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1. Data from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer

Author

Hammerman, Peter S., primary, Sos, Martin L., primary, Ramos, Alex H., primary, Xu, Chunxiao, primary, Dutt, Amit, primary, Zhou, Wenjun, primary, Brace, Lear E., primary, Woods, Brittany A., primary, Lin, Wenchu, primary, Zhang, Jianming, primary, Deng, Xianming, primary, Lim, Sang Min, primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Simard, Jeffrey R., primary, Lawrence, Michael S., primary, Onofrio, Robert C., primary, Salvesen, Helga B., primary, Seidel, Danila, primary, Zander, Thomas, primary, Heuckmann, Johannes M., primary, Soltermann, Alex, primary, Moch, Holger, primary, Koker, Mirjam, primary, Leenders, Frauke, primary, Gabler, Franziska, primary, Querings, Silvia, primary, Ansén, Sascha, primary, Brambilla, Elisabeth, primary, Brambilla, Christian, primary, Lorimier, Philippe, primary, Brustugun, Odd Terje, primary, Helland, Åslaug, primary, Petersen, Iver, primary, Clement, Joachim H., primary, Groen, Harry, primary, Timens, Wim, primary, Sietsma, Hannie, primary, Stoelben, Erich, primary, Wolf, Jürgen, primary, Beer, David G., primary, Tsao, Ming Sound, primary, Hanna, Megan, primary, Hatton, Charles, primary, Eck, Michael J., primary, Janne, Pasi A., primary, Johnson, Bruce E., primary, Winckler, Wendy, primary, Greulich, Heidi, primary, Bass, Adam J., primary, Cho, Jeonghee, primary, Rauh, Daniel, primary, Gray, Nathanael S., primary, Wong, Kwok-Kin, primary, Haura, Eric B., primary, Thomas, Roman K., primary, and Meyerson, Matthew, primary

Published
2023
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2. Interview with Dr. Meyerson from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer

Author

Hammerman, Peter S., primary, Sos, Martin L., primary, Ramos, Alex H., primary, Xu, Chunxiao, primary, Dutt, Amit, primary, Zhou, Wenjun, primary, Brace, Lear E., primary, Woods, Brittany A., primary, Lin, Wenchu, primary, Zhang, Jianming, primary, Deng, Xianming, primary, Lim, Sang Min, primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Simard, Jeffrey R., primary, Lawrence, Michael S., primary, Onofrio, Robert C., primary, Salvesen, Helga B., primary, Seidel, Danila, primary, Zander, Thomas, primary, Heuckmann, Johannes M., primary, Soltermann, Alex, primary, Moch, Holger, primary, Koker, Mirjam, primary, Leenders, Frauke, primary, Gabler, Franziska, primary, Querings, Silvia, primary, Ansén, Sascha, primary, Brambilla, Elisabeth, primary, Brambilla, Christian, primary, Lorimier, Philippe, primary, Brustugun, Odd Terje, primary, Helland, Åslaug, primary, Petersen, Iver, primary, Clement, Joachim H., primary, Groen, Harry, primary, Timens, Wim, primary, Sietsma, Hannie, primary, Stoelben, Erich, primary, Wolf, Jürgen, primary, Beer, David G., primary, Tsao, Ming Sound, primary, Hanna, Megan, primary, Hatton, Charles, primary, Eck, Michael J., primary, Janne, Pasi A., primary, Johnson, Bruce E., primary, Winckler, Wendy, primary, Greulich, Heidi, primary, Bass, Adam J., primary, Cho, Jeonghee, primary, Rauh, Daniel, primary, Gray, Nathanael S., primary, Wong, Kwok-Kin, primary, Haura, Eric B., primary, Thomas, Roman K., primary, and Meyerson, Matthew, primary

Published
2023
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3. Supplementary Figure Legends 1-7 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer

Author

Hammerman, Peter S., primary, Sos, Martin L., primary, Ramos, Alex H., primary, Xu, Chunxiao, primary, Dutt, Amit, primary, Zhou, Wenjun, primary, Brace, Lear E., primary, Woods, Brittany A., primary, Lin, Wenchu, primary, Zhang, Jianming, primary, Deng, Xianming, primary, Lim, Sang Min, primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Simard, Jeffrey R., primary, Lawrence, Michael S., primary, Onofrio, Robert C., primary, Salvesen, Helga B., primary, Seidel, Danila, primary, Zander, Thomas, primary, Heuckmann, Johannes M., primary, Soltermann, Alex, primary, Moch, Holger, primary, Koker, Mirjam, primary, Leenders, Frauke, primary, Gabler, Franziska, primary, Querings, Silvia, primary, Ansén, Sascha, primary, Brambilla, Elisabeth, primary, Brambilla, Christian, primary, Lorimier, Philippe, primary, Brustugun, Odd Terje, primary, Helland, Åslaug, primary, Petersen, Iver, primary, Clement, Joachim H., primary, Groen, Harry, primary, Timens, Wim, primary, Sietsma, Hannie, primary, Stoelben, Erich, primary, Wolf, Jürgen, primary, Beer, David G., primary, Tsao, Ming Sound, primary, Hanna, Megan, primary, Hatton, Charles, primary, Eck, Michael J., primary, Janne, Pasi A., primary, Johnson, Bruce E., primary, Winckler, Wendy, primary, Greulich, Heidi, primary, Bass, Adam J., primary, Cho, Jeonghee, primary, Rauh, Daniel, primary, Gray, Nathanael S., primary, Wong, Kwok-Kin, primary, Haura, Eric B., primary, Thomas, Roman K., primary, and Meyerson, Matthew, primary

Published
2023
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4. Supplementary Figures 1-7 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer

Author

Hammerman, Peter S., primary, Sos, Martin L., primary, Ramos, Alex H., primary, Xu, Chunxiao, primary, Dutt, Amit, primary, Zhou, Wenjun, primary, Brace, Lear E., primary, Woods, Brittany A., primary, Lin, Wenchu, primary, Zhang, Jianming, primary, Deng, Xianming, primary, Lim, Sang Min, primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Simard, Jeffrey R., primary, Lawrence, Michael S., primary, Onofrio, Robert C., primary, Salvesen, Helga B., primary, Seidel, Danila, primary, Zander, Thomas, primary, Heuckmann, Johannes M., primary, Soltermann, Alex, primary, Moch, Holger, primary, Koker, Mirjam, primary, Leenders, Frauke, primary, Gabler, Franziska, primary, Querings, Silvia, primary, Ansén, Sascha, primary, Brambilla, Elisabeth, primary, Brambilla, Christian, primary, Lorimier, Philippe, primary, Brustugun, Odd Terje, primary, Helland, Åslaug, primary, Petersen, Iver, primary, Clement, Joachim H., primary, Groen, Harry, primary, Timens, Wim, primary, Sietsma, Hannie, primary, Stoelben, Erich, primary, Wolf, Jürgen, primary, Beer, David G., primary, Tsao, Ming Sound, primary, Hanna, Megan, primary, Hatton, Charles, primary, Eck, Michael J., primary, Janne, Pasi A., primary, Johnson, Bruce E., primary, Winckler, Wendy, primary, Greulich, Heidi, primary, Bass, Adam J., primary, Cho, Jeonghee, primary, Rauh, Daniel, primary, Gray, Nathanael S., primary, Wong, Kwok-Kin, primary, Haura, Eric B., primary, Thomas, Roman K., primary, and Meyerson, Matthew, primary

