Research Topics
| M MeyersonSummaryAffiliation: Harvard University Country: USA Publications
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Publications
Homozygous deletions and chromosome amplifications in human lung carcinomas revealed by single nucleotide polymorphism array analysisXiaojun 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...
Inferring loss-of-heterozygosity from unpaired tumors using high-density oligonucleotide SNP arraysRameen 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...- Characterizing the cancer genome in lung adenocarcinomaBarbara 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... - A novel totivirus and piscine reovirus (PRV) in Atlantic salmon (Salmo salar) with cardiomyopathy syndrome (CMS)Marie Løvoll
Section for Virology and Serology, National Veterinary Institute, P, O, Box 750 Sentrum, 0106 Oslo, Norway
Virol J 7:309. 2010..In the present work we have studied whether PRV or other infectious agents may be involved in the etiology of CMS... - GISTIC2.0 facilitates sensitive and confident localization of the targets of focal somatic copy-number alteration in human cancersCraig H Mermel
Cancer Program, The Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, MA 02142, USA
Genome Biol 12:R41. 2011..Here we detail this revised computational approach, GISTIC2.0, and validate its performance in real and simulated datasets... - Major copy proportion analysis of tumor samples using SNP arraysCheng 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... - Telomerase enzyme activation and human cell immortalizationM Meyerson
Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Toxicol Lett 102:41-5. 1998..In contrast, disruption of the mouse telomerase RNA subunit gene, mTERC, results in a delayed failure of cell proliferation. Telomerase activity therefore appears to be necessary for the prolonged survival of mammalian cells... 
Advances in understanding cancer genomes through second-generation sequencingMatthew Meyerson
Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Nat Rev Genet 11:685-96. 2010..This Review focuses on the methodological considerations for characterizing somatic genome alterations in cancer and the future prospects for these approaches...- Human genetic variation and diseaseMatthew Meyerson
Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Lancet 362:259-60. 2003 - Role of telomerase in normal and cancer cellsM Meyerson
Department of Adult Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
J Clin Oncol 18:2626-34. 2000..Moreover, data on the experimental use of telomerase assays for cancer detection and diagnosis are reviewed. Finally, the review considers the evidence regarding whether telomerase inhibitors could be used to treat human cancers... - Transcriptional profiling identifies cyclin D1 as a critical downstream effector of mutant epidermal growth factor receptor signalingSusumu Kobayashi
Division of Hematology/Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
Cancer Res 66:11389-98. 2006..These studies suggest that cyclin D1 may contribute to the emergence of EGFR-driven tumorigenesis and can be an alternative target of therapy... - Genome coverage and sequence fidelity of phi29 polymerase-based multiple strand displacement whole genome amplificationJ Guillermo Paez
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA
Nucleic Acids Res 32:e71. 2004..These results suggest that phi29MDA yields high fidelity, near-complete genome representation suitable for high resolution genetic analysis... - Allele-specific amplification in cancer revealed by SNP array analysisThomas LaFramboise
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America
PLoS Comput Biol 1:e65. 2005..An R software package containing the methods described in this paper is freely available at http://genome.dfci.harvard.edu/~tlaframb/PLASQ... - High-resolution single-nucleotide polymorphism array and clustering analysis of loss of heterozygosity in human lung cancer cell linesPasi A Janne
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Oncogene 23:2716-26. 2004..Using this array, we identified small regions of LOH that were not detected by lower density SNP arrays or by standard microsatellite marker panels... - EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapyJ 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... - Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutantsHeidi 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... - Genome-wide loss of heterozygosity analysis from laser capture microdissected prostate cancer using single nucleotide polymorphic allele (SNP) arrays and a novel bioinformatics platform dChipSNPMarshall E Lieberfarb
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Res 63:4781-5. 2003..This organizational strategy revealed apparently distinct genetic subsets of prostate cancer... - EGFR mutation and resistance of non-small-cell lung cancer to gefitinibSusumu Kobayashi
Division of Hematology Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA
N Engl J Med 352:786-92. 2005..Structural modeling and biochemical studies showed that this second mutation led to gefitinib resistance... - Activating mutations in ALK provide a therapeutic target in neuroblastomaRani E George
Department of Pediatric Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 455:975-8. 2008.... - Modeling genomic diversity and tumor dependency in malignant melanomaWilliam 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... - Exon 19 deletion mutations of epidermal growth factor receptor are associated with prolonged survival in non-small cell lung cancer patients treated with gefitinib or erlotinibDavid M Jackman
