CHI DANG

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. doi request reprint Therapeutic targeting of Myc-reprogrammed cancer cell metabolism
    C V Dang
    Johns Hopkins University School of Medicine, Baltimore, Maryland 21212, USA
    Cold Spring Harb Symp Quant Biol 76:369-74. 2011
  2. pmc An integrated database of genes responsive to the Myc oncogenic transcription factor: identification of direct genomic targets
    Karen I Zeller
    Division of Hematology, Department of Medicine, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Genome Biol 4:R69. 2003
  3. pmc Stimulation of Myc transactivation by the TATA binding protein in promoter-reporter assays
    John F Barrett
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    BMC Biochem 6:7. 2005
  4. pmc Rethinking the Warburg effect with Myc micromanaging glutamine metabolism
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Cancer Res 70:859-62. 2010
  5. ncbi request reprint The great MYC escape in tumorigenesis
    Chi V Dang
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Cancer Cell 8:177-8. 2005
  6. ncbi request reprint Could MYC induction of mitochondrial biogenesis be linked to ROS production and genomic instability?
    Chi V Dang
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Cell Cycle 4:1465-6. 2005
  7. ncbi request reprint The c-Myc target gene network
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Semin Cancer Biol 16:253-64. 2006
  8. doi request reprint PKM2 tyrosine phosphorylation and glutamine metabolism signal a different view of the Warburg effect
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Sci Signal 2:pe75. 2009
  9. ncbi request reprint The interplay between MYC and HIF in cancer
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nat Rev Cancer 8:51-6. 2008
  10. pmc Antimalarial therapy prevents Myc-induced lymphoma
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Clin Invest 118:15-7. 2008

Detail Information

Publications63

  1. doi request reprint Therapeutic targeting of Myc-reprogrammed cancer cell metabolism
    C V Dang
    Johns Hopkins University School of Medicine, Baltimore, Maryland 21212, USA
    Cold Spring Harb Symp Quant Biol 76:369-74. 2011
    ..This addictive state can be exploited for cancer therapy, because nutrient deprivation kills Myc-driven cells and inhibition of the Myc targets, lactate dehydrogenase A or glutaminase, diminishes tumor xenograft growth in vivo...
  2. pmc An integrated database of genes responsive to the Myc oncogenic transcription factor: identification of direct genomic targets
    Karen I Zeller
    Division of Hematology, Department of Medicine, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Genome Biol 4:R69. 2003
    ..This database is essential for the understanding of the genetic regulatory networks underlying the genesis of cancers...
  3. pmc Stimulation of Myc transactivation by the TATA binding protein in promoter-reporter assays
    John F Barrett
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    BMC Biochem 6:7. 2005
    ....
  4. pmc Rethinking the Warburg effect with Myc micromanaging glutamine metabolism
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Cancer Res 70:859-62. 2010
    ..Thus, a reevaluation of cancer metabolism considering glutamine catabolism with a better understanding of the tumor histological complexity is needed before cancer metabolism can be effectively targeted in therapy...
  5. ncbi request reprint The great MYC escape in tumorigenesis
    Chi V Dang
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Cancer Cell 8:177-8. 2005
    ..In contrast, the MYC point mutants failed to induce Bim, promoting murine lymphomas that escaped both wild-type p53 and p19ARF, and in doing so, evaded apoptosis...
  6. ncbi request reprint Could MYC induction of mitochondrial biogenesis be linked to ROS production and genomic instability?
    Chi V Dang
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Cell Cycle 4:1465-6. 2005
    ....
  7. ncbi request reprint The c-Myc target gene network
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Semin Cancer Biol 16:253-64. 2006
    ..Despite tremendous advances, the downstream target genes that distinguish between physiologic and tumorigenic functions of c-Myc remain to be delineated...