Published
2023
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5. Supplementary Table 1 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer

Author

Hammerman, Peter S., primary, Sos, Martin L., primary, Ramos, Alex H., primary, Xu, Chunxiao, primary, Dutt, Amit, primary, Zhou, Wenjun, primary, Brace, Lear E., primary, Woods, Brittany A., primary, Lin, Wenchu, primary, Zhang, Jianming, primary, Deng, Xianming, primary, Lim, Sang Min, primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Simard, Jeffrey R., primary, Lawrence, Michael S., primary, Onofrio, Robert C., primary, Salvesen, Helga B., primary, Seidel, Danila, primary, Zander, Thomas, primary, Heuckmann, Johannes M., primary, Soltermann, Alex, primary, Moch, Holger, primary, Koker, Mirjam, primary, Leenders, Frauke, primary, Gabler, Franziska, primary, Querings, Silvia, primary, Ansén, Sascha, primary, Brambilla, Elisabeth, primary, Brambilla, Christian, primary, Lorimier, Philippe, primary, Brustugun, Odd Terje, primary, Helland, Åslaug, primary, Petersen, Iver, primary, Clement, Joachim H., primary, Groen, Harry, primary, Timens, Wim, primary, Sietsma, Hannie, primary, Stoelben, Erich, primary, Wolf, Jürgen, primary, Beer, David G., primary, Tsao, Ming Sound, primary, Hanna, Megan, primary, Hatton, Charles, primary, Eck, Michael J., primary, Janne, Pasi A., primary, Johnson, Bruce E., primary, Winckler, Wendy, primary, Greulich, Heidi, primary, Bass, Adam J., primary, Cho, Jeonghee, primary, Rauh, Daniel, primary, Gray, Nathanael S., primary, Wong, Kwok-Kin, primary, Haura, Eric B., primary, Thomas, Roman K., primary, and Meyerson, Matthew, primary

Published
2023
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6. Data from ALK Mutations Conferring Differential Resistance to Structurally Diverse ALK Inhibitors

Author

Heuckmann, Johannes M., primary, Hölzel, Michael, primary, Sos, Martin L., primary, Heynck, Stefanie, primary, Balke-Want, Hyatt, primary, Koker, Mirjam, primary, Peifer, Martin, primary, Weiss, Jonathan, primary, Lovly, Christine M., primary, Grütter, Christian, primary, Rauh, Daniel, primary, Pao, William, primary, and Thomas, Roman K., primary

Published
2023
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7. Supplementary Figures 1-9 from ALK Mutations Conferring Differential Resistance to Structurally Diverse ALK Inhibitors

Author

Heuckmann, Johannes M., primary, Hölzel, Michael, primary, Sos, Martin L., primary, Heynck, Stefanie, primary, Balke-Want, Hyatt, primary, Koker, Mirjam, primary, Peifer, Martin, primary, Weiss, Jonathan, primary, Lovly, Christine M., primary, Grütter, Christian, primary, Rauh, Daniel, primary, Pao, William, primary, and Thomas, Roman K., primary

Published
2023
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8. Supplementary Figure Legends 1-9 from ALK Mutations Conferring Differential Resistance to Structurally Diverse ALK Inhibitors

Author

Heuckmann, Johannes M., primary, Hölzel, Michael, primary, Sos, Martin L., primary, Heynck, Stefanie, primary, Balke-Want, Hyatt, primary, Koker, Mirjam, primary, Peifer, Martin, primary, Weiss, Jonathan, primary, Lovly, Christine M., primary, Grütter, Christian, primary, Rauh, Daniel, primary, Pao, William, primary, and Thomas, Roman K., primary

Published
2023
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9. Supplementary Table 1 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation

Author

Sos, Martin L., primary, Rode, Haridas B., primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Fischer, Florian, primary, Klüter, Sabine, primary, Pawar, Vijaykumar G., primary, Reuter, Cecile, primary, Heuckmann, Johannes M., primary, Weiss, Jonathan, primary, Ruddigkeit, Lars, primary, Rabiller, Matthias, primary, Koker, Mirjam, primary, Simard, Jeffrey R., primary, Getlik, Matthäus, primary, Yuza, Yuki, primary, Chen, Tzu-Hsiu, primary, Greulich, Heidi, primary, Thomas, Roman K., primary, and Rauh, Daniel, primary

Published
2023
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10. Supplementary Figure 2 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation

Author

Sos, Martin L., primary, Rode, Haridas B., primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Fischer, Florian, primary, Klüter, Sabine, primary, Pawar, Vijaykumar G., primary, Reuter, Cecile, primary, Heuckmann, Johannes M., primary, Weiss, Jonathan, primary, Ruddigkeit, Lars, primary, Rabiller, Matthias, primary, Koker, Mirjam, primary, Simard, Jeffrey R., primary, Getlik, Matthäus, primary, Yuza, Yuki, primary, Chen, Tzu-Hsiu, primary, Greulich, Heidi, primary, Thomas, Roman K., primary, and Rauh, Daniel, primary

Published
2023
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11. Supplementary Methods, Figure Legends 1-3 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation

Author

Sos, Martin L., primary, Rode, Haridas B., primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Fischer, Florian, primary, Klüter, Sabine, primary, Pawar, Vijaykumar G., primary, Reuter, Cecile, primary, Heuckmann, Johannes M., primary, Weiss, Jonathan, primary, Ruddigkeit, Lars, primary, Rabiller, Matthias, primary, Koker, Mirjam, primary, Simard, Jeffrey R., primary, Getlik, Matthäus, primary, Yuza, Yuki, primary, Chen, Tzu-Hsiu, primary, Greulich, Heidi, primary, Thomas, Roman K., primary, and Rauh, Daniel, primary

Published
2023
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12. Supplementary Figure 3 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation

Author

Sos, Martin L., primary, Rode, Haridas B., primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Fischer, Florian, primary, Klüter, Sabine, primary, Pawar, Vijaykumar G., primary, Reuter, Cecile, primary, Heuckmann, Johannes M., primary, Weiss, Jonathan, primary, Ruddigkeit, Lars, primary, Rabiller, Matthias, primary, Koker, Mirjam, primary, Simard, Jeffrey R., primary, Getlik, Matthäus, primary, Yuza, Yuki, primary, Chen, Tzu-Hsiu, primary, Greulich, Heidi, primary, Thomas, Roman K., primary, and Rauh, Daniel, primary

Published
2023
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13. Supplementary Table 2 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation

Author

Sos, Martin L., primary, Rode, Haridas B., primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Fischer, Florian, primary, Klüter, Sabine, primary, Pawar, Vijaykumar G., primary, Reuter, Cecile, primary, Heuckmann, Johannes M., primary, Weiss, Jonathan, primary, Ruddigkeit, Lars, primary, Rabiller, Matthias, primary, Koker, Mirjam, primary, Simard, Jeffrey R., primary, Getlik, Matthäus, primary, Yuza, Yuki, primary, Chen, Tzu-Hsiu, primary, Greulich, Heidi, primary, Thomas, Roman K., primary, and Rauh, Daniel, primary

Published
2023
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14. Supplementary Figure from PTEN Loss Contributes to Erlotinib Resistance in EGFR-Mutant Lung Cancer by Activation of Akt and EGFR

Author

Sos, Martin L., primary, Koker, Mirjam, primary, Weir, Barbara A., primary, Heynck, Stefanie, primary, Rabinovsky, Rosalia, primary, Zander, Thomas, primary, Seeger, Jens M., primary, Weiss, Jonathan, primary, Fischer, Florian, primary, Frommolt, Peter, primary, Michel, Kathrin, primary, Peifer, Martin, primary, Mermel, Craig, primary, Girard, Luc, primary, Peyton, Michael, primary, Gazdar, Adi F., primary, Minna, John D., primary, Garraway, Levi A., primary, Kashkar, Hamid, primary, Pao, William, primary, Meyerson, Matthew, primary, and Thomas, Roman K., primary

Published
2023
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15. Supplementary Figure 4 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation

Author

Sos, Martin L., primary, Rode, Haridas B., primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Fischer, Florian, primary, Klüter, Sabine, primary, Pawar, Vijaykumar G., primary, Reuter, Cecile, primary, Heuckmann, Johannes M., primary, Weiss, Jonathan, primary, Ruddigkeit, Lars, primary, Rabiller, Matthias, primary, Koker, Mirjam, primary, Simard, Jeffrey R., primary, Getlik, Matthäus, primary, Yuza, Yuki, primary, Chen, Tzu-Hsiu, primary, Greulich, Heidi, primary, Thomas, Roman K., primary, and Rauh, Daniel, primary

Published
2023
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16. Supplementary Materials & Methods and Figure Legend from PTEN Loss Contributes to Erlotinib Resistance in EGFR-Mutant Lung Cancer by Activation of Akt and EGFR

Author

Sos, Martin L., primary, Koker, Mirjam, primary, Weir, Barbara A., primary, Heynck, Stefanie, primary, Rabinovsky, Rosalia, primary, Zander, Thomas, primary, Seeger, Jens M., primary, Weiss, Jonathan, primary, Fischer, Florian, primary, Frommolt, Peter, primary, Michel, Kathrin, primary, Peifer, Martin, primary, Mermel, Craig, primary, Girard, Luc, primary, Peyton, Michael, primary, Gazdar, Adi F., primary, Minna, John D., primary, Garraway, Levi A., primary, Kashkar, Hamid, primary, Pao, William, primary, Meyerson, Matthew, primary, and Thomas, Roman K., primary

Published
2023
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17. Supplementary Figure 1 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation

Author

Sos, Martin L., primary, Rode, Haridas B., primary, Heynck, Stefanie, primary, Peifer, Martin, primary, Fischer, Florian, primary, Klüter, Sabine, primary, Pawar, Vijaykumar G., primary, Reuter, Cecile, primary, Heuckmann, Johannes M., primary, Weiss, Jonathan, primary, Ruddigkeit, Lars, primary, Rabiller, Matthias, primary, Koker, Mirjam, primary, Simard, Jeffrey R., primary, Getlik, Matthäus, primary, Yuza, Yuki, primary, Chen, Tzu-Hsiu, primary, Greulich, Heidi, primary, Thomas, Roman K., primary, and Rauh, Daniel, primary

Published
2023
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18. Data from PTEN Loss Contributes to Erlotinib Resistance in EGFR-Mutant Lung Cancer by Activation of Akt and EGFR

Author

Sos, Martin L., primary, Koker, Mirjam, primary, Weir, Barbara A., primary, Heynck, Stefanie, primary, Rabinovsky, Rosalia, primary, Zander, Thomas, primary, Seeger, Jens M., primary, Weiss, Jonathan, primary, Fischer, Florian, primary, Frommolt, Peter, primary, Michel, Kathrin, primary, Peifer, Martin, primary, Mermel, Craig, primary, Girard, Luc, primary, Peyton, Michael, primary, Gazdar, Adi F., primary, Minna, John D., primary, Garraway, Levi A., primary, Kashkar, Hamid, primary, Pao, William, primary, Meyerson, Matthew, primary, and Thomas, Roman K., primary

Published
2023
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19. Supplementary Table from PTEN Loss Contributes to Erlotinib Resistance in EGFR-Mutant Lung Cancer by Activation of Akt and EGFR

Author

Sos, Martin L., primary, Koker, Mirjam, primary, Weir, Barbara A., primary, Heynck, Stefanie, primary, Rabinovsky, Rosalia, primary, Zander, Thomas, primary, Seeger, Jens M., primary, Weiss, Jonathan, primary, Fischer, Florian, primary, Frommolt, Peter, primary, Michel, Kathrin, primary, Peifer, Martin, primary, Mermel, Craig, primary, Girard, Luc, primary, Peyton, Michael, primary, Gazdar, Adi F., primary, Minna, John D., primary, Garraway, Levi A., primary, Kashkar, Hamid, primary, Pao, William, primary, Meyerson, Matthew, primary, and Thomas, Roman K., primary

Published
2023
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20. A framework for identification of actionable cancer genome dependencies in small cell lung cancer

Author

Sos, Martin L., Dietlein, Felix, Peifer, Martin, Schöttle, Jakob, Balke-Want, Hyatt, Müller, Christian, Koker, Mirjam, Richters, André, Heynck, Stefanie, Malchers, Florian, Heuckmann, Johannes M., Seidel, Danila, Eyers, Patrick A., Ullrich, Rolad T., Antonchick, Andrey P., Vintonyak, Viktor V., Schneider, Peter M., Ninomiya, Takashi, Waldmann, Herbert, Büttner, Reinhard, Rauh, Daniel, Heukamp, Lukas C., and Thomas, Roman K.

Published
2012

21. Identifying Genotype-Dependent Efficacy of Single and Combined PI3K- and MAPK-Pathway Inhibition in Cancer

Author

Sos, Martin L., Fischer, Stefanie, Ullrich, Roland, Peifer, Martin, Heuckmann, Johannes M., Koker, Mirjam, Heynck, Stefanie, Stückrath, Isabel, Weiss, Jonathan, Fischer, Florian, Michel, Kathrin, Goel, Aviva, Regales, Lucia, Politi, Katerina A., Perera, Samanthi, Getlik, Matthäus, Heukamp, Lukas C., Ansén, Sascha, Zander, Thomas, Beroukhim, Rameen, Kashkar, Hamid, Shokat, Kevan M., Sellers, William R., Rauh, Daniel, Orr, Christine, Hoeflich, Klaus P., Friedman, Lori, Wong, Kwok-Kin, Pao, William, and Thomas, Roman K.

