistance Mechanisms to Second-Generation ALK Inhibitors Alectinib and Ceritinib in Non–Small Cell Lung Cancer Cells , 2016, Neoplasia.

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

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

[30]  I. Lax,et al.  Augmentor α and β (FAM150) are ligands of the receptor tyrosine kinases ALK and LTK: Hierarchy and specificity of ligand–receptor interactions , 2015, Proceedings of the National Academy of Sciences.

[31]  R. Palmer,et al.  FAM150A and FAM150B are activating ligands for anaplastic lymphoma kinase , 2015, eLife.

[32]  Y. Ichinose,et al.  Insights into brain metastasis in patients with ALK+ lung cancer: is the brain truly a sanctuary? , 2015, Cancer and Metastasis Reviews.

[33]  Y. Ichinose,et al.  Insights into brain metastasis in patients with ALK+ lung cancer: is the brain truly a sanctuary? , 2015, Cancer and Metastasis Reviews.

[34]  Thomas J. Smith,et al.  Systemic Therapy for Stage IV Non-Small-Cell Lung Cancer: American Society of Clinical Oncology Clinical Practice Guideline Update. , 2015, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[35]  C. Sima,et al.  A phase 1 study of crizotinib and ganetespib (STA-9090) in ALK positive lung cancers. , 2015 .

[36]  A. Shaw,et al.  Therapeutic Targeting of Anaplastic Lymphoma Kinase in Lung Cancer: A Paradigm for Precision Cancer Medicine , 2015, Clinical Cancer Research.

[37]  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.

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

[39]  I. Lax,et al.  Heparin is an activating ligand of the orphan receptor tyrosine kinase ALK , 2015, Science Signaling.

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

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

[42]  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.

[43]  M. Tsao,et al.  The Cost-Effectiveness of Second-Line Crizotinib in Eml4-Alk Rearranged Advanced Non-Small Cell Lung Cancer. , 2014, Value in health : the journal of the International Society for Pharmacoeconomics and Outcomes Research.

[44]  Joana A. Vidigal,et al.  In vivo engineering of oncogenic chromosomal rearrangements with the CRISPR/Cas9 system , 2014, Nature.

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

[46]  Ruey-min Lee,et al.  Safety and activity of alectinib against systemic disease and brain metastases in patients with crizotinib-resistant ALK-rearranged non-small-cell lung cancer (AF-002JG): results from the dose-finding portion of a phase 1/2 study. , 2014, The Lancet. Oncology.

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

[48]  Steven J. M. Jones,et al.  Comprehensive molecular profiling of lung adenocarcinoma , 2014, Nature.

[49]  Murray Krahn,et al.  Cost effectiveness of EML4-ALK fusion testing and first-line crizotinib treatment for patients with advanced ALK-positive non-small-cell lung cancer. , 2014, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[50]  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.

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

[52]  A. Delmonte,et al.  Targeting ALK in patients with advanced non small cell lung cancer: biology, diagnostic and therapeutic options. , 2014, Critical reviews in oncology/hematology.

[53]  Toyokawa Gouji,et al.  Crizotinib can overcome acquired resistance to CH5424802: is amplification of the MET gene a key factor? , 2014, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[54]  R. Palmer,et al.  Mechanistic insight into ALK receptor tyrosine kinase in human cancer biology , 2013, Nature Reviews Cancer.

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

[56]  W. Guo,et al.  A Multicenter Phase II Study of Ganetespib Monotherapy in Patients with Genotypically Defined Advanced Non–Small Cell Lung Cancer , 2013, Clinical Cancer Research.

[57]  A. Shaw,et al.  Targeted inhibition of the molecular chaperone Hsp90 overcomes ALK inhibitor resistance in non-small cell lung cancer. , 2013, Cancer discovery.

[58]  William H. Bisson,et al.  Crizotinib-Resistant NPM-ALK Mutants Confer Differential Sensitivity to Unrelated Alk Inhibitors , 2012, Molecular Cancer Research.

[59]  Dong-Wan Kim,et al.  Immunohistochemical screening for anaplastic lymphoma kinase (ALK) rearrangement in advanced non-small cell lung cancer patients. , 2012, Lung cancer.

[60]  Kazuko Sakai,et al.  Activation of HER Family Signaling as a Mechanism of Acquired Resistance to ALK Inhibitors in EML4-ALK–Positive Non–Small Cell Lung Cancer , 2012, Clinical Cancer Research.

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

[62]  P. Jänne,et al.  Combined effect of ALK and MEK inhibitors in EML4–ALK-positive non-small-cell lung cancer cells , 2012, British Journal of Cancer.

[63]  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.

[64]  田中 俊典.  National Center for Biotechnology Information (NCBI) , 2012 .

[65]  William Pao,et al.  ALK Mutations Conferring Differential Resistance to Structurally Diverse ALK Inhibitors , 2011, Clinical Cancer Research.

[66]  Wei Zheng,et al.  A novel ALK secondary mutation and EGFR signaling cause resistance to ALK kinase inhibitors. , 2011, Cancer research.

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

[68]  Ryohei Katayama,et al.  Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK , 2011, Proceedings of the National Academy of Sciences.

