Hai Yan

Summary

Affiliation: Duke University Medical Center
Country: USA

Publications

  1. pmc Mutant IDH1 is required for IDH1 mutated tumor cell growth
    Genglin Jin
    The Preston Robert Tisch Brain Tumor Center, The Pediatric Brain Tumor Foundation Institute, and the Department of Pathology, Duke University Medical Center, Durham, North Carolina, USA
    Oncotarget 3:774-82. 2012
  2. pmc Disruption of wild-type IDH1 suppresses D-2-hydroxyglutarate production in IDH1-mutated gliomas
    Genglin Jin
    The Preston Robert Tisch Brain Tumor Center, The Pediatric Brain Tumor Foundation Institute, and the Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Cancer Res 73:496-501. 2013
  3. ncbi request reprint Allelic variations in gene expression
    Hai Yan
    Duke University Medical Center, Department of Pathology, Durham, North Carolina 27710, USA
    Curr Opin Oncol 16:39-43. 2004
  4. pmc Mutant metabolic enzymes are at the origin of gliomas
    Hai Yan
    The Pediatric Brain Tumor Foundation Institute, Duke University Medical Center, Durham, North Carolina, USA
    Cancer Res 69:9157-9. 2009
  5. pmc Identification of microbial DNA in human cancer
    Christopher G Duncan
    Preston Robert Tisch Brain Tumor Center, Pediatric Brain Tumor Foundation Institute, Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
    BMC Med Genomics 2:22. 2009
  6. pmc IDH1 and IDH2 mutations in gliomas
    Hai Yan
    Department of Pathology, Pediatric Brain Tumor Foundation Institute, Duke University Medical Center, Durham, NC 27710, USA
    N Engl J Med 360:765-73. 2009
  7. pmc Profiling the effects of isocitrate dehydrogenase 1 and 2 mutations on the cellular metabolome
    Zachary J Reitman
    The Preston Robert Tisch Brain Tumor Center at Duke, Pediatric Brain Tumor Foundation Institute, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 108:3270-5. 2011
  8. pmc 2-hydroxyglutarate production, but not dominant negative function, is conferred by glioma-derived NADP-dependent isocitrate dehydrogenase mutations
    Genglin Jin
    The Preston Robert Tisch Brain Tumor Center at Duke, Pediatric Brain Tumor Foundation Institute, and Department of Pathology, Duke University Medical Center, Durham, North Carolina, United States of America
    PLoS ONE 6:e16812. 2011
  9. pmc OTX2 is critical for the maintenance and progression of Shh-independent medulloblastomas
    David C Adamson
    Department of Surgery, The Pediatric Brain Tumor Foundation Institute, and The Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center, Veterans Affairs Medical Center, Durham, North Carolina 27710, USA
    Cancer Res 70:181-91. 2010
  10. pmc HDMX regulates p53 activity and confers chemoresistance to 3-bis(2-chloroethyl)-1-nitrosourea
    Genglin Jin
    Department of Pathology, Pediatric Brain Tumor Foundation Institute and Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center, Durham, North Carolina 27710, USA
    Neuro Oncol 12:956-66. 2010