Published
2009
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23. Predicting drug susceptibility of non--small cell lung cancers based on genetic lesions

Author

Sos, Martin L., Michel, Kathrin, Zander, Thomas, Weiss, Jonathan, Frommolt, Peter, Peifer, Martin, Li, Danan, Ullrich, Roland, Koker, Mirjam, Fischer, Florian, Shimamura, Takeshi, Rauh, Daniel, Mermel, Craig, Fischer, Stefanie, Stuckrath, Isabel, Heynck, Stefanie, Beroukhim, Rameen, Lin, William, Winckler, Wendy, Shah, Kinjal, LaFramboise, Thomas, Moriarty, Whei F., Hanna, Megan, Tolosi, Laura, Rahnenfuhrer, Jorg, Verhaak, Roel, Chiang, Derek, Getz, Gad, Hellmich, Martin, Wolf, Jurgen, Girard, Luc, Peyton, Michael, Weir, Barbara A., Chen, Tzu-Hsiu, Greulich, Heidi, Barretina, Jordi, Shapiro, Geoffrey I., Garraway, Levi A., Gazdar, Adi F., Minna, John D., Meyerson, Matthew, Wong, Kwok-Kin, and Thomas, Roman K.

Subjects
Gene mutations -- Health aspects, Genetic susceptibility -- Research, Heat shock proteins -- Health aspects, Heat shock proteins -- Genetic aspects, Heat shock proteins -- Research, Lung cancer, Non-small cell -- Risk factors, Lung cancer, Non-small cell -- Genetic aspects, Lung cancer, Non-small cell -- Care and treatment, Lung cancer, Non-small cell -- Research
Abstract

Somatic genetic alterations in cancers have been linked with response to targeted therapeutics by creation of specific dependency on activated oncogenic signaling pathways. However, no tools currently exist to systematically connect such genetic lesions to therapeutic vulnerability. We have therefore developed a genomics approach to identify lesions associated with therapeutically relevant oncogene dependency. Using integrated genomic profiling, we have demonstrated that the genomes of a large panel of human non--small cell lung cancer (NSCLC) cell lines are highly representative of those of primary NSCLC tumors. Using cell-based compound screening coupled with diverse computational approaches to integrate orthogonal genomic and biochemical data sets, we identified molecular and genomic predictors of therapeutic response to clinically relevant compounds. Using this approach, we showed that v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations confer enhanced Hsp90 dependency and validated this finding in mice with KRAS-driven lung adenocarcinoma, as these mice exhibited dramatic tumor regression when treated with an Hsp90 inhibitor. In addition, we found that cells with copy number enhancement of v-abl Abelson murine leukemia viral oncogene homolog 2 (ABL2) and ephrin receptor kinase and v-src sarcoma (Schmidt-Ruppin A-2) viral oncogene homolog (avian) (SRC) kinase family genes were exquisitely sensitive to treatment with the SRC/ABL inhibitor dasatinib, both in vitro and when it xenografted into mice. Thus, genomically annotated cell-line collections may help translate cancer genomics information into clinical practice by defining critical pathway dependencies amenable to therapeutic inhibition., Introduction The dynamics of ongoing efforts to fully annotate the genomes of all major cancer types are reminiscent of those of the Human Genome Project. The analysis of somatic gene [...]

Published
2009

24. Telomerase activation by genomic rearrangements in high-risk neuroblastoma

Author

Peifer, Martin, Hertwig, Falk, Roels, Frederik, Dreidax, Daniel, Gartlgruber, Moritz, Menon, Roopika, Kraemer, Andrea, Roncaioli, Justin L., Sand, Frederik, Heuckmann, Johannes M., Ikram, Fakhera, Schmidt, Rene, Ackermann, Sandra, Engesser, Anne, Kahlert, Yvonne, Vogel, Wenzel, Altmueller, Janine, Nuernberg, Peter, Thierry-Mieg, Jean, Thierry-Mieg, Danielle, Mariappan, Aruljothi, Heynck, Stefanie, Mariotti, Erika, Henrich, Kai-Oliver, Gloeckner, Christian, Bosco, Graziella, Leuschner, Ivo, Schweiger, Michal R., Savelyeva, Larissa, Watkins, Simon C., Shao, Chunxuan, Bell, Emma, Hoefer, Thomas, Achter, Viktor, Lang, Ulrich, Theissen, Jessica, Volland, Ruth, Saadati, Maral, Eggert, Angelika, de Wilde, Bram, Berthold, Frank, Peng, Zhiyu, Zhao, Chen, Shi, Leming, Ortmann, Monika, Buettner, Reinhard, Perner, Sven, Hero, Barbara, Schramm, Alexander, Schulte, Johannes H., Herrmann, Carl, O'Sullivan, Roderick J., Westermann, Frank, Thomas, Roman K., Fischer, Matthias, Peifer, Martin, Hertwig, Falk, Roels, Frederik, Dreidax, Daniel, Gartlgruber, Moritz, Menon, Roopika, Kraemer, Andrea, Roncaioli, Justin L., Sand, Frederik, Heuckmann, Johannes M., Ikram, Fakhera, Schmidt, Rene, Ackermann, Sandra, Engesser, Anne, Kahlert, Yvonne, Vogel, Wenzel, Altmueller, Janine, Nuernberg, Peter, Thierry-Mieg, Jean, Thierry-Mieg, Danielle, Mariappan, Aruljothi, Heynck, Stefanie, Mariotti, Erika, Henrich, Kai-Oliver, Gloeckner, Christian, Bosco, Graziella, Leuschner, Ivo, Schweiger, Michal R., Savelyeva, Larissa, Watkins, Simon C., Shao, Chunxuan, Bell, Emma, Hoefer, Thomas, Achter, Viktor, Lang, Ulrich, Theissen, Jessica, Volland, Ruth, Saadati, Maral, Eggert, Angelika, de Wilde, Bram, Berthold, Frank, Peng, Zhiyu, Zhao, Chen, Shi, Leming, Ortmann, Monika, Buettner, Reinhard, Perner, Sven, Hero, Barbara, Schramm, Alexander, Schulte, Johannes H., Herrmann, Carl, O'Sullivan, Roderick J., Westermann, Frank, Thomas, Roman K., and Fischer, Matthias