  8. doi request reprint PKM2 tyrosine phosphorylation and glutamine metabolism signal a different view of the Warburg effect
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Sci Signal 2:pe75. 2009
    ..This effect, which describes the propensity for cancer cells to convert glucose to lactate at a high rate, must now accommodate links among glycolysis, the tricarboxylic acid cycle, and glutamine metabolism in cancer cells...
  9. ncbi request reprint The interplay between MYC and HIF in cancer
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nat Rev Cancer 8:51-6. 2008
    ..This Perspective emphasizes the differences between the transcriptional network that operates under normal homeostatic conditions and the network in a tumorigenic milieu...
  10. pmc Antimalarial therapy prevents Myc-induced lymphoma
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Clin Invest 118:15-7. 2008
    ..These findings suggest that a new use of an old drug for cancer prevention may profoundly affect disease outcome...
  11. pmc Therapeutic targeting of cancer cell metabolism
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21212, USA
    J Mol Med (Berl) 89:205-12. 2011
    ....
  12. ncbi request reprint Glutaminolysis: supplying carbon or nitrogen or both for cancer cells?
    Chi V Dang
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Cell Cycle 9:3884-6. 2010
    ..As such, cancer cells have many degrees of freedom for re-programming cell metabolism, which with better understanding will result in novel therapeutic approaches...
  13. pmc Have you seen...?: Micro-managing and restraining pluripotent stem cells by MYC
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    EMBO J 28:3065-6. 2009
    ....
  14. pmc MYC-induced cancer cell energy metabolism and therapeutic opportunities
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Clin Cancer Res 15:6479-83. 2009
    ..Collectively, these studies indicate that Myc-mediated altered cancer cell energy metabolism could be translated for the development of new anticancer therapies...
  15. doi request reprint Edging toward new therapeutics with cyclin D1 Egl'ng on cancer
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cancer Cell 16:361-2. 2009
    ..Their observations through loss of function studies suggest the potential for drug-like molecules inhibiting EglN to serve as new cancer therapeutics...
  16. doi request reprint Muscle fatigue from losing your PHD
    Chi V Dang
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cell Metab 7:191-2. 2008
    ..A new study by Aragones et al. (2008) demonstrates that mice lacking skeletal muscle PHD1 have decreased exercise tolerance and oxygen consumption but remarkably tolerate ischemia in a HIF-2alpha- and PPARalpha-dependent fashion...
  17. ncbi request reprint Runner's anemia
    C V Dang
    Ross Research Bldg, Room 1025, Johns Hopkins University School of Medicine, 720 Rutland Ave, Baltimore, MD 21205, USA
    JAMA 286:714-6. 2001
    ..Runner's anemia should be considered when, amidst a constellation of signs and symptoms, mild anemia is well tolerated by an avid runner...
  18. pmc Global mapping of c-Myc binding sites and target gene networks in human B cells
    Karen I Zeller
    Department of Medicine and The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 103:17834-9. 2006
    ....
  19. ncbi request reprint c-Myc-regulated microRNAs modulate E2F1 expression
    Kathryn A O'Donnell
    Program in Human Genetics and Molecular Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nature 435:839-43. 2005
    ....
  20. pmc Hypoxia-inducible factor 1 and dysregulated c-Myc cooperatively induce vascular endothelial growth factor and metabolic switches hexokinase 2 and pyruvate dehydrogenase kinase 1
    Jung whan Kim
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Mol Cell Biol 27:7381-93. 2007
    ....
  21. pmc Widespread microRNA repression by Myc contributes to tumorigenesis
    Tsung Cheng Chang
    McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nat Genet 40:43-50. 2008
    ..We further show that enforced expression of repressed miRNAs diminishes the tumorigenic potential of lymphoma cells. These results demonstrate that extensive reprogramming of the miRNA transcriptome by Myc contributes to tumorigenesis...
  22. pmc Global regulation of nucleotide biosynthetic genes by c-Myc
    Yen Chun Liu
    Program in Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 3:e2722. 2008
    ....
