1. A Synergistic Interaction between Chk1- and MK2 Inhibitors in KRAS-Mutant Cancer.

    Cell 162(1):146 (2015) PMID 26140595

    KRAS is one of the most frequently mutated oncogenes in human cancer. Despite substantial efforts, no clinically applicable strategy has yet been developed to effectively treat KRAS-mutant tumors. Here, we perform a cell-line-based screen and identify strong synergistic interactions between cell...
  2. Spatial Tumor Heterogeneity in Lung Cancer with Acquired Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor Resistance: Targeting High-Level MET-Amplification and EGFR T790M Mutation Occurring at Different Sites in the Same Patient.

    Journal of Thoracic Oncology 10(6):e40 (2015) PMID 26001148

  3. Molecular Pathways: Targeting NRG1 Fusions in Lung Cancer.

    Clinical Cancer Research 21(9):1989 (2015) PMID 25501131

    The four members of the ERBB (HER) family of transmembrane receptor tyrosine kinases are frequently activated in cancer by several mechanisms, such as mutation, amplification, or autocrine ligand-receptor stimulation. We recently identified gene fusions involving the ERBB ligand gene, NRG1, whic...
  4. Crizotinib therapy for advanced lung adenocarcinoma and a ROS1 rearrangement: results from the EUROS1 cohort.

    Journal of Clinical Oncology 33(9):992 (2015) PMID 25667280

    Approximately 1% of lung adenocarcinomas are driven by oncogenic ROS1 rearrangement. Crizotinib is a potent inhibitor of both ROS1 and ALK kinase domains. In the absence of a prospective clinical trial in Europe, we conducted a retrospective study in centers that tested for ROS1 rearrangement. E...
  5. PD-L1 expression in small cell neuroendocrine carcinomas.

    European Journal of Cancer 51(3):421 (2015) PMID 25582496

    Small cell lung cancer and extrapulmonary small cell carcinomas are the most aggressive type of neuroendocrine carcinomas. Clinical treatment relies on conventional chemotherapy and radiotherapy; relapses are frequent. The PD-1/PD-L1/PD-L2 pathway is a major target of anti-tumour immunotherapy. ...
  6. Identification and Further Development of Potent TBK1 Inhibitors.

    ACS Chemical Biology 10(1):289 (2015) PMID 25540906

    The cytosolic Ser/Thr kinase TBK1 was discovered to be an essential element in the mediation of signals that lead to tumor migration and progression. These findings meet the need for the identification of novel tool compounds and potential therapeutics to gain deeper insights into TBK1 related s...
  7. Identification and further development of potent TBK1 inhibitors.

    ACS Chemical Biology 10(1):289 (2015) PMID 25540906

    The cytosolic Ser/Thr kinase TBK1 was discovered to be an essential element in the mediation of signals that lead to tumor migration and progression. These findings meet the need for the identification of novel tool compounds and potential therapeutics to gain deeper insights into TBK1 related s...
  8. Identification and further development of potent TBK1 inhibitors.

    ACS Chemical Biology 10(1):289 (2015) PMID 25540906

    The cytosolic Ser/Thr kinase TBK1 was discovered to be an essential element in the mediation of signals that lead to tumor migration and progression. These findings meet the need for the identification of novel tool compounds and potential therapeutics to gain deeper insights into TBK1 related s...
  9. Identification of novel fusion genes in lung cancer using breakpoint assembly of transcriptome sequencing data.

    Genome biology 16(1):7 (2015) PMID 25650807 PMCID PMC4300615

    Genomic translocation events frequently underlie cancer development through generation of gene fusions with oncogenic properties. Identification of such fusion transcripts by transcriptome sequencing might help to discover new potential therapeutic targets. We developed TRUP (Tumor-specimen suit...
  10. Identification of novel fusion genes in lung cancer using breakpoint assembly of transcriptome sequencing data.

    Genome biology 16(1):7 (2015) PMID 25650807 PMCID PMC4300615

    Genomic translocation events frequently underlie cancer development through generation of gene fusions with oncogenic properties. Identification of such fusion transcripts by transcriptome sequencing might help to discover new potential therapeutic targets. We developed TRUP (Tumor-specimen suit...
  11. Era of comprehensive cancer genome analyses.

    Journal of Clinical Oncology 32(36):4029 (2014) PMID 25385732

  12. Era of comprehensive cancer genome analyses.

    Journal of Clinical Oncology 32(36):4029 (2014) PMID 25385732

  13. Era of comprehensive cancer genome analyses.

    Journal of Clinical Oncology 32(36):4029 (2014) PMID 25385732

  14. Era of comprehensive cancer genome analyses.

    Journal of Clinical Oncology 32(36):4029 (2014) PMID 25385732

  15. Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer.

    Nature Medicine 20(9):1027 (2014) PMID 25173427 PMCID PMC4159407

    Crizotinib, a selective tyrosine kinase inhibitor (TKI), shows marked activity in patients whose lung cancers harbor fusions in the gene encoding anaplastic lymphoma receptor tyrosine kinase (ALK), but its efficacy is limited by variable primary responses and acquired resistance. In work arising...
  16. Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer.

    Nature Medicine 20(9):1027 (2014) PMID 25173427 PMCID PMC4159407

    Crizotinib, a selective tyrosine kinase inhibitor (TKI), shows marked activity in patients whose lung cancers harbor fusions in the gene encoding anaplastic lymphoma receptor tyrosine kinase (ALK), but its efficacy is limited by variable primary responses and acquired resistance. In work arising...
  17. Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer.

    Nature Medicine 20(9):1027 (2014) PMID 25173427 PMCID PMC4159407

    Crizotinib, a selective tyrosine kinase inhibitor (TKI), shows marked activity in patients whose lung cancers harbor fusions in the gene encoding anaplastic lymphoma receptor tyrosine kinase (ALK), but its efficacy is limited by variable primary responses and acquired resistance. In work arising...
  18. Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer.

    Nature Medicine 20(9):1027 (2014) PMID 25173427 PMCID PMC4159407

    Crizotinib, a selective tyrosine kinase inhibitor (TKI), shows marked activity in patients whose lung cancers harbor fusions in the gene encoding anaplastic lymphoma receptor tyrosine kinase (ALK), but its efficacy is limited by variable primary responses and acquired resistance. In work arising...
  19. Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer.

    Nature Medicine 20(9):1027 (2014) PMID 25173427 PMCID PMC4159407

    Crizotinib, a selective tyrosine kinase inhibitor (TKI), shows marked activity in patients whose lung cancers harbor fusions in the gene encoding anaplastic lymphoma receptor tyrosine kinase (ALK), but its efficacy is limited by variable primary responses and acquired resistance. In work arising...
  20. Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer.

    Nature Medicine 20(9):1027 (2014) PMID 25173427 PMCID PMC4159407

    Crizotinib, a selective tyrosine kinase inhibitor (TKI), shows marked activity in patients whose lung cancers harbor fusions in the gene encoding anaplastic lymphoma receptor tyrosine kinase (ALK), but its efficacy is limited by variable primary responses and acquired resistance. In work arising...