Barry S Taylor

Summary

Affiliation: Memorial Sloan-Kettering Cancer Center
Country: USA

Publications

  1. pmc Frequent alterations and epigenetic silencing of differentiation pathway genes in structurally rearranged liposarcomas
    Barry S Taylor
    Memorial Sloan Kettering Cancer Center, NY 10065, USA
    Cancer Discov 1:587-97. 2011
  2. doi request reprint Clinical cancer genomics: how soon is now?
    Barry S Taylor
    Program in Computational Biology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    J Pathol 223:318-26. 2011
  3. pmc The RAF inhibitor PLX4032 inhibits ERK signaling and tumor cell proliferation in a V600E BRAF-selective manner
    Eric W Joseph
    Weill Cornell Graduate School of Medical Sciences, New York, NY 10065, USA
    Proc Natl Acad Sci U S A 107:14903-8. 2010
  4. pmc Genomic and biological characterization of exon 4 KRAS mutations in human cancer
    Manickam Janakiraman
    Departments of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Cancer Res 70:5901-11. 2010
  5. pmc Copy number losses define subgroups of dedifferentiated liposarcoma with poor prognosis and genomic instability
    Aimee M Crago
    Sarcoma Disease Management Program, Department of Surgery, Bioinformatics Core, Computational Biology Center, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Clin Cancer Res 18:1334-40. 2012
  6. doi request reprint Somatic mutations of the Parkinson's disease-associated gene PARK2 in glioblastoma and other human malignancies
    Selvaraju Veeriah
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Nat Genet 42:77-82. 2010
  7. pmc Integrative genomic profiling of human prostate cancer
    Barry S Taylor
    Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA
    Cancer Cell 18:11-22. 2010
  8. pmc Genome sequencing identifies a basis for everolimus sensitivity
    Gopa Iyer
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Science 338:221. 2012
  9. pmc MYC cooperates with AKT in prostate tumorigenesis and alters sensitivity to mTOR inhibitors
    Nicola J Clegg
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 6:e17449. 2011
  10. pmc ZIC1 overexpression is oncogenic in liposarcoma
    Elliott Brill
    Department of Surgery, Computational Biology Center, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Cancer Res 70:6891-901. 2010