  23. ncbi request reprint HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia
    Jung whan Kim
    Graduate Program of Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Cell Metab 3:177-85. 2006
    ..These studies reveal a hypoxia-induced metabolic switch that shunts glucose metabolites from the mitochondria to glycolysis to maintain ATP production and to prevent toxic ROS production...
  24. pmc Myc stimulates nuclearly encoded mitochondrial genes and mitochondrial biogenesis
    Feng Li
    Division of Hematology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Mol Cell Biol 25:6225-34. 2005
    ..These observations support a pivotal role for Myc in regulating mitochondrial biogenesis...
  25. pmc Evaluation of myc E-box phylogenetic footprints in glycolytic genes by chromatin immunoprecipitation assays
    Jung whan Kim
    Graduate Program of Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Mol Cell Biol 24:5923-36. 2004
    ..In aggregate, these observations indicate that Myc is an important regulator of glycolytic genes, suggesting that MYC plays a key role in a switch to glycolytic metabolism during cell proliferation or tumorigenesis...
  26. pmc Lin-28B transactivation is necessary for Myc-mediated let-7 repression and proliferation
    Tsung Cheng Chang
    McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 106:3384-9. 2009
    ..These findings highlight an important role for Lin-28B in Myc-driven cellular phenotypes and uncover an orchestration of transcriptional and posttranscriptional mechanisms in Myc-mediated reprogramming of miRNA expression...
  27. ncbi request reprint c-myc overexpression causes anaplasia in medulloblastoma
    Duncan Stearns
    Department of Neuropathology, Johns Hopkins University School of Medicine, 558 Ross Building, 720 Rutland Avenue, Baltimore, MD 21205, USA
    Cancer Res 66:673-81. 2006
    ..Because anaplastic changes are often observed in recurrent medulloblastoma, we propose that c-myc dysregulation is involved in the progression of these malignant embryonal neoplasms...
  28. ncbi request reprint Biology and treatment of Burkitt's lymphoma
    Jason T Yustein
    Division of Pediatric Hematology Oncology, Johns Hopkins University, Baltimore, Maryland 21205, USA
    Curr Opin Hematol 14:375-81. 2007
    ..This review will focus on those features, and discuss recent advances in the molecular biology and advancing treatment options for the disease...
  29. pmc Inhibition of lactate dehydrogenase A induces oxidative stress and inhibits tumor progression
    Anne Le
    Division of Hematology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 107:2037-42. 2010
    ....
  30. ncbi request reprint HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activity
    Huafeng Zhang
    Vascular Biology Program, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cancer Cell 11:407-20. 2007
    ..We demonstrate that transcription of the gene encoding the coactivator PGC-1beta is C-MYC dependent and that loss of PGC-1beta expression is a major factor contributing to reduced respiration in VHL-deficient renal carcinoma cells...
  31. ncbi request reprint Histopathological and molecular prognostic markers in medulloblastoma: c-myc, N-myc, TrkC, and anaplasia
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Neuropathol Exp Neurol 63:441-9. 2004
    ..The association we describe between c-myc expression, tumor anaplasia, and worse clinical outcomes provides further evidence for the importance of this oncogene in medulloblastoma pathobiology...
  32. pmc Induction of ectopic Myc target gene JAG2 augments hypoxic growth and tumorigenesis in a human B-cell model
    Jason T Yustein
    Departments of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 107:3534-9. 2010
    ..Furthermore, the expression of Jagged2 in P493-6 tumors often overlapped with regions of hypoxia. These observations suggest that Notch signaling downstream of Myc enables cells to adapt in the tumor hypoxic microenvironment...
  33. pmc c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism
    Ping Gao
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nature 458:762-5. 2009
    ..The unique means by which Myc regulates glutaminase uncovers a previously unsuspected link between Myc regulation of miRNAs, glutamine metabolism, and energy and reactive oxygen species homeostasis...