Detail Information

Publications39

  1. pmc Mutant IDH1 is required for IDH1 mutated tumor cell growth
    Genglin Jin
    The Preston Robert Tisch Brain Tumor Center, The Pediatric Brain Tumor Foundation Institute, and the Department of Pathology, Duke University Medical Center, Durham, North Carolina, USA
    Oncotarget 3:774-82. 2012
    ..Our findings offer insights into changes that may contribute to the inhibition of cell proliferation and offer a strong preclinical rationale for utilizing mutant IDH1 as a valid therapeutic target...
  2. pmc Disruption of wild-type IDH1 suppresses D-2-hydroxyglutarate production in IDH1-mutated gliomas
    Genglin Jin
    The Preston Robert Tisch Brain Tumor Center, The Pediatric Brain Tumor Foundation Institute, and the Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Cancer Res 73:496-501. 2013
    ..Expression of wild-type IDH1 was also critical for mutant IDH1-associated D-2HG production in the colorectal cancer cell line HCT116. These insights may aid in the development of therapeutic strategies to target IDH1-mutated cancers...
  3. ncbi request reprint Allelic variations in gene expression
    Hai Yan
    Duke University Medical Center, Department of Pathology, Durham, North Carolina 27710, USA
    Curr Opin Oncol 16:39-43. 2004
    ..Thus, it has been hypothesized that the study of natural differential expression presenting within and among populations may enhance understanding of human phenotypic variation...
  4. pmc Mutant metabolic enzymes are at the origin of gliomas
    Hai Yan
    The Pediatric Brain Tumor Foundation Institute, Duke University Medical Center, Durham, North Carolina, USA
    Cancer Res 69:9157-9. 2009
    ..IDH1 and IDH2 mutations define a specific subtype of gliomas and may have significant utility for the diagnosis, prognosis, and treatment of patients with these tumors...
  5. pmc Identification of microbial DNA in human cancer
    Christopher G Duncan
    Preston Robert Tisch Brain Tumor Center, Pediatric Brain Tumor Foundation Institute, Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
    BMC Med Genomics 2:22. 2009
    ..CONCLUSION: DK-MICROBE can identify previously unknown infectious agents in human tumors, and is now available for further applications for the identification of pathogen DNA in human cancer and other diseases...
  6. pmc IDH1 and IDH2 mutations in gliomas
    Hai Yan
    Department of Pathology, Pediatric Brain Tumor Foundation Institute, Duke University Medical Center, Durham, NC 27710, USA
    N Engl J Med 360:765-73. 2009
    ....
  7. pmc Profiling the effects of isocitrate dehydrogenase 1 and 2 mutations on the cellular metabolome
    Zachary J Reitman
    The Preston Robert Tisch Brain Tumor Center at Duke, Pediatric Brain Tumor Foundation Institute, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 108:3270-5. 2011
    ..NAAG also was significantly lower in human glioma tissues containing IDH mutations than in gliomas without such mutations. These metabolic changes provide clues to the pathogenesis of tumors associated with IDH gene mutations...
  8. pmc 2-hydroxyglutarate production, but not dominant negative function, is conferred by glioma-derived NADP-dependent isocitrate dehydrogenase mutations
    Genglin Jin
    The Preston Robert Tisch Brain Tumor Center at Duke, Pediatric Brain Tumor Foundation Institute, and Department of Pathology, Duke University Medical Center, Durham, North Carolina, United States of America
    PLoS ONE 6:e16812. 2011
    ..Genetic evidence indicates that these mutations share a common gain of function, but it is unclear whether the shared function is dominant negative activity, neomorphic production of (R)-2-hydroxyglutarate (2HG), or both...
  9. pmc OTX2 is critical for the maintenance and progression of Shh-independent medulloblastomas
    David C Adamson
    Department of Surgery, The Pediatric Brain Tumor Foundation Institute, and The Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center, Veterans Affairs Medical Center, Durham, North Carolina 27710, USA
    Cancer Res 70:181-91. 2010
    ..Mechanistic investigations revealed upregulation of MYC as a potential mechanism whereby OTX2 promotes tumor progression. Our findings define OTX2 as an important oncogenic driver in medulloblastoma...
  10. pmc HDMX regulates p53 activity and confers chemoresistance to 3-bis(2-chloroethyl)-1-nitrosourea
    Genglin Jin
    Department of Pathology, Pediatric Brain Tumor Foundation Institute and Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center, Durham, North Carolina 27710, USA
    Neuro Oncol 12:956-66. 2010
    ..In summary, HDMX exhibits bona fide oncogenic properties and offers a promising molecular target for GBM therapeutic intervention...
  11. pmc A heterozygous IDH1R132H/WT mutation induces genome-wide alterations in DNA methylation
    Christopher G Duncan
    The Preston Robert Tisch Brain Tumor Center, The Pediatric Brain Tumor Foundation Institute, The Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Genome Res 22:2339-55. 2012
    ..These data provide insight on epigenetic alterations induced by IDH1 mutations and support a causal role for IDH1(R132H/WT) mutants in driving epigenetic instability in human cancer cells...
  12. pmc Isocitrate dehydrogenase 1 and 2 mutations in cancer: alterations at a crossroads of cellular metabolism
    Zachary J Reitman
    Department of Pathology, The Pediatric Brain Tumor Foundation Institute, Duke University Medical Center, Durham, NC 27710, USA
    J Natl Cancer Inst 102:932-41. 2010
