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KRAS-driven lung adenocarcinoma: combined DDR1/Notch inhibition as an effective therapy
  1. Chiara Ambrogio1,2,
  2. Ernest Nadal3,
  3. Alberto Villanueva4,5,
  4. Gonzalo Gómez-López6,
  5. Timothy P Cash7,
  6. Mariano Barbacid1,
  7. David Santamaría1
  1. 1Experimental Oncology, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain
  2. 2Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
  3. 3Department of Medical Oncology, Multidisciplinary Thoracic Oncology Unit, Catalan Institute of Oncology, Barcelona, Spain
  4. 4Xenopat S.L., Business Bioincubator, Bellvitge Health Science Campus, Barcelona, Spain
  5. 5Chemoresistance and Predictive Factors Group, Program Against Cancer Therapeutic Resistance (ProCURE), Catalan Institute of Oncology (ICO), Bellvitge Institute for Biomedical Research (IDIBELL), L'Hospitalet del Llobregat, Barcelona, Spain
  6. 6Bioinformatics Unit, Structural Biology and Biocomputing Programme, Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain
  7. 7Tumour Suppression, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain
  1. Correspondence to Dr Chiara Ambrogio; chiara_ambrogio{at}dfci.harvard.edu

Abstract

Understanding the early evolution of cancer heterogeneity during the initial steps of tumorigenesis can uncover vulnerabilities of cancer cells that may be masked at later stages. We describe a comprehensive approach employing gene expression analysis in early lesions to identify novel therapeutic targets and the use of mouse models to test synthetic lethal drug combinations to treat human Kirsten rat sarcoma viral oncogene homologue (KRAS)-driven lung adenocarcinoma.

  • KRAS
  • Lung adenocarcinoma

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