<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Zimmermann S</dc:creator>
  <dc:creator>Peters S</dc:creator>
  <dc:date>2012</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">a substantial proportion of non-small-cell lung cancer (NSCLC), and adenocarcinoma in particular, depends on a so-called 'driver mutation' for their malignant phenotype. This genetic alteration induces and sustains tumorigenesis, and targeting of its protein product can result in growth inhibition, tumor response and increased patient survival. NSCLC can thus be subdivided into clinically relevant molecular subsets. Mutations in EGFR best illustrate the therapeutic relevance of molecular classification. This article reviews the scope of presently known driving molecular alterations, including ROS1, BRAF, KRAS, HER2 and PIK3CA, with a special emphasis on aLK rearrangements, and outlines their potential therapeutic applications.</dc:description>
  <dc:identifier>https://sonar.ch/global/documents/20643</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1093/annonc/mds319</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/22987962</dc:relation>
  <dc:source>Annals of oncology : official journal of the European Society for Medical Oncology. - 2012</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Adenocarcinoma</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Anaplastic Lymphoma Kinase</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Carcinoma, Non-Small-Cell Lung</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Class I Phosphatidylinositol 3-Kinases</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">ErbB Receptors</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Humans</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Molecular Targeted Therapy</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Mutation</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">Oncogene Proteins, Fusion</dc:subject>
  <dc:subject xmlns:ns10="xml" ns10:lang="en">Phosphatidylinositol 3-Kinases</dc:subject>
  <dc:subject xmlns:ns11="xml" ns11:lang="en">Protein-Tyrosine Kinases</dc:subject>
  <dc:subject xmlns:ns12="xml" ns12:lang="en">Proto-Oncogene Proteins</dc:subject>
  <dc:subject xmlns:ns13="xml" ns13:lang="en">Proto-Oncogene Proteins B-raf</dc:subject>
  <dc:subject xmlns:ns14="xml" ns14:lang="en">Proto-Oncogene Proteins c-met</dc:subject>
  <dc:subject xmlns:ns15="xml" ns15:lang="en">Proto-Oncogene Proteins p21(ras)</dc:subject>
  <dc:subject xmlns:ns16="xml" ns16:lang="en">Receptor Protein-Tyrosine Kinases</dc:subject>
  <dc:subject xmlns:ns17="xml" ns17:lang="en">Receptor, ErbB-2</dc:subject>
  <dc:subject xmlns:ns18="xml" ns18:lang="en">ras Proteins</dc:subject>
  <dc:title xmlns:ns19="xml" ns19:lang="en">Going beyond EGFR.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>