[69]  E. Grande,et al.  Targeting Oncogenic ALK: A Promising Strategy for Cancer Treatment , 2011, Molecular Cancer Therapeutics.

[70]  P. Jänne,et al.  Role of ERK-BIM and STAT3-Survivin Signaling Pathways in ALK Inhibitor–Induced Apoptosis in EML4-ALK–Positive Lung Cancer , 2011, Clinical Cancer Research.

[71]  J. Zha,et al.  Evaluation of EML4-ALK fusion proteins in non-small cell lung cancer using small molecule inhibitors. , 2011, Neoplasia.

[72]  P. Jänne,et al.  Inhibition of ALK, PI3K/MEK, and HSP90 in murine lung adenocarcinoma induced by EML4-ALK fusion oncogene. , 2010, Cancer research.

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

[74]  Young Lim Choi,et al.  EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors. , 2010, The New England journal of medicine.

[75]  A. Iafrate,et al.  A Novel, Highly Sensitive Antibody Allows for the Routine Detection of ALK-Rearranged Lung Adenocarcinomas by Standard Immunohistochemistry , 2010, Clinical Cancer Research.

[76]  Magali Olivier,et al.  TP53 mutations in human cancers: origins, consequences, and clinical use. , 2010, Cold Spring Harbor perspectives in biology.

[77]  A. Iafrate,et al.  Unique Clinicopathologic Features Characterize ALK-Rearranged Lung Adenocarcinoma in the Western Population , 2009, Clinical Cancer Research.

[78]  Y. Ishikawa,et al.  A mouse model for EML4-ALK-positive lung cancer , 2008, Proceedings of the National Academy of Sciences.

[79]  H. Carén,et al.  High incidence of DNA mutations and gene amplifications of the ALK gene in advanced sporadic neuroblastoma tumours. , 2008, The Biochemical journal.

[80]  Gudrun Schleiermacher,et al.  Somatic and germline activating mutations of the ALK kinase receptor in neuroblastoma , 2008, Nature.

[81]  S. Ogawa,et al.  Oncogenic mutations of ALK kinase in neuroblastoma , 2008, Nature.

[82]  Y. Ishikawa,et al.  Multiplex Reverse Transcription-PCR Screening for EML4-ALK Fusion Transcripts , 2008, Clinical Cancer Research.

[83]  John Kuriyan,et al.  Activation of tyrosine kinases by mutation of the gatekeeper threonine , 2008, Nature Structural &Molecular Biology.

[84]  Petr Znamenskiy,et al.  Behavioral and Neurochemical Alterations in Mice Deficient in Anaplastic Lymphoma Kinase Suggest Therapeutic Potential for Psychiatric Indications , 2008, Neuropsychopharmacology.

[85]  T. Mathivet,et al.  In contrast to agonist monoclonal antibodies, both C-terminal truncated form and full length form of Pleiotrophin failed to activate vertebrate ALK (anaplastic lymphoma kinase)? , 2007, Cellular signalling.

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

[87]  Shinji Yamazaki,et al.  An orally available small-molecule inhibitor of c-Met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanisms. , 2007, Cancer research.

[88]  M. Wasik,et al.  Nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) oncoprotein induces the T regulatory cell phenotype by activating STAT3. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[89]  R. Palmer,et al.  Characterization of the expression of the ALK receptor tyrosine kinase in mice. , 2006, Gene expression patterns : GEP.

[90]  C. Créminon,et al.  Activation and Inhibition of Anaplastic Lymphoma Kinase Receptor Tyrosine Kinase by Monoclonal Antibodies and Absence of Agonist Activity of Pleiotrophin* , 2005, Journal of Biological Chemistry.

[91]  Hitoshi Sakuraba,et al.  ALK receptor tyrosine kinase promotes cell growth and neurite outgrowth , 2004, Journal of Cell Science.

[92]  C. Powers,et al.  Midkine Binds to Anaplastic Lymphoma Kinase (ALK) and Acts as a Growth Factor for Different Cell Types* , 2002, The Journal of Biological Chemistry.

[93]  D. Wen,et al.  Identification of Anaplastic Lymphoma Kinase as a Receptor for the Growth Factor Pleiotrophin* , 2001, The Journal of Biological Chemistry.

[94]  A. Rosenwald,et al.  TRK-fused gene (TFG) is a new partner of ALK in anaplastic large cell lymphoma producing two structurally different TFG-ALK translocations. , 1999, Blood.

[95]  K. Pulford,et al.  A new fusion gene TPM3-ALK in anaplastic large cell lymphoma created by a (1;2)(q25;p23) translocation. , 1999, Blood.

[96]  S. Morris,et al.  Nucleophosmin-Anaplastic Lymphoma Kinase of Large-Cell Anaplastic Lymphoma Is a Constitutively Active Tyrosine Kinase That Utilizes Phospholipase C-γ To Mediate Its Mitogenicity , 1998, Molecular and Cellular Biology.

[97]  T. Arakawa,et al.  Molecular characterization of ALK, a receptor tyrosine kinase expressed specifically in the nervous system , 1997, Oncogene.

[98]  D N Shapiro,et al.  Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma. , 1994, Science.

[99]  M. Watson,et al.  Cloning and expression of a developmentally regulated protein that induces mitogenic and neurite outgrowth activity. , 1990, Science.