Heidi Greulich

Summary

Publications

  1. pmc Functional analysis of receptor tyrosine kinase mutations in lung cancer identifies oncogenic extracellular domain mutations of ERBB2
    Heidi Greulich
    Department of Medical Oncology, Center for Cancer Genome Discovery, and Cancer Biology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 109:14476-81. 2012
  2. doi request reprint Targeting mutant fibroblast growth factor receptors in cancer
    Heidi Greulich
    Dana Farber Cancer Institute, Boston, MA 02115, USA
    Trends Mol Med 17:283-92. 2011
  3. ncbi request reprint Allele-dependent variation in the relative cellular potency of distinct EGFR inhibitors
    Yuki Yuza
    Department of Medical Oncology, Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Cancer Biol Ther 6:661-7. 2007
  4. doi request reprint Modeling genomic diversity and tumor dependency in malignant melanoma
    William M Lin
    Department of Medical Oncology, Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 68:664-73. 2008
  5. pmc The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP
    Cai Hong Yun
    Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 105:2070-5. 2008
  6. ncbi request reprint Signal transducer and activator of transcription 3 is required for the oncogenic effects of non-small-cell lung cancer-associated mutations of the epidermal growth factor receptor
    James V Alvarez
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 66:3162-8. 2006
  7. pmc Hsp90 inhibition suppresses mutant EGFR-T790M signaling and overcomes kinase inhibitor resistance
    Takeshi Shimamura
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215, USA
    Cancer Res 68:5827-38. 2008
  8. pmc HER2YVMA drives rapid development of adenosquamous lung tumors in mice that are sensitive to BIBW2992 and rapamycin combination therapy
    Samanthi A Perera
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 106:474-9. 2009
  9. pmc Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivity
    Cai Hong Yun
    Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, MA 02115, USA
    Cancer Cell 11:217-27. 2007
  10. pmc Activating mutations in ALK provide a therapeutic target in neuroblastoma
    Rani E George
    Department of Pediatric Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 455:975-8. 2008