Abstract

Neuroblastoma is a malignant paediatric tumour of the sympathetic nervous system(1). Roughly half of these tumours regress spontaneously or are cured by limited therapy. By contrast, high-risk neuroblastomas have an unfavourable clinical course despite intensive multimodal treatment, and their molecular basis has remained largely elusive(2-4). Here we have performed whole-genome sequencing of 56 neuroblastomas (high-risk, n = 39; low-risk, n = 17) and discovered recurrent genomic rearrangements affecting a chromosomal region at 5p15.33 proximal of the telomerase reverse transcriptase gene (TERT). These rearrangements occurred only in high-risk neuroblastomas (12/39, 31%) in a mutually exclusive fashion with MYCN amplifications and ATRX mutations, which are known genetic events in this tumour type(1,2,5). In an extended case series (n = 217), TERT rearrangements defined a subgroup of high-risk tumours with particularly poor outcome. Despite a large structural diversity of these rearrangements, they all induced massive transcriptional upregulation of TERT. In the remaining high-risk tumours, TERT expression was also elevated in MYCN-amplified tumours, whereas alternative lengthening of telomeres was present in neuroblastomas without TERT or MYCN alterations, suggesting that telomere lengthening represents a central mechanism defining this subtype. The 5p15.33 rearrangements juxtapose the TERT coding sequence to strong enhancer elements, resulting in massive chromatin remodelling and DNA methylation of the affected region. Supporting a functional role of TERT, neuroblastoma cell lines bearing rearrangements or amplified MYCN exhibited both upregulated TERT expression and enzymatic telomerase activity. In summary, our findings show that remodelling of the genomic context abrogates transcriptional silencing of TERT in high-risk neuroblastoma and places telomerase activation in the centre of transformation in a large fraction of these tumours.

Published
2015

25. Telomerase activation by genomic rearrangements in high-risk neuroblastoma

Author

Peifer, Martin, primary, Hertwig, Falk, additional, Roels, Frederik, additional, Dreidax, Daniel, additional, Gartlgruber, Moritz, additional, Menon, Roopika, additional, Krämer, Andrea, additional, Roncaioli, Justin L., additional, Sand, Frederik, additional, Heuckmann, Johannes M., additional, Ikram, Fakhera, additional, Schmidt, Rene, additional, Ackermann, Sandra, additional, Engesser, Anne, additional, Kahlert, Yvonne, additional, Vogel, Wenzel, additional, Altmüller, Janine, additional, Nürnberg, Peter, additional, Thierry-Mieg, Jean, additional, Thierry-Mieg, Danielle, additional, Mariappan, Aruljothi, additional, Heynck, Stefanie, additional, Mariotti, Erika, additional, Henrich, Kai-Oliver, additional, Gloeckner, Christian, additional, Bosco, Graziella, additional, Leuschner, Ivo, additional, Schweiger, Michal R., additional, Savelyeva, Larissa, additional, Watkins, Simon C., additional, Shao, Chunxuan, additional, Bell, Emma, additional, Höfer, Thomas, additional, Achter, Viktor, additional, Lang, Ulrich, additional, Theissen, Jessica, additional, Volland, Ruth, additional, Saadati, Maral, additional, Eggert, Angelika, additional, de Wilde, Bram, additional, Berthold, Frank, additional, Peng, Zhiyu, additional, Zhao, Chen, additional, Shi, Leming, additional, Ortmann, Monika, additional, Büttner, Reinhard, additional, Perner, Sven, additional, Hero, Barbara, additional, Schramm, Alexander, additional, Schulte, Johannes H., additional, Herrmann, Carl, additional, O’Sullivan, Roderick J., additional, Westermann, Frank, additional, Thomas, Roman K., additional, and Fischer, Matthias, additional

Published
2015
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26. Integrative genome analyses identify key somatic driver mutations of small-cell lung cancer

Author

Peifer, Martin, Fernandez-Cuesta, Lynnette, Sos, Martin L., George, Julie, Seidel, Danila, Kasper, Lawryn H., Plenker, Dennis, Leenders, Frauke, Sun, Ruping, Zander, Thomas, Menon, Roopika, Koker, Mirjam, Dahmen, Ilona, Mueller, Christian, Di Cerbo, Vincenzo, Schildhaus, Hans-Ulrich, Altmueller, Janine, Baessmann, Ingelore, Becker, Christian, de Wilde, Bram, Vandesompele, Jo, Boehm, Diana, Ansen, Sascha, Gabler, Franziska, Wilkening, Ines, Heynck, Stefanie, Heuckmann, Johannes M., Lu, Xin, Carter, Scott L., Cibulskis, Kristian, Banerji, Shantanu, Getz, Gad, Park, Kwon-Sik, Rauh, Daniel, Gruetter, Christian, Fischer, Matthias, Pasqualucci, Laura, Wright, Gavin, Wainer, Zoe, Russell, Prudence, Petersen, Iver, Chen, Yuan, Stoelben, Erich, Ludwig, Corinna, Schnabel, Philipp, Hoffmann, Hans, Muley, Thomas, Brockmann, Michael, Engel-Riedel, Walburga, Muscarella, Lucia A., Fazio, Vito M., Groen, Harry, Timens, Wim, Sietsma, Hannie, Thunnissen, Erik, Smit, Egbert, Heideman, Danielle A. M., Snijders, Peter J. F., Cappuzzo, Federico, Ligorio, Claudia, Damiani, Stefania, Field, John, Solberg, Steinar, Brustugun, Odd Terje, Lund-Iversen, Marius, Saenger, Joerg, Clement, Joachim H., Soltermann, Alex, Moch, Holger, Weder, Walter, Solomon, Benjamin, Soria, Jean-Charles, Validire, Pierre, Besse, Benjamin, Brambilla, Elisabeth, Brambilla, Christian, Lantuejoul, Sylvie, Lorimier, Philippe, Schneider, Peter M., Hallek, Michael, Pao, William, Meyerson, Matthew, Sage, Julien, Shendure, Jay, Schneider, Robert, Buettner, Reinhard, Wolf, Juergen, Nuernberg, Peter, Perner, Sven, Heukamp, Lukas C., Brindle, Paul K., Haas, Stefan, Thomas, Roman K., Peifer, Martin, Fernandez-Cuesta, Lynnette, Sos, Martin L., George, Julie, Seidel, Danila, Kasper, Lawryn H., Plenker, Dennis, Leenders, Frauke, Sun, Ruping, Zander, Thomas, Menon, Roopika, Koker, Mirjam, Dahmen, Ilona, Mueller, Christian, Di Cerbo, Vincenzo, Schildhaus, Hans-Ulrich, Altmueller, Janine, Baessmann, Ingelore, Becker, Christian, de Wilde, Bram, Vandesompele, Jo, Boehm, Diana, Ansen, Sascha, Gabler, Franziska, Wilkening, Ines, Heynck, Stefanie, Heuckmann, Johannes M., Lu, Xin, Carter, Scott L., Cibulskis, Kristian, Banerji, Shantanu, Getz, Gad, Park, Kwon-Sik, Rauh, Daniel, Gruetter, Christian, Fischer, Matthias, Pasqualucci, Laura, Wright, Gavin, Wainer, Zoe, Russell, Prudence, Petersen, Iver, Chen, Yuan, Stoelben, Erich, Ludwig, Corinna, Schnabel, Philipp, Hoffmann, Hans, Muley, Thomas, Brockmann, Michael, Engel-Riedel, Walburga, Muscarella, Lucia A., Fazio, Vito M., Groen, Harry, Timens, Wim, Sietsma, Hannie, Thunnissen, Erik, Smit, Egbert, Heideman, Danielle A. M., Snijders, Peter J. F., Cappuzzo, Federico, Ligorio, Claudia, Damiani, Stefania, Field, John, Solberg, Steinar, Brustugun, Odd Terje, Lund-Iversen, Marius, Saenger, Joerg, Clement, Joachim H., Soltermann, Alex, Moch, Holger, Weder, Walter, Solomon, Benjamin, Soria, Jean-Charles, Validire, Pierre, Besse, Benjamin, Brambilla, Elisabeth, Brambilla, Christian, Lantuejoul, Sylvie, Lorimier, Philippe, Schneider, Peter M., Hallek, Michael, Pao, William, Meyerson, Matthew, Sage, Julien, Shendure, Jay, Schneider, Robert, Buettner, Reinhard, Wolf, Juergen, Nuernberg, Peter, Perner, Sven, Heukamp, Lukas C., Brindle, Paul K., Haas, Stefan, and Thomas, Roman K.

