Levi Garraway

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Malignant melanoma: genetics and therapeutics in the genomic era
    Lynda Chin
    Melanoma Program, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Genes Dev 20:2149-82. 2006
  2. 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
  3. ncbi request reprint From integrated genomics to tumor lineage dependency
    Levi A Garraway
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 66:2506-8. 2006
  4. pmc Profiling critical cancer gene mutations in clinical tumor samples
    Laura E MacConaill
    Center for Cancer Genome Discovery, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA
    PLoS ONE 4:e7887. 2009
  5. pmc COT drives resistance to RAF inhibition through MAP kinase pathway reactivation
    Cory M Johannessen
    Broad Institute of Harvard and Massachusetts Institute of Technology, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA
    Nature 468:968-72. 2010
  6. pmc The genomic landscape of prostate cancer
    Sylvan C Baca
    Harvard Medical School, Boston, MA, USA
    Front Endocrinol (Lausanne) 3:69. 2012
  7. pmc The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity
    Jordi Barretina
    The Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA
    Nature 483:603-7. 2012
  8. doi request reprint Genomics-driven oncology: framework for an emerging paradigm
    Levi A Garraway
    Dana Farber Cancer Institute, 450 Brookline Ave, Boston, MA 02215, USA
    J Clin Oncol 31:1806-14. 2013
  9. doi request reprint Whole-genome sequencing and cancer therapy: is too much ever enough?
    Levi A Garraway
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02215, USA
    Cancer Discov 2:766-8. 2012
  10. pmc Targeted next-generation sequencing of a cancer transcriptome enhances detection of sequence variants and novel fusion transcripts
    Joshua Z Levin
    Genome Sequencing and Analysis Program, Broad Institute of MIT and Harvard, 320 Charles Street, Cambridge, MA 02141, USA
    Genome Biol 10:R115. 2009