  34. ncbi request reprint Effects of hypoxia on tumor metabolism
    Jung whan Kim
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cancer Metastasis Rev 26:291-8. 2007
    ..These new insights into hypoxic metabolic alterations in tumors will hopefully lead us to target tumor bioenergetics for the treatment of cancers...
  35. pmc Digoxin and other cardiac glycosides inhibit HIF-1alpha synthesis and block tumor growth
    Huafeng Zhang
    Vascular Program, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 105:19579-86. 2008
    ....
  36. pmc The c-Myc target gene PRDX3 is required for mitochondrial homeostasis and neoplastic transformation
    Diane R Wonsey
    Program in Human Genetics and Molecular Biology and Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 99:6649-54. 2002
    ..These data provide evidence that PRDX3 is a c-Myc target gene that is required to maintain normal mitochondrial function...
  37. pmc hTERT gene amplification and increased mRNA expression in central nervous system embryonal tumors
    Xing Fan
    Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Am J Pathol 162:1763-9. 2003
    ..Our data indicate that hTERT gene amplification is relatively common in embryonal brain tumors, and that increased expression of hTERT mRNA may be associated with biologically aggressive tumor behavior...
  38. pmc The Myc target gene JPO1/CDCA7 is frequently overexpressed in human tumors and has limited transforming activity in vivo
    Rebecca C Osthus
    Program in Human Genetics and Molecular Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Cancer Res 65:5620-7. 2005
    ..We observed a significant increased incidence of transgenic animal solid tumors, which were not seen in littermate controls. These observations suggest that JPO1/CDCA7 may contribute to Myc-mediated tumorigenesis...
  39. pmc Activation of transferrin receptor 1 by c-Myc enhances cellular proliferation and tumorigenesis
    Kathryn A O'Donnell
    Program in Human Genetics and Molecular Biology, The Johns Hopkins School of Medicine, Baltimore, MD 21205, USA
    Mol Cell Biol 26:2373-86. 2006
    ..These findings provide a molecular basis for increased TFRC1 expression in human tumors, illuminate the role of TFRC1 in the c-Myc target gene network, and support strategies that target TFRC1 for cancer therapy...
  40. pmc MYC overexpression induces prostatic intraepithelial neoplasia and loss of Nkx3.1 in mouse luminal epithelial cells
    Tsuyoshi Iwata
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 5:e9427. 2010
    ..We also identified a novel histopathologically identifiable intermediate step prior to invasion that should facilitate studies of molecular pathway alterations occurring during early progression of prostatic adenocarcinomas...
  41. ncbi request reprint Highlights of the National Cancer Institute Workshop on mitochondrial function and cancer
    Mary Ellen Perry
    Division of Cancer Biology, National Cancer Institute, NIH, Bethesda, Maryland, USA
    Cancer Res 64:7640-4. 2004
  42. pmc A strategy for identifying transcription factor binding sites reveals two classes of genomic c-Myc target sites
    Timothy J Haggerty
    Division of Hematology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 100:5313-8. 2003
    ....
  43. ncbi request reprint HIF-1 regulates cytochrome oxidase subunits to optimize efficiency of respiration in hypoxic cells
    Ryo Fukuda
    Vascular Biology Program, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cell 129:111-22. 2007
    ..Thus, mammalian cells respond to hypoxia by altering COX subunit composition, as previously observed in yeast, but by a completely different molecular mechanism...
  44. pmc Role of NADPH oxidase in arsenic-induced reactive oxygen species formation and cytotoxicity in myeloid leukemia cells
    Wen Chien Chou
    Program of Human Genetics and Molecular Biology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 101:4578-83. 2004
    ..Our findings pinpoint the arsenic target of ROS production and provide a conceptual basis for an anticancer regimen...