Lowe Center of Thoracic Oncology, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Clin Cancer Res 12:3908-14. 2006..Our study explored the relationship between the two most common types of somatic EGFR mutations, exon 19 deletions and the L858R point mutation, and outcomes of patients following treatment with gefitinib or erlotinib... - Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1David A Barbie
Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115 USA
Nature 462:108-12. 2009..These observations indicate that TBK1 and NF-kappaB signalling are essential in KRAS mutant tumours, and establish a general approach for the rational identification of co-dependent pathways in cancer... - Cancer genomes evolve by pulverizing single chromosomesMatthew Meyerson
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115 Department of Pathology, Harvard Medical School, Boston, MA 02115 Broad Institute, Cambridge, MA 02142
Cell 144:9-10. 2011..Chromothripsis appears to be a cataclysmic event in which a single chromosome is fragmented and then reassembled. The phenomenon raises important questions of how chromosome rearrangements can be confined to defined genome segments... - An integrated view of copy number and allelic alterations in the cancer genome using single nucleotide polymorphism arraysXiaojun Zhao
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Res 64:3060-71. 2004..The simultaneous measurement of DNA copy number changes and loss of heterozygosity events by SNP arrays should strengthen our ability to discover cancer-causing genes and to refine cancer diagnosis... - Allele-dependent variation in the relative cellular potency of distinct EGFR inhibitorsYuki 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... - A rapid and sensitive enzymatic method for epidermal growth factor receptor mutation screeningPasi A Janne
Lowe Center for Thoracic Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Clin Cancer Res 12:751-8. 2006..Here we describe the use of a sensitive screening method that overcomes many of these limitations... - Hsp90 inhibition suppresses mutant EGFR-T790M signaling and overcomes kinase inhibitor resistanceTakeshi 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... - Phase II clinical trial of chemotherapy-naive patients > or = 70 years of age treated with erlotinib for advanced non-small-cell lung cancerDavid M Jackman
Dana Farber Cancer Institute, Boston, MA 02115, USA
J Clin Oncol 25:760-6. 2007..The secondary end points include radiographic response rate, time to progression (TTP), toxicity, and symptom improvement... - Genome-wide analysis of neuroblastomas using high-density single nucleotide polymorphism arraysRani E George
Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, United States of America
PLoS ONE 2:e255. 2007..We analyzed paired blood and primary tumor samples from 22 children with high-risk neuroblastoma for loss of heterozygosity (LOH) and DNA copy number change using the Affymetrix 10K single nucleotide polymorphism (SNP) array... - LKB1 modulates lung cancer differentiation and metastasisHongbin Ji
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Nature 448:807-10. 2007..These studies establish LKB1 as a critical barrier to pulmonary tumorigenesis, controlling initiation, differentiation and metastasis... - 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-272Takeshi 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... - Frequent HIN-1 promoter methylation and lack of expression in multiple human tumor typesIan Krop
Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, D740C, Boston, MA 02115, USA
Mol Cancer Res 2:489-94. 2004..Thus, silencing of HIN-1 expression and methylation of its promoter occurs in multiple human cancer types, suggesting that elimination of HIN-1 function may contribute to several forms of epithelial tumorigenesis... - Gefitinib induces apoptosis in the EGFRL858R non-small-cell lung cancer cell line H3255Sean Tracy
Lowe Center for Thoracic Oncology and Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Res 64:7241-4. 2004..These findings further characterize a mechanism by which gefitinib treatment of NSCLC harboring EGFR(L858R) leads to a dramatic response to gefitinib... - Activating mutations of the noonan syndrome-associated SHP2/PTPN11 gene in human solid tumors and adult acute myelogenous leukemiaMohamed Bentires-Alj
Cancer Biology Program, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
Cancer Res 64:8816-20. 2004..Our data demonstrate that mutations in PTPN11 occur at low frequency in several human cancers, especially neuroblastoma and AML, and suggest that Shp2 may be a novel target for antineoplastic therapy... - Patterns of gene expression and copy-number alterations in von-hippel lindau disease-associated and sporadic clear cell carcinoma of the kidneyRameen Beroukhim
Departments of Medical Oncology, Harvard Medical School, Boston, Massachusetts, USA
Cancer Res 69:4674-81. 2009.... - PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinibJeffrey A Engelman
Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA, USA
Cancer Res 67:11924-32. 2007..These preclinical evaluations support further clinical development of PF00299804 for cancers with mutations and/or amplifications of ERBB family members... - Epidermal growth factor-independent transformation of Ba/F3 cells with cancer-derived epidermal growth factor receptor mutants induces gefitinib-sensitive cell cycle progressionJingrui 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... - Loss of heterozygosity and its correlation with expression profiles in subclasses of invasive breast cancersZhigang C Wang