Abstract

Small-cell lung cancer (SCLC) is an aggressive lung tumor subtype with poor prognosis(1-3). We sequenced 29 SCLC exomes, 2 genomes and 15 transcriptomes and found an extremely high mutation rate of 7.4 +/- 1 protein-changing mutations per million base pairs. Therefore, we conducted integrated analyses of the various data sets to identify pathogenetically relevant mutated genes. In all cases, we found evidence for inactivation of TP53 and RB1 and identified recurrent mutations in the CREBBP, EP300 and MLL genes that encode histone modifiers. Furthermore, we observed mutations in PTEN, SLIT2 and EPHA7, as well as focal amplifications of the FGFR1 tyrosine kinase gene. Finally, we detected many of the alterations found in humans in SCLC tumors from Tp53 and Rb1 double knockout mice(4). Our study implicates histone modification as a major feature of SCLC, reveals potentially therapeutically tractable genomic alterations and provides a generalizable framework for the identification of biologically relevant genes in the context of high mutational background.

Published
2012

27. ALK Mutations Conferring Differential Resistance to Structurally Diverse ALK Inhibitors

Author

Heuckmann, Johannes M., Hoelzel, Michael, Sos, Martin L., Heynck, Stefanie, Balke-Want, Hyatt, Koker, Mirjam, Peifer, Martin, Weiss, Jonathan, Lovly, Christine M., Gruetter, Christian, Rauh, Daniel, Pao, William, Thomas, Roman K., Heuckmann, Johannes M., Hoelzel, Michael, Sos, Martin L., Heynck, Stefanie, Balke-Want, Hyatt, Koker, Mirjam, Peifer, Martin, Weiss, Jonathan, Lovly, Christine M., Gruetter, Christian, Rauh, Daniel, Pao, William, and Thomas, Roman K.

Abstract

Purpose: EML4-ALK fusions define a subset of lung cancers that can be effectively treated with anaplastic lymphoma kinase (ALK) inhibitors. Unfortunately, the duration of response is heterogeneous and acquired resistance limits their ultimate efficacy. Thus, a better understanding of resistance mechanisms will help to enhance tumor control in EML4-ALK-positive tumors. Experimental Design: By applying orthogonal functional mutagenesis screening approaches, we screened for mutations inducing resistance to the aminopyridine PF02341066 (crizotinib) and/or the diaminopyrimidine TAE684. Results: Here, we show that the resistance mutation, L1196M, as well as other crizotinib resistance mutations (F1174L and G1269S), are highly sensitive to the structurally unrelated ALK inhibitor TAE684. In addition, we identified two novel EML4-ALK resistance mutations (L1198P and D1203N), which unlike previously reported mutations, induced resistance to both ALK inhibitors. An independent resistance screen in ALK-mutant neuroblastoma cells yielded the same L1198P resistance mutation but defined two additional mutations conferring resistance to TAE684 but not to PF02341066. Conclusions: Our results show that different ALK resistance mutations as well as different ALK inhibitors impact the therapeutic efficacy in the setting of EML4-ALK fusions and ALK mutations. Clin Cancer Res; 17(23); 7394-401. (C)2011 AACR.

Published
2011

28. Frequent and Focal FGFR1 Amplification Associates with Therapeutically Tractable FGFR1 Dependency in Squamous Cell Lung Cancer

Author

Weiss, Jonathan, Sos, Martin L., Seidel, Danila, Peifer, Martin, Zander, Thomas, Heuckmann, Johannes M., Ullrich, Roland T., Menon, Roopika, Maier, Sebastian, Soltermann, Alex, Moch, Holger, Wagener, Patrick, Fischer, Florian, Heynck, Stefanie, Koker, Mirjam, Schoettle, Jakob, Leenders, Frauke, Gabler, Franziska, Dabow, Ines, Querings, Silvia, Heukamp, Lukas C., Balke-Want, Hyatt, Ansen, Sascha, Rauh, Daniel, Baessmann, Ingelore, Altmueller, Janine, Wainer, Zoe, Conron, Matthew, Wright, Gavin, Russell, Prudence, Solomon, Ben, Brambilla, Elisabeth, Brambilla, Christian, Lorimier, Philippe, Sollberg, Steinar, Brustugun, Odd Terje, Engel-Riedel, Walburga, Ludwig, Corinna, Petersen, Iver, Saenger, Joerg, Clement, Joachim, Groen, Harry, Timens, Wim, Sietsma, Hannie, Thunnissen, Erik, Smit, Egbert, Heideman, Danielle, Cappuzzo, Federico, Ligorio, Claudia, Damiani, Stefania, Hallek, Michael, Beroukhim, Rameen, Pao, William, Klebl, Bert, Baumann, Matthias, Buettner, Reinhard, Ernestus, Karen, Stoelben, Erich, Wolf, Juergen, Nuernberg, Peter, Perner, Sven, Thomas, Roman K., Weiss, Jonathan, Sos, Martin L., Seidel, Danila, Peifer, Martin, Zander, Thomas, Heuckmann, Johannes M., Ullrich, Roland T., Menon, Roopika, Maier, Sebastian, Soltermann, Alex, Moch, Holger, Wagener, Patrick, Fischer, Florian, Heynck, Stefanie, Koker, Mirjam, Schoettle, Jakob, Leenders, Frauke, Gabler, Franziska, Dabow, Ines, Querings, Silvia, Heukamp, Lukas C., Balke-Want, Hyatt, Ansen, Sascha, Rauh, Daniel, Baessmann, Ingelore, Altmueller, Janine, Wainer, Zoe, Conron, Matthew, Wright, Gavin, Russell, Prudence, Solomon, Ben, Brambilla, Elisabeth, Brambilla, Christian, Lorimier, Philippe, Sollberg, Steinar, Brustugun, Odd Terje, Engel-Riedel, Walburga, Ludwig, Corinna, Petersen, Iver, Saenger, Joerg, Clement, Joachim, Groen, Harry, Timens, Wim, Sietsma, Hannie, Thunnissen, Erik, Smit, Egbert, Heideman, Danielle, Cappuzzo, Federico, Ligorio, Claudia, Damiani, Stefania, Hallek, Michael, Beroukhim, Rameen, Pao, William, Klebl, Bert, Baumann, Matthias, Buettner, Reinhard, Ernestus, Karen, Stoelben, Erich, Wolf, Juergen, Nuernberg, Peter, Perner, Sven, and Thomas, Roman K.

