Research Topics
Genomes and Genes
| Daphne W BellSummaryAffiliation: National Institutes of Health Country: USA Publications
| Collaborators
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Detail Information
Publications
Our changing view of the genomic landscape of cancerDaphne W Bell
National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA
J Pathol 220:231-43. 2010....- Predisposition to cancer caused by genetic and functional defects of mammalian Atad5Daphne W Bell
Cancer Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America
PLoS Genet 7:e1002245. 2011..Taken together, our findings indicate that loss-of-function mutations in mammalian Atad5 are sufficient to cause genomic instability and tumorigenesis... - Genetic and functional analysis of CHEK2 (CHK2) variants in multiethnic cohortsDaphne W Bell
Massachusetts General Hospital Cancer Center, Charlestown, MA, USA
Int J Cancer 121:2661-7. 2007.... - Prevalence and functional analysis of sequence variants in the ATR checkpoint mediator ClaspinJianmin Zhang
Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA
Mol Cancer Res 7:1510-6. 2009.... - Oncogenic activity of epidermal growth factor receptor kinase mutant alleles is enhanced by the T790M drug resistance mutationNadia Godin-Heymann
Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA
Cancer Res 67:7319-26. 2007.... - Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752Gromoslaw A Smolen
Cancer Center and Department of Pathology, Molecular Pathology Research Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
Proc Natl Acad Sci U S A 103:2316-21. 2006..MET amplification may thus identify a subset of epithelial cancers that are uniquely sensitive to disruption of this pathway and define a patient group that is appropriate for clinical trials of targeted therapy using MET inhibitors... 
Molecular predictors of response to epidermal growth factor receptor antagonists in non-small-cell lung cancerLecia V Sequist
Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA
J Clin Oncol 25:587-95. 2007....- Epidermal growth factor receptor mutations and gene amplification in non-small-cell lung cancer: molecular analysis of the IDEAL/INTACT gefitinib trialsDaphne W Bell
Massachusetts General Hospital Cancer Center and Department of Pathology, Harvard Medical School, Charlestown, MA 02129, USA
J Clin Oncol 23:8081-92. 2005..The combination of gefitinib with chemotherapy does not improve survival in patients with these molecular markers... - Inherited susceptibility to lung cancer may be associated with the T790M drug resistance mutation in EGFRDaphne W Bell
Massachusetts General Hospital Cancer Center, Harvard Medical School, 13th Street, Charlestown, Massachusetts 02129, USA
Nat Genet 37:1315-6. 2005..Four of six tumors analyzed showed a secondary somatic activating EGFR mutation, arising in cis with the germline EGFR mutation T790M. These observations implicate altered EGFR signaling in genetic susceptibility to lung cancer... - Increased prevalence of EGFR-mutant lung cancer in women and in East Asian populations: analysis of estrogen-related polymorphismsDaphne W Bell
Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA
Clin Cancer Res 14:4079-84. 2008.... - Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinibEunice L Kwak
Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA 02129, USA
Proc Natl Acad Sci U S A 102:7665-70. 2005..Our findings suggest that one of these, HKI-272, may prove highly effective in the treatment of EGFR-mutant NSCLCs, including tumors that have become resistant to gefitinib or erlotinib... - Epidermal growth factor receptor kinase domain mutations in esophageal and pancreatic adenocarcinomasEunice L Kwak
Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA
Clin Cancer Res 12:4283-7. 2006..Given recent reports of TKI-responsive cases of esophageal and pancreatic cancer, this study was designed to determine the prevalence of EGFR mutations in these gastrointestinal cancers... - Epidermal growth factor receptor mutants from human lung cancers exhibit enhanced catalytic activity and increased sensitivity to gefitinibRoseann Mulloy
Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
Cancer Res 67:2325-30. 2007.... - Epidermal growth factor receptor mutations in lung cancerSreenath V Sharma
Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA
Nat Rev Cancer 7:169-81. 2007.... - A unique spectrum of somatic PIK3CA (p110alpha) mutations within primary endometrial carcinomasMeghan L Rudd
Cancer Genetics Branch, National Human Genome Research Institute, National Cancer Institute, Bethesda, Maryland, USA