Collaborators

Detail Information

Publications19

  1. pmc Frequent alterations and epigenetic silencing of differentiation pathway genes in structurally rearranged liposarcomas
    Barry S Taylor
    Memorial Sloan Kettering Cancer Center, NY 10065, USA
    Cancer Discov 1:587-97. 2011
    ..Pharmacologic inhibition of DNA methylation promoted apoptosis and differentiated DLPS cells in vitro and inhibited tumor growth in vivo, providing a rationale for investigating methylation inhibitors in this disease...
  2. doi request reprint Clinical cancer genomics: how soon is now?
    Barry S Taylor
    Program in Computational Biology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    J Pathol 223:318-26. 2011
    ..Whether these will impact routine clinical practice and the treatment of disease is no longer debatable, but how precisely this will happen is a source of ongoing speculation and development...
  3. pmc The RAF inhibitor PLX4032 inhibits ERK signaling and tumor cell proliferation in a V600E BRAF-selective manner
    Eric W Joseph
    Weill Cornell Graduate School of Medical Sciences, New York, NY 10065, USA
    Proc Natl Acad Sci U S A 107:14903-8. 2010
    ..This selectivity may lead to a broader therapeutic index and help explain the greater antitumor activity observed with this drug than with MEK inhibitors...
  4. pmc Genomic and biological characterization of exon 4 KRAS mutations in human cancer
    Manickam Janakiraman
    Departments of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Cancer Res 70:5901-11. 2010
    ..These results also provide a rationale for broader KRAS testing beyond the most common hotspot alleles in exons 2 and 3...
  5. pmc Copy number losses define subgroups of dedifferentiated liposarcoma with poor prognosis and genomic instability
    Aimee M Crago
    Sarcoma Disease Management Program, Department of Surgery, Bioinformatics Core, Computational Biology Center, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Clin Cancer Res 18:1334-40. 2012
    ..This study sought to identify copy number alterations (CNA) associated with dedifferentiation of WDLS, with DDLS morphology, and with patient outcomes...
  6. doi request reprint Somatic mutations of the Parkinson's disease-associated gene PARK2 in glioblastoma and other human malignancies
    Selvaraju Veeriah
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Nat Genet 42:77-82. 2010
    ..These data strongly point to PARK2 as a tumor suppressor on 6q25.2-q27. Thus, PARK2, a gene that causes neuronal dysfunction when mutated in the germline, may instead contribute to oncogenesis when altered in non-neuronal somatic cells...
  7. pmc Integrative genomic profiling of human prostate cancer
    Barry S Taylor
    Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA
    Cancer Cell 18:11-22. 2010
    ..The genomic and clinical outcome data from these patients are now made available as a public resource...
  8. pmc Genome sequencing identifies a basis for everolimus sensitivity
    Gopa Iyer
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Science 338:221. 2012
    ....
  9. pmc MYC cooperates with AKT in prostate tumorigenesis and alters sensitivity to mTOR inhibitors
    Nicola J Clegg
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 6:e17449. 2011
    ..Since increased MYC expression is an early feature of many human prostate cancers, these data have implications for treatment of human prostate cancers with PI3K-pathway alterations using mTOR inhibitors...
  10. pmc ZIC1 overexpression is oncogenic in liposarcoma
    Elliott Brill
    Department of Surgery, Computational Biology Center, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Cancer Res 70:6891-901. 2010
    ..Our results show that ZIC1 expression is essential for liposarcomagenesis and that targeting ZIC1 or its downstream targets might lead to novel therapy for liposarcoma...
  11. pmc Advances in sarcoma genomics and new therapeutic targets
    Barry S Taylor
    Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA
    Nat Rev Cancer 11:541-57. 2011
    ....
  12. pmc Small RNA sequencing and functional characterization reveals MicroRNA-143 tumor suppressor activity in liposarcoma
    Stacy Ugras
    Department of Surgery, Sarcoma Biology Laboratory, Sarcoma Disease Management Program, The Rockefeller University, New York, New York, USA
    Cancer Res 71:5659-69. 2011
    ..Taken together, our findings suggest that miR-143 re-expression vectors or selective agents directed at miR-143 or its targets may have therapeutic value in dedifferentiated liposarcoma...
  13. pmc Genomic complexity and AKT dependence in serous ovarian cancer
    Aphrothiti J Hanrahan
    Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10471, USA
    Cancer Discov 2:56-67. 2012
    ....
  14. pmc Automated network analysis identifies core pathways in glioblastoma
    Ethan Cerami
    Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 5:e8918. 2010
    ..A central challenge in large-scale genome projects, such as the TCGA GBM project, is the ability to distinguish cancer-causing "driver" mutations from passively selected "passenger" mutations...
  15. pmc Functional copy-number alterations in cancer
    Barry S Taylor
    Computational Biology Center, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 3:e3179. 2008
    ..Taken together, we present a statistically robust methodology applicable to high-resolution genomic data to assess the extent and function of copy-number alterations in cancer...
  16. doi request reprint The nuclear deubiquitinase BAP1 is commonly inactivated by somatic mutations and 3p21.1 losses in malignant pleural mesothelioma
    Matthew Bott
    Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Nat Genet 43:668-72. 2011
    ..These findings implicate transcriptional deregulation in the pathogenesis of MPM...
  17. pmc Genetic predictors of MEK dependence in non-small cell lung cancer
    Christine A Pratilas
    Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Cancer Res 68:9375-83. 2008
    ....
  18. pmc Genomic dissection of the epidermal growth factor receptor (EGFR)/PI3K pathway reveals frequent deletion of the EGFR phosphatase PTPRS in head and neck cancers
    Luc G T Morris
    Human Oncology and Pathogenesis Program, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Proc Natl Acad Sci U S A 108:19024-9. 2011
    ..These findings have important implications for our understanding of head and neck cancer tumorigenesis and for the use of targeted agents for this malignancy...
  19. pmc (V600E)BRAF is associated with disabled feedback inhibition of RAF-MEK signaling and elevated transcriptional output of the pathway
    Christine A Pratilas
    Department of Pediatrics, Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Proc Natl Acad Sci U S A 106:4519-24. 2009
    ..Physiologic feedback inhibition of RAF/MEK signaling down-regulates ERK output in RTK cells; evasion of this feedback in mutant BRAF cells is associated with increased transcriptional output and MEK/ERK-dependent transformation...