    ..Study of alterations in these metabolic enzymes may provide insights into the metabolism of cancer cells and uncover novel avenues for development of anticancer therapeutics...
  13. pmc Isocitrate dehydrogenase 1: what it means to the neurosurgeon: a review
    Tiffany R Hodges
    Duke Brain Tumor Immunotherapy Program, Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Neurosurg 118:1176-80. 2013
    ..However, given that IDH1 mutations are homogeneously expressed and are limited solely to tumor tissue, targeting this mutation could potentially yield novel treatment strategies for patients with glioblastoma multiforme...
  14. pmc Integrated genomic analyses identify ERRFI1 and TACC3 as glioblastoma-targeted genes
    Christopher G Duncan
    The Preston Robert Tisch Brain Tumor Center, The Pediatric Brain Tumor Foundation, The Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
    Oncotarget 1:265-77. 2010
    ..Our multifaceted genomic evaluation of glioblastoma establishes ERRFI1 as a potential candidate tumor suppressor gene and TACC3 as a potential oncogene, and provides insight on targets for oncogenic pathway-based therapy...
  15. pmc The genetic landscape of anaplastic astrocytoma
    Patrick J Killela
    Department of Pathology, Duke University Medical Center, The Preston Robert Tisch Brain Tumor Center at Duke, and Pediatric Brain Tumor Foundation Institute at Duke, Durham, NC
    Oncotarget 5:1452-7. 2014
    ..This study suggests genetic signatures will be useful for the classification of gliomas. ..
  16. pmc IDH1(R132) mutation identified in one human melanoma metastasis, but not correlated with metastases to the brain
    Giselle Y Lopez
    The Preston Robert Tisch Brain Tumor Center, The Pediatric Brain Tumor Foundation, and the Department of Pathology, Duke University Medical Center, DUMC 3156, Durham, NC 27710, USA
    Biochem Biophys Res Commun 398:585-7. 2010
    ..Studies on the cell-lineages of tumors with IDH1/2 mutations may help clarify the role of these mutations in the development of brain tumors...
  17. pmc Glioblastoma proto-oncogene SEC61gamma is required for tumor cell survival and response to endoplasmic reticulum stress
    Zheming Lu
    Department of Pathology, The Pediatric Brain Tumor Foundation Institute, Duke University Medical Center, Durham, North Carolina 27710, USA
    Cancer Res 69:9105-11. 2009
    ....
  18. pmc Isocitrate dehydrogenase mutations in gliomas: mechanisms, biomarkers and therapeutic target
    Changcun Guo
    The Preston Robert Tisch Brain Tumor Center at Duke, Pediatric Brain Tumor Foundation Institute, Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Curr Opin Neurol 24:648-52. 2011
    ..The mechanisms of IDH mutations in gliomagenesis, and their value as diagnostic, prognostic marker and therapeutic target have been extensively studied. This review is to summarize the findings of these studies...
  19. pmc Aberrant Otx2 expression enhances migration and induces ectopic proliferation of hindbrain neuronal progenitor cells
    Matthew Wortham
    Department of Pathology, The Pediatric Brain Tumor Foundation Institute, and The Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center, Durham, North Carolina, USA
    PLoS ONE 7:e36211. 2012
    ..These studies implicate a role for Otx2 in altering the dynamics of neuronal progenitor cell proliferation...
  20. pmc TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal
    Patrick J Killela
    Pediatric Brain Tumor Foundation Institute at Duke, and Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 110:6021-6. 2013
    ....
  21. ncbi request reprint Identification of OTX2 as a medulloblastoma oncogene whose product can be targeted by all-trans retinoic acid
    Chunhui Di
    Brain Tumor Center, Department of Pathology, Duke University Medical Center, Research Drive, Durham, NC 27710, USA
    Cancer Res 65:919-24. 2005
    ..These observations suggest that OTX2 is essential for the pathogenesis of anaplastic medulloblastomas and that these tumors may be amenable to therapy with all-trans-retinoic acid...
  22. pmc A monoclonal antibody IMab-1 specifically recognizes IDH1R132H, the most common glioma-derived mutation
    Yukinari Kato
    Department of Pathology, Duke University Medical Center, DUMC 3156, Durham, NC 27710, USA
    Biochem Biophys Res Commun 390:547-51. 2009
    ..In conclusion, we established an anti-IDH1(R132H)-specific monoclonal antibody IMab-1, which should be significantly useful for diagnosis and biological evaluation of mutation-bearing gliomas...
  23. pmc Mutations in IDH1, IDH2, and in the TERT promoter define clinically distinct subgroups of adult malignant gliomas
    Patrick J Killela
    Department of Pathology, Duke University Medical Center, The Preston Robert Tisch Brain Tumor Center at Duke, and Pediatric Brain Tumor Foundation Institute at Duke, Durham, NC, USA
    Oncotarget 5:1515-25. 2014
    ..Analyzing gliomas based on their genetic signatures allows for the stratification of these patients into distinct cohorts, with unique prognosis and survival. ..
  24. doi request reprint Releasing the block: setting differentiation free with mutant IDH inhibitors
    Christopher J Pirozzi
    The Preston Robert Tisch Brain Tumor Center at Duke, Pediatric Brain Tumor Foundation Institute at Duke, Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
    Cancer Cell 23:570-2. 2013
    ....
  25. pmc Enzyme redesign guided by cancer-derived IDH1 mutations
    Zachary J Reitman
    Department of Pathology, Duke University Medical Center, Durham, NC, USA
    Nat Chem Biol 8:887-9. 2012