Clin Cancer Res 17:1331-40. 2011..The goal of this study was to comprehensively define the incidence of mutations in all exons of PIK3CA in both endometrioid endometrial cancer (EEC) and nonendometrioid endometrial cancer (NEEC)... - Frequent met oncogene amplification in a Brca1/Trp53 mouse model of mammary tumorigenesisGromoslaw A Smolen
Massachusetts General Hospital Cancer Center, Harvard Medical School, 13th Street, Charlestown, MA 02129, USA
Cancer Res 66:3452-5. 2006.... - A novel Wilms tumor 1 (WT1) target gene negatively regulates the WNT signaling pathwayMyoung Shin Kim
Genetics of Development and Disease Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 285:14585-93. 2010..Taken together, our results demonstrate that the WT1 negatively regulates WNT/beta-catenin pathway via its target gene WID and further suggest a role for WID in nephrogenesis... - Infrequent mutations of Archipelago (hAGO, hCDC4, Fbw7) in primary ovarian cancerEunice L Kwak
Massachusetts General Hospital Cancer Center and Harvard Medical School, Building 149, CNY-7, 13th Street, Charlestown, MA 02129, USA
Gynecol Oncol 98:124-8. 2005..Reconstitution experiments, rather than measuring tumor levels of cyclin E and c-Myc, provide an effective approach to determine the functional significance of AGO mutations identified in human cancers... - Mutations in the neutral sphingomyelinase gene SMPD3 implicate the ceramide pathway in human leukemiasWoo Jae Kim
Massachusetts General Hospital Cancer Center, Boston, MA, USA
Blood 111:4716-22. 2008..Taken together, these observations suggest that disruption of the ceramide pathway may contribute to a subset of human leukemias... - salvador Promotes both cell cycle exit and apoptosis in Drosophila and is mutated in human cancer cell linesNicolas Tapon
Massachusetts General Hospital Cancer Center, Building 149, 13th Street, Charlestown 02129, USA
Cell 110:467-78. 2002..The human ortholog of salvador (hWW45) is mutated in three cancer cell lines. Thus, salvador restricts cell numbers in vivo by functioning as a dual regulator of cell proliferation and apoptosis... - Detection of mutations in EGFR in circulating lung-cancer cellsShyamala Maheswaran
Massachusetts General Hospital Cancer Center, Boston 02129, USA
N Engl J Med 359:366-77. 2008..Molecular characterization of circulating tumor cells may provide a strategy for noninvasive serial monitoring of tumor genotypes during treatment... - Exome sequencing of serous endometrial tumors identifies recurrent somatic mutations in chromatin-remodeling and ubiquitin ligase complex genesMatthieu Le Gallo
Cancer Genetics Branch, National Human Genome Research Institute, US National Institutes of Health NIH, Bethesda, MD, USA
Nat Genet 44:1310-5. 2012.... - DOCK4, a GTPase activator, is disrupted during tumorigenesisVijay Yajnik
Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA 02129, USA
Cell 112:673-84. 2003..DOCK4 therefore encodes a CDM family member that regulates intercellular junctions and is disrupted during tumorigenesis... - An X chromosome gene, WTX, is commonly inactivated in Wilms tumorMiguel N Rivera
Massachusetts General Hospital Cancer Center, Harvard Medical Center, Boston, MA 02114, USA
Science 315:642-5. 2007.... - Regulation of expression of BIK proapoptotic protein in human breast cancer cells: p53-dependent induction of BIK mRNA by fulvestrant and proteasomal degradation of BIK proteinJingyung Hur
Department of Tumor Biology, Massachusetts General Hospital Center for Cancer Research, Charlestown, Massachusetts 02129, USA
Cancer Res 66:10153-61. 2006..These results suggest that expression of BIK in human breast cancer cells is regulated at the mRNA level by a mechanism involving a nontranscriptional activity of p53 and by proteasomal degradation of BIK protein... - Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathwaysRaffaella Sordella
Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, Building 149, 13th Street, Charlestown, MA 02129, USA
Science 305:1163-7. 2004..Thus, mutant EGFRs selectively transduce survival signals on which NSCLCs become dependent; inhibition of those signals by gefitinib may contribute to the drug's efficacy... - PIK3R1 (p85α) is somatically mutated at high frequency in primary endometrial cancerMary E Urick
Cancer Genetics Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland 20892, USA
Cancer Res 71:4061-7. 2011.... - Selective loss of heterozygosity in multiple breast cancers from a carrier of mutations in both BRCA1 and BRCA2Daphne W Bell
Center for Cancer Risk Analysis, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
Cancer Res 62:2741-3. 2002..The distinct histopathological features of these tumors may reflect the acquisition of subsequent genetic events...