Detail Information

Publications37

  1. ncbi request reprint Malignant melanoma: genetics and therapeutics in the genomic era
    Lynda Chin
    Melanoma Program, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Genes Dev 20:2149-82. 2006
    ..In addition, we look forward toward how these new insights will impact on therapeutic options for metastatic melanoma in the near future...
  2. 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...
  3. ncbi request reprint From integrated genomics to tumor lineage dependency
    Levi A Garraway
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 66:2506-8. 2006
    ..Similar combined genomic approaches may be useful in other cancer types to learn how critical regulators of tumor lineage are linked to genomic alterations in cancer cells...
  4. pmc Profiling critical cancer gene mutations in clinical tumor samples
    Laura E MacConaill
    Center for Cancer Genome Discovery, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA
    PLoS ONE 4:e7887. 2009
    ..We report the implementation of a genotyping and validation algorithm that enables robust tumor mutation profiling in the clinical setting...
  5. pmc COT drives resistance to RAF inhibition through MAP kinase pathway reactivation
    Cory M Johannessen
    Broad Institute of Harvard and Massachusetts Institute of Technology, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA
    Nature 468:968-72. 2010
    ....
  6. pmc The genomic landscape of prostate cancer
    Sylvan C Baca
    Harvard Medical School, Boston, MA, USA
    Front Endocrinol (Lausanne) 3:69. 2012
    ..The widespread application of massively parallel sequencing technology to the analysis of prostate cancer genomes should continue to advance both discovery-oriented and diagnostic avenues...
  7. pmc The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity
    Jordi Barretina
    The Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA
    Nature 483:603-7. 2012
    ..The generation of genetic predictions of drug response in the preclinical setting and their incorporation into cancer clinical trial design could speed the emergence of 'personalized' therapeutic regimens...
  8. doi request reprint Genomics-driven oncology: framework for an emerging paradigm
    Levi A Garraway
    Dana Farber Cancer Institute, 450 Brookline Ave, Boston, MA 02215, USA
    J Clin Oncol 31:1806-14. 2013
    ..The results of these efforts and the rigor with which they are implemented will determine whether and how comprehensive tumor genomic information may become incorporated into the routine care of patients with cancer...
  9. doi request reprint Whole-genome sequencing and cancer therapy: is too much ever enough?
    Levi A Garraway
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02215, USA
    Cancer Discov 2:766-8. 2012
    ..This finding highlights the growing debate surrounding the optimal deployment of powerful new genomics technologies in the clinical oncology arena...
  10. pmc Targeted next-generation sequencing of a cancer transcriptome enhances detection of sequence variants and novel fusion transcripts
    Joshua Z Levin
    Genome Sequencing and Analysis Program, Broad Institute of MIT and Harvard, 320 Charles Street, Cambridge, MA 02141, USA
    Genome Biol 10:R115. 2009
    ..Thus, targeted RNA-Seq produces an enhanced view of the molecular state of a set of "high interest" genes...
  11. pmc Major copy proportion analysis of tumor samples using SNP arrays
    Cheng Li
    Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute and Harvard School of Public Health, 3 Blackfan Circle, Boston, MA 02115, USA
    BMC Bioinformatics 9:204. 2008
    ..We have previously used Hidden Markov Models (HMM) to analyze SNP array data for inferring copy numbers and loss-of-heterozygosity (LOH) from paired normal and tumor samples and unpaired tumor samples...
  12. ncbi request reprint On or off target: mutations, models, and predictions
    Levi A Garraway
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Sci Transl Med 2:35ps28. 2010
    ..In this issue of Science Translational Medicine, Whittaker et al. describe research that reconciles some of the bewildering aspects of the discovery and development of drugs that inhibit such protein kinase targets in cancer...
  13. ncbi request reprint Lineage dependency and lineage-survival oncogenes in human cancer
    Levi A Garraway
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nat Rev Cancer 6:593-602. 2006
    ..MITF and other lineage-survival genes therefore implicate lineage dependency (or lineage addiction) as a newly recognized mechanism that is affected by tumour genetic alterations...
  14. pmc RAS mutations are associated with the development of cutaneous squamous cell tumors in patients treated with RAF inhibitors
    Patrick A Oberholzer
    Broad Institute of Massachusetts Institute of Technology, Cambridge, USA
    J Clin Oncol 30:316-21. 2012
    ..The potential of these agents to promote secondary malignancies is concerning. We analyzed cSCC and KA lesions for genetic mutations in an attempt to identify an underlying mechanism for their formation...
  15. pmc Clinical implications of the cancer genome
    Laura E MacConaill
    Center for Cancer Genome Discovery, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA, USA
    J Clin Oncol 28:5219-28. 2010
    ..We also discuss how the convergence of cancer genome biology, technology, and targeted therapeutics articulates a cohesive framework for the advent of personalized cancer medicine...
  16. ncbi request reprint Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma
    Levi A Garraway
    Department of Medical Oncology, and Melanoma Program in Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA
    Nature 436:117-22. 2005
    ..Together, these data suggest that MITF represents a distinct class of 'lineage survival' or 'lineage addiction' oncogenes required for both tissue-specific cancer development and tumour progression...
  17. 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
    ....
  18. pmc An oncogenic role for ETV1 in melanoma
    Judit Jane-Valbuena
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Res 70:2075-84. 2010
    ..These observations implicate deregulated ETV1 in melanoma genesis and suggest a pivotal lineage dependency mediated by oncogenic ETS transcription factors in this malignancy...
  19. 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...
  20. pmc MEK1 mutations confer resistance to MEK and B-RAF inhibition
    Caroline M Emery
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 106:20411-6. 2009
    ..These results affirm the importance of MEK dependency in BRAF-mutant melanoma and suggest novel mechanisms of resistance to MEK and B-RAF inhibitors that may have important clinical implications...
  21. pmc High-throughput genotyping in osteosarcoma identifies multiple mutations in phosphoinositide-3-kinase and other oncogenes
    Edwin Choy
    Division of Hematology Oncology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    Cancer 118:2905-14. 2012
    ..The identification of new genes that are mutated in osteosarcomas is critical to developing a better understanding of the molecular pathogenesis of this disease and discovering new targets for therapeutic development...
  22. pmc Nuclear factor I/B is an oncogene in small cell lung cancer
    Alison L Dooley
    David H Koch Institute for Integrative Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, USA
    Genes Dev 25:1470-5. 2011
    ..Functional studies indicate that NFIB regulates cell viability and proliferation during transformation...
  23. pmc Attitudes of patients with cancer about personalized medicine and somatic genetic testing
    Stacy W Gray
    Center for Population Sciences, Department of Medical Oncology, Dana Farber Cancer Institute, 450 Brookline Ave, LW 633, Boston, MA 02215, USA
    J Oncol Pract 8:329-35, 2 p following 335. 2012
    ..Dramatic advances in genomic technology stand to revolutionize cancer care; however, little is known about patients' understanding and acceptance of personalized medicine and widespread genetic testing (GT)...
  24. pmc Inferring loss-of-heterozygosity from unpaired tumors using high-density oligonucleotide SNP arrays
    Rameen Beroukhim
    Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    PLoS Comput Biol 2:e41. 2006
    ..We have developed a method for analyzing high-density oligonucleotide SNP array data to accurately identify of regions of LOH and retention in tumors without the need for paired normal samples...
  25. ncbi request reprint Homozygous deletions and chromosome amplifications in human lung carcinomas revealed by single nucleotide polymorphism array analysis
    Xiaojun Zhao
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 65:5561-70. 2005
    ..EGFR amplification was shown to be independent of kinase domain mutational status...
  26. pmc AKT-independent signaling downstream of oncogenic PIK3CA mutations in human cancer
    Krishna M Vasudevan
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 16:21-32. 2009
    ..Thus, PI3K may promote cancer through both AKT-dependent and AKT-independent mechanisms. Knowledge of differential PI3K/PDK1 signaling could inform rational therapeutics in cancers harboring PIK3CA mutations...
  27. 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...
  28. 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...
  29. pmc Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling
    Nikhil Wagle
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney St, D1542, Boston, MA, USA
    J Clin Oncol 29:3085-96. 2011
    ..These results provide an instructive framework for assessing mechanisms of acquired resistance to kinase inhibition and illustrate the use of emerging technologies in a manner that may accelerate personalized cancer medicine...
  30. ncbi request reprint Androgen-dependent regulation of Her-2/neu in prostate cancer cells
    Raanan Berger
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Cancer Res 66:5723-8. 2006
    ..These data provide the biochemical rationale to target Her-2/neu in hormone-refractory prostate cancer...
  31. ncbi request reprint Mutations in BRAF and KRAS converge on activation of the mitogen-activated protein kinase pathway in lung cancer mouse models
    Hongbin Ji
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 67:4933-9. 2007
    ..These results unveil a potential common vulnerability of BRAF and KRas mutant lung tumors that potentially affects rational deployment of MEK targeted therapies to non-small-cell lung cancer patients...
  32. 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...
  33. ncbi request reprint A 2-Mb critical region implicated in the microcephaly associated with terminal 1q deletion syndrome
    Anthony D Hill
    Howard Hughes Medical Institute, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    Am J Med Genet A 143:1692-8. 2007
    ..0-Mb microcephaly critical region including the 1q43-1q44 boundary and no more than 11 genes...
  34. pmc Recurrent BRAF mutations in Langerhans cell histiocytosis
    Gayane Badalian-Very
    Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
    Blood 116:1919-23. 2010
    ..High prevalence, recurrent BRAF mutations in LCH indicate that it is a neoplastic disease that may respond to RAF pathway inhibitors...
  35. ncbi request reprint Intermediate basal cells of the prostate: in vitro and in vivo characterization
    Levi A Garraway
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Prostate 55:206-18. 2003
    ..Progenitor cells within the prostate basal layer may play important roles in differentiation and carcinogenesis; however, prostate stem cell populations remain uncharacterized...
  36. pmc Assessing the significance of chromosomal aberrations in cancer: methodology and application to glioma
    Rameen Beroukhim
    Broad Institute, Massachusetts Institute of Technology and Harvard University, 7 Cambridge Center, Cambridge, MA 02142, USA
    Proc Natl Acad Sci U S A 104:20007-12. 2007
    ..Our results support the feasibility and utility of systematic characterization of the cancer genome...
  37. pmc BRAF mutation predicts sensitivity to MEK inhibition
    David B Solit
    Department of Medicine, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
    Nature 439:358-62. 2006
    ..These data suggest an exquisite dependency on MEK activity in BRAF mutant tumours, and offer a rational therapeutic strategy for this genetically defined tumour subtype...