    ..Thus, we provide a prototypic example of how insights from cancer genome sequencing and functional studies can aid in enzyme redesign...
  26. ncbi request reprint Mutations of PIK3CA in anaplastic oligodendrogliomas, high-grade astrocytomas, and medulloblastomas
    Daniel K Broderick
    Brain Tumor Center, Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
    Cancer Res 64:5048-50. 2004
    ..These observations implicate PIK3CA as an oncogene in a wider spectrum of adult and pediatric brain tumors and suggest that PIK3CA may be a useful diagnostic marker or a therapeutic target in these cancers...
  27. pmc Apples to origins: identifying brain tumor stem cell genes by comparing transcriptomes of normal and cancer stem cells
    Matthew Wortham
    Department of Pathology, The Pediatric Brain Tumor Foundation Institute, and The Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center, Durham, North Carolina 27710, USA
    Cancer Discov 2:492-4. 2012
    ....
  28. pmc Global identification of MLL2-targeted loci reveals MLL2's role in diverse signaling pathways
    Changcun Guo
    The Preston Robert Tisch Brain Tumor Center at Duke, Pediatric Brain Tumor Foundation Institute, cDepartment of Pathology, Duke University, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 109:17603-8. 2012
    ..Our results present a genome-wide integrative analysis of the MLL2 target loci and suggest potential mechanisms underlying tumorigenesis driven by MLL2 alterations...
  29. ncbi request reprint Digital karyotyping technology: exploring the cancer genome
    Timothy J Parrett
    Department of Pathology, Brain Tumor Center, Duke University Medical Center, 3156, Durham, NC 27710, USA
    Expert Rev Mol Diagn 5:917-25. 2005
    ....
  30. ncbi request reprint IDH1 and IDH2: not your typical oncogenes
    Zachary J Reitman
    The Preston Robert Tisch Brain Tumor Center at Duke, The Pediatric Brain Tumor Institute, and the Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
    Cancer Cell 17:215-6. 2010
    ..However, seemingly oncogenic mutations in IDH1 and IDH2 reduce their native enzyme activity. In this issue of Cancer Cell, Ward et al. pin down a neomorphic enzyme activity as a possible oncogenic function for these alterations...
  31. pmc Altered telomeres in tumors with ATRX and DAXX mutations
    Christopher M Heaphy
    Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Science 333:425. 2011
    ..ATRX mutations also correlate with abnormal telomeres in tumors of the central nervous system. These data suggest that an alternative telomere maintenance function may operate in human tumors with alterations in the ATRX or DAXX genes...
  32. ncbi request reprint Snapshot of the allele-specific variation in human gene expression
    Hai Yan
    Department of Pathology, Duke University Meeical Center, Durham, NC, USA
    Methods Mol Biol 311:31-8. 2005
    ..The studies of allele-specific expression revealed that differential expression is relatively common in the human population...
  33. ncbi request reprint Allelic variation in human gene expression
    Hai Yan
    Sidney Kimmel Comprehensive Cancer Center and Howard Hughes Medical Institute, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Science 297:1143. 2002
  34. ncbi request reprint Allele separation facilitates interpretation of potential splicing alterations and genomic rearrangements
    Hidewaki Nakagawa
    Human Cancer Genetics Program, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA
    Cancer Res 62:4579-82. 2002
    ..These results allowed pathogenicity to be unambiguously assigned to the mutations and increased the sensitivity of genomic testing...
  35. ncbi request reprint High frequency of mutations of the PIK3CA gene in human cancers
    Yardena Samuels
    Sidney Kimmel Comprehensive Cancer Center, Howard Hughes Medical Institute, The Johns Hopkins University Medical Institutions, Baltimore, MD 21231, USA
    Science 304:554. 2004
  36. pmc Detection of allelic variations of human gene expression by polymerase colonies
    James A Butz
    Department of Chemical Engineering, University of Delaware, Newark, DE 19716, USA
    BMC Genet 5:3. 2004
    ..Herein, we describe the application of an immobilized polymerase chain reaction technique as an alternative approach to measure relative allelic differential expression...
  37. ncbi request reprint Somatic mutations of GUCY2F, EPHA3, and NTRK3 in human cancers
    Laura D Wood
    The Ludwig Center for Cancer Genetics and Therapeutics, The Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, Maryland 21231, USA
    Hum Mutat 27:1060-1. 2006
    ..Our results implicate these tyrosine kinase genes in the pathogenesis of other tumor types and suggest that they may be useful targets for diagnostic and therapeutic intervention in selected patients...
  38. pmc An integrated genomic analysis of human glioblastoma multiforme
    D Williams Parsons
    Ludwig Center for Cancer Genetics and Therapeutics, and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA
    Science 321:1807-12. 2008
    ..These studies demonstrate the value of unbiased genomic analyses in the characterization of human brain cancer and identify a potentially useful genetic alteration for the classification and targeted therapy of GBMs...
  39. ncbi request reprint Small changes in expression affect predisposition to tumorigenesis
    Hai Yan
    The Howard Hughes Medical Institute, The Oncology Center, and the Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Nat Genet 30:25-6. 2002
    ....