Hai Yan

Summary

Affiliation: Duke University Medical Center
Country: USA

Publications

  1. 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
  2. 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
  3. 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
  4. 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
  5. 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
  6. 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
  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 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
  9. 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
  10. 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

Detail Information

Publications33

  1. 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...
  2. 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...
  3. 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...
  4. 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
    ....
  5. 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...
  6. 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...
  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 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...
  9. 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...
  10. 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...
  11. 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...
  12. 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...
  13. 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. ..
  14. 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...
  15. 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
    ....
  16. 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
    ....
  17. 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...
  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 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...
  20. 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. ..
  21. 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
    ....
  22. 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...
  23. 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...
  24. 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
    ....
  25. ncbi request reprint Glioblastoma multiforme: a review of therapeutic targets
    Okezie O Kanu
    Duke and Durham VAMC, Neurosurgery, DUMC Box 2624, NC 27710, USA
    Expert Opin Ther Targets 13:701-18. 2009
    ..This review describes the epidemiology, clinical presentation, pathology and tumor immunology, with a focus on understanding the molecular biology that underlies the current targeted therapeutics being tested...
  26. 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...
  27. 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...
  28. 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
    ....
  29. 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...
  30. 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...
  31. 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...
  32. 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...
  33. 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...