Variability in lung cancer response to ALK inhibitors cannot be explained by the diversity of ALK fusion variants.

[1]  A. Warth,et al.  EML4‐ALK fusion variant V3 is a high‐risk feature conferring accelerated metastatic spread, early treatment failure and worse overall survival in ALK+ non‐small cell lung cancer , 2018, International journal of cancer.

[2]  S. Chuai,et al.  Response to crizotinib in advanced ALK-rearranged non-small cell lung cancers with different ALK-fusion variants. , 2018, Lung cancer.

[3]  Benjamin Solomon,et al.  Updated Molecular Testing Guideline for the Selection of Lung Cancer Patients for Treatment With Targeted Tyrosine Kinase Inhibitors: Guideline From the College of American Pathologists, the International Association for the Study of Lung Cancer, and the Association for Molecular Pathology , 2018, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[4]  Robyn L. Temple-Smolkin,et al.  Updated Molecular Testing Guideline for the Selection of Lung Cancer Patients for Treatment With Targeted Tyrosine Kinase Inhibitors: Guideline From the College of American Pathologists, the International Association for the Study of Lung Cancer, and the Association for Molecular Pathology. , 2018, The Journal of molecular diagnostics : JMD.

[5]  P. Hainaut,et al.  ALK fusion variants detection by targeted RNA-next generation sequencing and clinical responses to crizotinib in ALK-positive non-small cell lung cancer. , 2018, Lung cancer.

[6]  A. Iafrate,et al.  Impact of EML4-ALK Variant on Resistance Mechanisms and Clinical Outcomes in ALK-Positive Lung Cancer. , 2018, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[7]  Hyun-Tae Shin,et al.  Molecular breakdown: a comprehensive view of anaplastic lymphoma kinase (ALK)‐rearranged non‐small cell lung cancer , 2017, The Journal of pathology.

[8]  R. Bayliss,et al.  EML4-ALK Variants: Biological and Molecular Properties, and the Implications for Patients , 2017, Cancers.

[9]  Gregory Riely,et al.  Diagnosis and Treatment of Anaplastic Lymphoma Kinase-Positive Non-Small Cell Lung Cancer. , 2017, Hematology/oncology clinics of North America.

[10]  K. Park,et al.  Differential protein stability and clinical responses of EML4-ALK fusion variants to various ALK inhibitors in advanced ALK-rearranged non-small cell lung cancer , 2016, Annals of oncology : official journal of the European Society for Medical Oncology.

[11]  H. Shim,et al.  Clinical outcomes in ALK-rearranged lung adenocarcinomas according to ALK fusion variants , 2016, Journal of Translational Medicine.

[12]  Y. Yatabe,et al.  Differential Crizotinib Response Duration Among ALK Fusion Variants in ALK-Positive Non-Small-Cell Lung Cancer. , 2016, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[13]  Yi-long Wu,et al.  Anaplastic Lymphoma Kinase Variants and the Percentage of ALK-Positive Tumor Cells and the Efficacy of Crizotinib in Advanced NSCLC. , 2016, Clinical lung cancer.

[14]  D. Fennell,et al.  Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs , 2016, Cellular and Molecular Life Sciences.

[15]  A. Sokolenko,et al.  Novel ALK fusion partners in lung cancer. , 2015, Cancer letters.

[16]  R. Bayliss,et al.  Microtubule association of EML proteins and the EML4-ALK variant 3 oncoprotein require an N-terminal trimerization domain. , 2015, The Biochemical journal.

[17]  F. López-Ríos,et al.  The anaplastic lymphoma kinase testing conundrum , 2015, Expert review of molecular diagnostics.

[18]  D. Fennell,et al.  Crystal structure of EML1 reveals the basis for Hsp90 dependence of oncogenic EML4-ALK by disruption of an atypical β-propeller domain , 2014, Proceedings of the National Academy of Sciences.

[19]  R. Pazdur,et al.  U.S. Food and Drug Administration Approval: Crizotinib for Treatment of Advanced or Metastatic Non–Small Cell Lung Cancer That Is Anaplastic Lymphoma Kinase Positive , 2014, Clinical Cancer Research.

[20]  E. Imyanitov,et al.  Detection of EGFR mutations and EML4‐ALK rearrangements in lung adenocarcinomas using archived cytological slides , 2013, Cancer cytopathology.

[21]  K. Prabhash,et al.  Crizotinib: A comprehensive review , 2013, South Asian journal of cancer.

[22]  R. Rosell,et al.  Targeting EML4-ALK driven non-small cell lung cancer (NSCLC). , 2013, Translational lung cancer research.

[23]  Jeffrey W. Clark,et al.  Activity and safety of crizotinib in patients with ALK-positive non-small-cell lung cancer: updated results from a phase 1 study. , 2012, The Lancet. Oncology.

[24]  Roman K. Thomas,et al.  Differential Protein Stability and ALK Inhibitor Sensitivity of EML4-ALK Fusion Variants , 2012, Clinical Cancer Research.

[25]  Y. Yatabe,et al.  A Screening Method for the ALK Fusion Gene in NSCLC , 2012, Front. Oncol..

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

[27]  P. Jänne,et al.  The biology and treatment of EML4-ALK non-small cell lung cancer. , 2010, European journal of cancer.

[28]  Laura A. Sullivan,et al.  Global Survey of Phosphotyrosine Signaling Identifies Oncogenic Kinases in Lung Cancer , 2007, Cell.

[29]  Shinji Yamazaki,et al.  Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma , 2007, Molecular Cancer Therapeutics.

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

[31]  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.