Departments of Surgery and Pathology, Brigham and Women's Hospital, Boston, MA 02115, USA
Cancer Res 64:64-71. 2004..Furthermore, exclusive association between biological subclasses and restricted LOH events provides rationale to search for targeted genes... - Epidermal growth factor receptor variant III mutations in lung tumorigenesis and sensitivity to tyrosine kinase inhibitorsHongbin Ji
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 103:7817-22. 2006..These findings suggest a therapeutic strategy for cancers harboring the EGFRvIII mutation... - Telomerase activation, cellular immortalization and cancerW C Hahn
Department of Adult Oncology, Dana Farber Cancer Institute and Brigham and Women s Hospital, Boston, MA 02115, USA
Ann Med 33:123-9. 2001..These applications include inhibiting or targeting telomerase as a novel antineoplastic strategy and using cells immortalized by telomerase for therapeutic applications... - SOS1 mutations are rare in human malignancies: implications for Noonan Syndrome patientsKenneth 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... - Lin28 promotes transformation and is associated with advanced human malignanciesSrinivas R Viswanathan
Children s Hospital Boston, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Harvard Stem Cell Institute, Boston, MA, USA
Nat Genet 41:843-8. 2009..Our work provides a mechanism for the coordinate repression of let-7 miRNAs observed in a subset of human cancers, and associates activation of LIN28 and LIN28B with poor clinical prognosis... - Amplification of chromosomal segment 4q12 in non-small cell lung cancerAlex H Ramos
Department of Medical Oncology and Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Boston, MA, USA
Cancer Biol Ther 8:2042-50. 2009..Together these observations implicate PDGFRA and KIT as potential oncogenes in NSCLC, but further study is needed to define the specific characteristics of those tumors that could respond to PDGFRalpha/KIT inhibitors... - CDK8 is a colorectal cancer oncogene that regulates beta-catenin activityRon Firestein
Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA
Nature 455:547-51. 2008..Together these observations suggest that therapeutic interventions targeting CDK8 may confer a clinical benefit in beta-catenin-driven malignancies... - Focal gains of VEGFA and molecular classification of hepatocellular carcinomaDerek Y Chiang
Department of Medical Oncology and Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Res 68:6779-88. 2008..Furthermore, the prevalence of VEGFA high-level gains in multiple tumor types suggests indications for clinical trials of antiangiogenic therapies... - 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 receptorJames 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... - Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivityCai 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... - Response to treatment and survival of patients with non-small cell lung cancer undergoing somatic EGFR mutation testingLecia V Sequist
Massachusetts General Hospital Cancer Center, Harvard Medical School Partners Healthcare Center for Genetics and Genomics, MGH Department of Pathology, Dana Farber Cancer Institute, Boston, Massachusetts 02114, USA
Oncologist 12:90-8. 2007..6 years in mutation-negative patients, after adjusting for age, gender, and stage at diagnosis. Integrating molecular profiling into clinical care is feasible in NSCLC patients and provides useful clinical information... - Genomic approaches to lung cancerRoman K Thomas
Department of Medical Oncology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
Clin Cancer Res 12:4384s-4391s. 2006..Taken together, the application of genomics technologies has led to important discoveries with clinical implications in lung cancer that might help to improve clinical care for patients suffering from this highly fatal tumor... - Integrative genomic approaches identify IKBKE as a breast cancer oncogeneJesse 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... - TSC1 loss synergizes with KRAS activation in lung cancer development in the mouse and confers rapamycin sensitivityM C Liang
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA, USA
Oncogene 29:1588-97. 2010..Rapamycin may have unique benefit for patients with lung cancer, for whom the TSC1/TSC2 function is limited... - Molecular classification and molecular genetics of human lung cancersMatthew Meyerson
Department of Medical Oncology, Dana-Farber Cancer Insitute, Boston, MA 02115, USA
Semin Oncol 31:4-19. 2004..These data may be useful in tailoring chemotherapeutic protocols to individual tumors and identifying new targets for therapeutic intervention... - Genomic representations using concatenates of Type IIB restriction endonuclease digestion fragmentsTorstein Tengs
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Nucleic Acids Res 32:e121. 2004..Here, we show that the RECORD libraries may be used for digital karyotyping and for pathogen identification by computational subtraction... - EML4-ALK fusion gene and efficacy of an ALK kinase inhibitor in lung cancerJussi P Koivunen
Lowe Center for Thoracic Oncology, Dana Farber Cancer Institute, D820A, 44 Binney Street, Boston, MA 02115, USA
Clin Cancer Res 14:4275-83. 2008..We determined the frequency of EML4-ALK in Caucasian NSCLC and in NSCLC cell lines. We also determined whether TAE684, a specific ALK kinase inhibitor, would inhibit the growth of EML4-ALK-containing cell lines in vitro and in vivo... - TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancerSven Perner
Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, EBRC 442A, 221 Longwood Avenue, Boston, MA 02115-6110, USA
Cancer Res 66:8337-41. 2006..The deletion as cause of TMPRSS2:ERG fusion is associated with clinical features for prostate cancer progression compared with tumors that lack the TMPRSS2:ERG rearrangement... - Missense mutations of the BRAF gene in human lung adenocarcinomaKatsuhiko Naoki
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Res 62:7001-3. 2002..These specimens belong to the same adenocarcinoma subgroup as defined by clustering of gene expression data. BRAF may provide a target for anticancer chemotherapy in a subset of lung adenocarcinoma patients... - The kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressorSusanne Schlisio
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Genes Dev 22:884-93. 2008.... - High-throughput oncogene mutation profiling in human cancerRoman 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... - Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosisRoss L Levine
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Cell 7:387-97. 2005..In vitro analysis demonstrated that JAK2V617F is a constitutively active tyrosine kinase... - A structure-guided approach to creating covalent FGFR inhibitorsWenjun Zhou
Department of Cancer Biology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Chem Biol 17:285-95. 2010..FIIN-1 is a useful probe of FGFR-dependent cellular phenomena and may provide a starting point of the development of therapeutically relevant irreversible inhibitors of wild-type and drug-resistant forms of FGFR kinases... - Identification of foreign gene sequences by transcript filtering against the human genomeGriffin Weber
Department of Adult Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA
Nat Genet 30:141-2. 2002..We demonstrate the potential of this method by identifying sequences from known pathogens in established expressed-sequence tag libraries... - Somatic alterations in the human cancer genomeBarbara Weir
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
Cancer Cell 6:433-8. 2004..With further development of targeted cancer therapies and improvement in genome analysis technology, genome-wide surveys of cancer will likely become tools for diagnosis as well as discovery... - HER2YVMA drives rapid development of adenosquamous lung tumors in mice that are sensitive to BIBW2992 and rapamycin combination therapySamanthi 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... - Phosphorylation of the menin tumor suppressor protein on serine 543 and serine 583Laura E MacConaill
Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
Mol Cancer Res 4:793-801. 2006..Chromatin immunoprecipitation experiments reveal that binding of menin to the Hoxc8 locus is not affected by phosphorylation on Ser543 or Ser583... - Sensitive mutation detection in heterogeneous cancer specimens by massively parallel picoliter reactor sequencingRoman 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... - The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATPCai 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.... - Drug-sensitive FGFR2 mutations in endometrial carcinomaAmit 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... - BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer modelsD Li
Department of Medical Oncology, Dana Farber Cancer Institute, MA, USA
Oncogene 27:4702-11. 2008..These findings encourage further testing of BIBW2992 in lung cancer patients harboring EGFR or HER2 oncogenes... - Identifying and characterizing a novel activating mutation of the FLT3 tyrosine kinase in AMLJingrui Jiang
Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney St, D720C, Boston, MA 02115, USA
Blood 104:1855-8. 2004..These results suggest that mutations at N841 represent a significant new activating mutation in patients with AML and that patients with such mutations may respond to small-molecule FLT3 inhibitors such as PKC412... - Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanomaLevi 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...
Research Grants
- Inhibitor-sensitive and -resistant EGFR mutants from lung cancer and glioblastomaMatthew L Meyerson; Fiscal Year: 2010..Specific Aim 4. Determine whether cancer-derived point mutations in the extracellular domain of EGFR are transforming and whether these mutants can be inhibited by small molecule kinase inhibitors. ..
- Center for Cancer Genome CharacterizationMatthew Meyerson; Fiscal Year: 2007..3) Cross-validate, integrate, and analyze CGCC data to determine regions of genome alteration for high-throughput sequencing. (4) Rapidly share data with the cancer research community. ..
- Elucidating the somatic genetics of prostate cancerMatthew Meyerson; Fiscal Year: 2007..4. To begin the functional validation of selected candidate tumor suppressor and oncogenes identified in aims 1 through 3. ..
- Inhibitor-sensitive and -resistant EGFR mutants from lung cancer and glioblastomaMatthew Meyerson; Fiscal Year: 2007..Specific Aim 4. Determine whether cancer-derived point mutations in the extracellular domain of EGFR are transforming and whether these mutants can be inhibited by small molecule kinase inhibitors. ..
- Cancer Virus Discovery by Computational SubtractionMatthew Meyerson; Fiscal Year: 2005..These include auto-immune diseases and inflammatory diseases, as well as uncharacterized epidemics, whether natural or bio-terrorist in origin. ..
- NKX2-1, A Candidate Lineage Survival Oncogene in Lung AdenocarcinomaMatthew L Meyerson; Fiscal Year: 2010..Our hope is that this understanding will lead to improved diagnosis and treatment of lung adenocarcinoma. ..