Abstract

Lung cancer remains one of the leading causes of cancer-related death in developed countries. Although lung adenocarcinomas with EGFR mutations or EML4-ALK fusions respond to treatment by epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) inhibition, respectively, squamous cell lung cancer currently lacks therapeutically exploitable genetic alterations. We conducted a systematic search in a set of 232 lung cancer specimens for genetic alterations that were therapeutically amenable and then performed high-resolution gene copy number analyses. We identified frequent and focal fibroblast growth factor receptor 1 (FGFR1) amplification in squamous cell lung cancer (n = 155), but not in other lung cancer subtypes, and, by fluorescence in situ hybridization, confirmed the presence of FGFR1 amplifications in an independent cohort of squamous cell lung cancer samples (22% of cases). Using cell-based screening with the FGFR inhibitor PD173074 in a large (n = 83) panel of lung cancer cell lines, we demonstrated that this compound inhibited growth and induced apoptosis specifically in those lung cancer cells carrying amplified FGFR1. We validated the FGFR1 dependence of FGFR1-amplified cell lines by FGFR1 knockdown and by ectopic expression of an FGFR1-resistant allele (FGFR1(V561M)), which rescued FGFR1-amplified cells from PD173074-mediated cytotoxicity. Finally, we showed that inhibition of FGFR1 with a small molecule led to significant tumor shrinkage in vivo. Thus, focal FGFR1 amplification is common in squamous cell lung cancer and associated with tumor growth and survival, suggesting that FGFR inhibitors may be a viable therapeutic option in this cohort of patients.

Published
2010

29. Targeting Gain of Function and Resistance Mutations in Abl and KIT by Hybrid Compound Design

Author

Richters, André, primary, Ketzer, Julia, additional, Getlik, Matthäus, additional, Grütter, Christian, additional, Schneider, Ralf, additional, Heuckmann, Johannes M., additional, Heynck, Stefanie, additional, Sos, Martin L., additional, Gupta, Anu, additional, Unger, Anke, additional, Schultz-Fademrecht, Carsten, additional, Thomas, Roman K., additional, Bauer, Sebastian, additional, and Rauh, Daniel, additional

Published
2013
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30. Integrative genome analyses identify key somatic driver mutations of small-cell lung cancer

Author

Peifer, Martin, primary, Fernández-Cuesta, Lynnette, additional, Sos, Martin L, additional, George, Julie, additional, Seidel, Danila, additional, Kasper, Lawryn H, additional, Plenker, Dennis, additional, Leenders, Frauke, additional, Sun, Ruping, additional, Zander, Thomas, additional, Menon, Roopika, additional, Koker, Mirjam, additional, Dahmen, Ilona, additional, Müller, Christian, additional, Di Cerbo, Vincenzo, additional, Schildhaus, Hans-Ulrich, additional, Altmüller, Janine, additional, Baessmann, Ingelore, additional, Becker, Christian, additional, de Wilde, Bram, additional, Vandesompele, Jo, additional, Böhm, Diana, additional, Ansén, Sascha, additional, Gabler, Franziska, additional, Wilkening, Ines, additional, Heynck, Stefanie, additional, Heuckmann, Johannes M, additional, Lu, Xin, additional, Carter, Scott L, additional, Cibulskis, Kristian, additional, Banerji, Shantanu, additional, Getz, Gad, additional, Park, Kwon-Sik, additional, Rauh, Daniel, additional, Grütter, Christian, additional, Fischer, Matthias, additional, Pasqualucci, Laura, additional, Wright, Gavin, additional, Wainer, Zoe, additional, Russell, Prudence, additional, Petersen, Iver, additional, Chen, Yuan, additional, Stoelben, Erich, additional, Ludwig, Corinna, additional, Schnabel, Philipp, additional, Hoffmann, Hans, additional, Muley, Thomas, additional, Brockmann, Michael, additional, Engel-Riedel, Walburga, additional, Muscarella, Lucia A, additional, Fazio, Vito M, additional, Groen, Harry, additional, Timens, Wim, additional, Sietsma, Hannie, additional, Thunnissen, Erik, additional, Smit, Egbert, additional, Heideman, Daniëlle A M, additional, Snijders, Peter J F, additional, Cappuzzo, Federico, additional, Ligorio, Claudia, additional, Damiani, Stefania, additional, Field, John, additional, Solberg, Steinar, additional, Brustugun, Odd Terje, additional, Lund-Iversen, Marius, additional, Sänger, Jörg, additional, Clement, Joachim H, additional, Soltermann, Alex, additional, Moch, Holger, additional, Weder, Walter, additional, Solomon, Benjamin, additional, Soria, Jean-Charles, additional, Validire, Pierre, additional, Besse, Benjamin, additional, Brambilla, Elisabeth, additional, Brambilla, Christian, additional, Lantuejoul, Sylvie, additional, Lorimier, Philippe, additional, Schneider, Peter M, additional, Hallek, Michael, additional, Pao, William, additional, Meyerson, Matthew, additional, Sage, Julien, additional, Shendure, Jay, additional, Schneider, Robert, additional, Büttner, Reinhard, additional, Wolf, Jürgen, additional, Nürnberg, Peter, additional, Perner, Sven, additional, Heukamp, Lukas C, additional, Brindle, Paul K, additional, Haas, Stefan, additional, and Thomas, Roman K, additional

Published
2012
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31. ALK Mutations Conferring Differential Resistance to Structurally Diverse ALK Inhibitors

Author

Heuckmann, Johannes M., primary, Hölzel, Michael, additional, Sos, Martin L., additional, Heynck, Stefanie, additional, Balke-Want, Hyatt, additional, Koker, Mirjam, additional, Peifer, Martin, additional, Weiss, Jonathan, additional, Lovly, Christine M., additional, Grütter, Christian, additional, Rauh, Daniel, additional, Pao, William, additional, and Thomas, Roman K., additional

Published
2011
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32. Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer

Author

Hammerman, Peter S., primary, Sos, Martin L., additional, Ramos, Alex H., additional, Xu, Chunxiao, additional, Dutt, Amit, additional, Zhou, Wenjun, additional, Brace, Lear E., additional, Woods, Brittany A., additional, Lin, Wenchu, additional, Zhang, Jianming, additional, Deng, Xianming, additional, Lim, Sang Min, additional, Heynck, Stefanie, additional, Peifer, Martin, additional, Simard, Jeffrey R., additional, Lawrence, Michael S., additional, Onofrio, Robert C., additional, Salvesen, Helga B., additional, Seidel, Danila, additional, Zander, Thomas, additional, Heuckmann, Johannes M., additional, Soltermann, Alex, additional, Moch, Holger, additional, Koker, Mirjam, additional, Leenders, Frauke, additional, Gabler, Franziska, additional, Querings, Silvia, additional, Ansén, Sascha, additional, Brambilla, Elisabeth, additional, Brambilla, Christian, additional, Lorimier, Philippe, additional, Brustugun, Odd Terje, additional, Helland, Åslaug, additional, Petersen, Iver, additional, Clement, Joachim H., additional, Groen, Harry, additional, Timens, Wim, additional, Sietsma, Hannie, additional, Stoelben, Erich, additional, Wolf, Jürgen, additional, Beer, David G., additional, Tsao, Ming Sound, additional, Hanna, Megan, additional, Hatton, Charles, additional, Eck, Michael J., additional, Janne, Pasi A., additional, Johnson, Bruce E., additional, Winckler, Wendy, additional, Greulich, Heidi, additional, Bass, Adam J., additional, Cho, Jeonghee, additional, Rauh, Daniel, additional, Gray, Nathanael S., additional, Wong, Kwok-Kin, additional, Haura, Eric B., additional, Thomas, Roman K., additional, and Meyerson, Matthew, additional

Published
2011
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33. Frequent and Focal FGFR1 Amplification Associates with Therapeutically Tractable FGFR1 Dependency in Squamous Cell Lung Cancer

Author

Weiss, Jonathan, primary, Sos, Martin L., additional, Seidel, Danila, additional, Peifer, Martin, additional, Zander, Thomas, additional, Heuckmann, Johannes M., additional, Ullrich, Roland T., additional, Menon, Roopika, additional, Maier, Sebastian, additional, Soltermann, Alex, additional, Moch, Holger, additional, Wagener, Patrick, additional, Fischer, Florian, additional, Heynck, Stefanie, additional, Koker, Mirjam, additional, Schöttle, Jakob, additional, Leenders, Frauke, additional, Gabler, Franziska, additional, Dabow, Ines, additional, Querings, Silvia, additional, Heukamp, Lukas C., additional, Balke-Want, Hyatt, additional, Ansén, Sascha, additional, Rauh, Daniel, additional, Baessmann, Ingelore, additional, Altmüller, Janine, additional, Wainer, Zoe, additional, Conron, Matthew, additional, Wright, Gavin, additional, Russell, Prudence, additional, Solomon, Ben, additional, Brambilla, Elisabeth, additional, Brambilla, Christian, additional, Lorimier, Philippe, additional, Sollberg, Steinar, additional, Brustugun, Odd Terje, additional, Engel-Riedel, Walburga, additional, Ludwig, Corinna, additional, Petersen, Iver, additional, Sänger, Jörg, additional, Clement, Joachim, additional, Groen, Harry, additional, Timens, Wim, additional, Sietsma, Hannie, additional, Thunnissen, Erik, additional, Smit, Egbert, additional, Heideman, Daniëlle, additional, Cappuzzo, Federico, additional, Ligorio, Claudia, additional, Damiani, Stefania, additional, Hallek, Michael, additional, Beroukhim, Rameen, additional, Pao, William, additional, Klebl, Bert, additional, Baumann, Matthias, additional, Buettner, Reinhard, additional, Ernestus, Karen, additional, Stoelben, Erich, additional, Wolf, Jürgen, additional, Nürnberg, Peter, additional, Perner, Sven, additional, and Thomas, Roman K., additional

Published
2010
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35. Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation

Author

Sos, Martin L., primary, Rode, Haridas B., additional, Heynck, Stefanie, additional, Peifer, Martin, additional, Fischer, Florian, additional, Klüter, Sabine, additional, Pawar, Vijaykumar G., additional, Reuter, Cecile, additional, Heuckmann, Johannes M., additional, Weiss, Jonathan, additional, Ruddigkeit, Lars, additional, Rabiller, Matthias, additional, Koker, Mirjam, additional, Simard, Jeffrey R., additional, Getlik, Matthäus, additional, Yuza, Yuki, additional, Chen, Tzu-Hsiu, additional, Greulich, Heidi, additional, Thomas, Roman K., additional, and Rauh, Daniel, additional

Published
2010
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37. PTEN Loss Contributes to Erlotinib Resistance in EGFR-Mutant Lung Cancer by Activation of Akt and EGFR

Author

Sos, Martin L., primary, Koker, Mirjam, additional, Weir, Barbara A., additional, Heynck, Stefanie, additional, Rabinovsky, Rosalia, additional, Zander, Thomas, additional, Seeger, Jens M., additional, Weiss, Jonathan, additional, Fischer, Florian, additional, Frommolt, Peter, additional, Michel, Kathrin, additional, Peifer, Martin, additional, Mermel, Craig, additional, Girard, Luc, additional, Peyton, Michael, additional, Gazdar, Adi F., additional, Minna, John D., additional, Garraway, Levi A., additional, Kashkar, Hamid, additional, Pao, William, additional, Meyerson, Matthew, additional, and Thomas, Roman K., additional

Published
2009
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39. Frequent and Focal FGFR1Amplification Associates with Therapeutically Tractable FGFR1 Dependency in Squamous Cell Lung Cancer

Author

Weiss, Jonathan, Sos, Martin L., Seidel, Danila, Peifer, Martin, Zander, Thomas, Heuckmann, Johannes M., Ullrich, Roland T., Menon, Roopika, Maier, Sebastian, Soltermann, Alex, Moch, Holger, Wagener, Patrick, Fischer, Florian, Heynck, Stefanie, Koker, Mirjam, Schöttle, Jakob, Leenders, Frauke, Gabler, Franziska, Dabow, Ines, Querings, Silvia, Heukamp, Lukas C., Balke-Want, Hyatt, Ansén, Sascha, Rauh, Daniel, Baessmann, Ingelore, Altmüller, Janine, Wainer, Zoe, Conron, Matthew, Wright, Gavin, Russell, Prudence, Solomon, Ben, Brambilla, Elisabeth, Brambilla, Christian, Lorimier, Philippe, Sollberg, Steinar, Brustugun, Odd Terje, Engel-Riedel, Walburga, Ludwig, Corinna, Petersen, Iver, Sänger, Jörg, Clement, Joachim, Groen, Harry, Timens, Wim, Sietsma, Hannie, Thunnissen, Erik, Smit, Egbert, Heideman, Daniëlle, Cappuzzo, Federico, Ligorio, Claudia, Damiani, Stefania, Hallek, Michael, Beroukhim, Rameen, Pao, William, Klebl, Bert, Baumann, Matthias, Buettner, Reinhard, Ernestus, Karen, Stoelben, Erich, Wolf, Jürgen, Nürnberg, Peter, Perner, Sven, and Thomas, Roman K.

Abstract

FGFR1amplification provides a therapeutic target for squamous cell lung cancer, which is resistant to other targeted lung cancer drugs.

Published
2010
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