Detail Information

Publications31

  1. pmc Functional analysis of receptor tyrosine kinase mutations in lung cancer identifies oncogenic extracellular domain mutations of ERBB2
    Heidi Greulich
    Department of Medical Oncology, Center for Cancer Genome Discovery, and Cancer Biology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 109:14476-81. 2012
    ....
  2. doi request reprint Targeting mutant fibroblast growth factor receptors in cancer
    Heidi Greulich
    Dana Farber Cancer Institute, Boston, MA 02115, USA
    Trends Mol Med 17:283-92. 2011
    ....
  3. ncbi request reprint Allele-dependent variation in the relative cellular potency of distinct EGFR inhibitors
    Yuki Yuza
    Department of Medical Oncology, Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Cancer Biol Ther 6:661-7. 2007
    ..More broadly, these results imply that the development and deployment of targeted therapies should focus on inhibition of specific cancer-causing mutations, not only on the mutated target...
  4. doi request reprint Modeling genomic diversity and tumor dependency in malignant melanoma
    William M Lin
    Department of Medical Oncology, Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 68:664-73. 2008
    ..Genetically defined cell culture collections therefore offer a rich framework for systematic functional studies in melanoma and other tumors...
  5. pmc The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP
    Cai Hong Yun
    Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 105:2070-5. 2008
    ....
  6. ncbi request reprint Signal transducer and activator of transcription 3 is required for the oncogenic effects of non-small-cell lung cancer-associated mutations of the epidermal growth factor receptor
    James V Alvarez
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 66:3162-8. 2006
    ..Thus, STAT3 is a critical mediator of the oncogenic effects of somatic EGFR mutations and targeting STAT3 may be an effective strategy for treating tumors characterized by these mutations...
  7. pmc Hsp90 inhibition suppresses mutant EGFR-T790M signaling and overcomes kinase inhibitor resistance
    Takeshi Shimamura
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215, USA
    Cancer Res 68:5827-38. 2008
    ..Nonetheless, these findings suggest that Hsp90 inhibitors may be effective in T790M-expressing cells and offer an alternative therapeutic strategy for this subset of lung cancers...
  8. pmc HER2YVMA drives rapid development of adenosquamous lung tumors in mice that are sensitive to BIBW2992 and rapamycin combination therapy
    Samanthi A Perera
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 106:474-9. 2009
    ..Based on these findings, clinical testing of the BIBW2992/rapamycin combination in non-small cell lung cancer patients with tumors expressing HER2 mutations is warranted...
  9. pmc Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivity
    Cai Hong Yun
    Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, MA 02115, USA
    Cancer Cell 11:217-27. 2007
    ..Strikingly, direct binding measurements show that gefitinib binds 20-fold more tightly to the L858R mutant than to the wild-type enzyme...
  10. pmc Activating mutations in ALK provide a therapeutic target in neuroblastoma
    Rani E George
    Department of Pediatric Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 455:975-8. 2008
    ....
  11. ncbi request reprint Non-small-cell lung cancer and Ba/F3 transformed cells harboring the ERBB2 G776insV_G/C mutation are sensitive to the dual-specific epidermal growth factor receptor and ERBB2 inhibitor HKI-272
    Takeshi Shimamura
    Department of Medical Oncology and Lowe Center for Thoracic Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    Cancer Res 66:6487-91. 2006
    ..Thus, the subset of NSCLC patients with tumors carrying the ERBB2 G776insV_G/C mutation may benefit from treatment with HKI-272...
  12. pmc Mutations in the DDR2 kinase gene identify a novel therapeutic target in squamous cell lung cancer
    Peter S Hammerman
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Cancer Discov 1:78-89. 2011
    ..As dasatinib is already approved for use, these findings could be rapidly translated into clinical trials...
  13. pmc Characterizing the cancer genome in lung adenocarcinoma
    Barbara A Weir
    Department of Medical Oncology and Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nature 450:893-8. 2007
    ..More generally, our results indicate that many of the genes that are involved in lung adenocarcinoma remain to be discovered...
  14. ncbi request reprint Epidermal growth factor-independent transformation of Ba/F3 cells with cancer-derived epidermal growth factor receptor mutants induces gefitinib-sensitive cell cycle progression
    Jingrui Jiang
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 65:8968-74. 2005
    ..Our results provide a model system to study the function of mutated EGFR and the differential effects of pharmacologic EGFR inhibition on the distinct mutant forms of this tyrosine kinase...
  15. pmc Inhibitor-sensitive FGFR1 amplification in human non-small cell lung cancer
    Amit Dutt
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
    PLoS ONE 6:e20351. 2011
    ..Although there are multiple genomically targeted therapies for lung adenocarcinoma, none has yet been reported in squamous cell lung carcinoma...
  16. pmc Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutants
    Heidi Greulich
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