Research Grants5

  1. FUNCTIONAL ANALYSIS OF THE PTEN TUMOR SUPPRESSOR PROTEIN
    Levi Garraway; Fiscal Year: 2005
    ..Based on this data we propose in specific aims 2 and 3: 2. To generate antibody reagents that selectively recognizes unphosphorylated PTEN. 3. To purify and identify proteins in the PTEN associated complex (PAC). ..
  2. FUNCTIONAL ANALYSIS OF THE PTEN TUMOR SUPPRESSOR PROTEIN
    Levi Garraway; Fiscal Year: 2006
    ..Based on this data we propose in specific aims 2 and 3: 2. To generate antibody reagents that selectively recognizes unphosphorylated PTEN. 3. To purify and identify proteins in the PTEN associated complex (PAC). ..
  3. FUNCTIONAL ANALYSIS OF THE PTEN TUMOR SUPPRESSOR PROTEIN
    Levi Garraway; Fiscal Year: 2007
    ..Based on this data we propose in specific aims 2 and 3: 2. To generate antibody reagents that selectively recognizes unphosphorylated PTEN. 3. To purify and identify proteins in the PTEN associated complex (PAC). ..
  4. FUNCTIONAL ANALYSIS OF THE PTEN TUMOR SUPPRESSOR PROTEIN
    Levi Garraway; Fiscal Year: 2009
    ..Based on this data we propose in specific aims 2 and 3: 2. To generate antibody reagents that selectively recognizes unphosphorylated PTEN. 3. To purify and identify proteins in the PTEN associated complex (PAC). ..