    PLoS Med 2:e313. 2005
    ..The presence of mutations correlates with tumor sensitivity to the EGFR inhibitors erlotinib and gefitinib, but the transforming potential of specific mutations and their relationship to drug sensitivity have not been described...
  17. pmc Drug-sensitive FGFR2 mutations in endometrial carcinoma
    Amit Dutt
    Department of Medical Oncology and Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 105:8713-7. 2008
    ..Inhibition of FGFR2 kinase activity in endometrial carcinoma cell lines bearing such FGFR2 mutations inhibits transformation and survival, implicating FGFR2 as a novel therapeutic target in endometrial carcinoma...
  18. pmc SNP panel identification assay (SPIA): a genetic-based assay for the identification of cell lines
    Francesca Demichelis
    Department of Pathology, Brigham and Women s Hospital, Boston, MA, USA
    Nucleic Acids Res 36:2446-56. 2008
    ....
  19. pmc Loss of the epigenetic tumor suppressor SNF5 leads to cancer without genomic instability
    Elizabeth S McKenna
    Department of Pediatric Oncology, Dana Farber Cancer Institute, Division of Hematology Oncology, Children s Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA
    Mol Cell Biol 28:6223-33. 2008
    ....
  20. ncbi request reprint Sensitive mutation detection in heterogeneous cancer specimens by massively parallel picoliter reactor sequencing
    Roman K Thomas
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
    Nat Med 12:852-5. 2006
    ..This technology can thereby facilitate accurate molecular diagnosis of heterogeneous cancer specimens and enable patient selection for targeted cancer therapies...
  21. pmc Integrative genomic analysis of medulloblastoma identifies a molecular subgroup that drives poor clinical outcome
    Yoon Jae Cho
    Children s Hospital Boston, Boston, MA 02115, USA
    J Clin Oncol 29:1424-30. 2011
    ....
  22. pmc The kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor
    Susanne Schlisio
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Genes Dev 22:884-93. 2008
    ....
  23. pmc An activated ErbB3/NRG1 autocrine loop supports in vivo proliferation in ovarian cancer cells
    Qing Sheng
    Department of Cancer Biology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Cell 17:298-310. 2010
    ..Furthermore, a monoclonal ErbB3-directed antibody (MM-121) also significantly inhibited tumor growth in vivo. These findings identify ErbB3 as a potential therapeutic target in ovarian cancer...
  24. ncbi request reprint High-throughput oncogene mutation profiling in human cancer
    Roman K Thomas
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
    Nat Genet 39:347-51. 2007
    ..These results offer a new dimension in tumor genetics, where mutations involving multiple cancer genes may be interrogated simultaneously and in 'real time' to guide cancer classification and rational therapeutic intervention...
  25. ncbi request reprint EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy
    J Guillermo Paez
    Departments of Medical Oncology and Cancer Biology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Science 304:1497-500. 2004
    ..These results suggest that EGFR mutations may predict sensitivity to gefitinib...
  26. pmc Subtype-specific genomic alterations define new targets for soft-tissue sarcoma therapy
    Jordi Barretina
    Department of Medical Oncology, Harvard Medical School, Boston, Massachusetts, USA
    Nat Genet 42:715-21. 2010
    ..Our study yields a detailed map of molecular alterations across diverse sarcoma subtypes and suggests potential subtype-specific targets for therapy...
  27. pmc Probing the cancer genome
    Heidi Greulich
    Dana Farber Cancer Institute, Binney St, Boston, MA 02115, and Broad Institute of MIT and Harvard, Cambridge Center, Cambridge, MA 02142, USA
    Genome Biol 9:309. 2008
  28. ncbi request reprint SOS1 mutations are rare in human malignancies: implications for Noonan Syndrome patients
    Kenneth D Swanson
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, Massachusetts, USA
    Genes Chromosomes Cancer 47:253-9. 2008
    ..Our findings suggest that SOS1 is not a significant human oncogene in most cancers. Furthermore, NS patients with SOS1 mutations may not be at increased risk of developing cancer...
  29. ncbi request reprint Integrative genomic approaches identify IKBKE as a breast cancer oncogene
    Jesse S Boehm
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cell 129:1065-79. 2007
    ..These observations suggest a mechanism for NF-kappaB activation in breast cancer, implicate the NF-kappaB pathway as a downstream mediator of PI3K, and provide a framework for integrated genomic approaches in oncogene discovery...
  30. pmc Activating Mutations in ERBB2 and Their Impact on Diagnostics and Treatment
    Grit S Herter-Sprie
    Department of Medical Oncology, Dana Farber Cancer Institute Boston, MA, USA Department of Medicine, Harvard Medical School Boston, MA, USA
    Front Oncol 3:86. 2013
    ..We will additionally discuss the current preclinical and clinical therapeutic strategies for targeting mutationally activated ERBB2...
  31. pmc Mapping the hallmarks of lung adenocarcinoma with massively parallel sequencing
    Marcin Imielinski
    Broad Institute of Harvard and MIT, 7 Cambridge Center, Cambridge, MA 02142, USA
    Cell 150:1107-20. 2012
    ..The candidate genes identified in this study are attractive targets for biological characterization and therapeutic targeting of lung adenocarcinoma...