  45. pmc Unexpected antitumorigenic effect of fenbendazole when combined with supplementary vitamins
    Ping Gao
    Department of Medicine, Division of Hematology, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA
    J Am Assoc Lab Anim Sci 47:37-40. 2008
    ..The mechanism for this synergy is unknown and deserves further investigation. Fenbendazole should be used with caution during tumor studies because it may interact with other treatments and confound research results...
  46. ncbi request reprint Cancer's molecular sweet tooth and the Warburg effect
    Jung whan Kim
    Division of Hematology, Department of Medicine, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Cancer Res 66:8927-30. 2006
    ..Molecular advances in this area may reveal tactics to exploit the cancer cell's "sweet tooth" for cancer therapy...
  47. ncbi request reprint Discovering robust protein biomarkers for disease from relative expression reversals in 2-D DIGE data
    Troy J Anderson
    Center for Cardiovascular Bioinformatics and Modeling and The Institute of Computational Medicine, Johns Hopkins University, Baltimore, MD 21218, USA
    Proteomics 7:1197-207. 2007
    ..We propose that by accounting for sources of within- and between-gel variation, RER classifiers applied to 2-D DIGE data provide a useful approach for identifying biomarkers that discriminate among protein samples of interest...
  48. ncbi request reprint Multifaceted roles of glycolytic enzymes
    Jung whan Kim
    Graduate Program in Pathobiology, The Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA
    Trends Biochem Sci 30:142-50. 2005
    ..These roles further underscore the need to consider the non-enzymatic functions of enzymes in proteomic studies of cells and tissues...
  49. ncbi request reprint Isolation of bone marrow-derived stem cells using density-gradient separation
    Tarja A Juopperi
    Graduate Program of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Exp Hematol 35:335-41. 2007
    ..We sought to provide the scientific community with an alternate approach to acquire our stem cells by replacing elutriation with the use of density-gradient centrifugation...
  50. ncbi request reprint Identification and characterization of the novel centrosome-associated protein CCCAP
    Andrew A Kenedy
    Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Gene 303:35-46. 2003
    ..We further discovered that the C-terminal portion of hCCCAP is identical to the human colon cancer autoantigen NY-CO-8 (Human Gene Nomenclature symbol SDCCAG8)...
  51. pmc HIF-dependent antitumorigenic effect of antioxidants in vivo
    Ping Gao
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cancer Cell 12:230-8. 2007
    ..These findings challenge the paradigm that antioxidants diminish tumorigenesis primarily through decreasing DNA damage and mutations and provide significant support for a key antitumorigenic effect of diminishing HIF levels...
  52. pmc Human-induced pluripotent stem cells from blood cells of healthy donors and patients with acquired blood disorders
    Zhaohui Ye
    Stem Cell Program, Institute for Cell Engineering, and Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Blood 114:5473-80. 2009
    ..These iPS cells provide a renewable cell source and a prospective hematopoiesis model for investigating MPD pathogenesis...
  53. pmc Development of human protein reference database as an initial platform for approaching systems biology in humans
    Suraj Peri
    McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University, Baltimore, Maryland 21287, USA
    Genome Res 13:2363-71. 2003
    ..hprd.org to the academic community. This unified bioinformatics platform will be useful in cataloging and mining the large number of proteomic interactions and alterations that will be discovered in the postgenomic era...
  54. pmc Unique conformation of cancer autoantigen B23 in hepatoma: a mechanism for specificity in the autoimmune response
    Danielle B Ulanet
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 100:12361-6. 2003
    ..We propose that unique features of autoantigens in the disease-relevant microenvironment may regulate susceptibility to cleavage by GB and their selection by the specific autoimmune response...
  55. ncbi request reprint Conditional deletion of c-myc does not impair liver regeneration
    Feng Li
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Cancer Res 66:5608-12. 2006
    ..Although c-myc is required for embryonic development, our findings indicate that it is not required for the maintenance of the adult liver...
  56. pmc Anoxic fibroblasts activate a replication checkpoint that is bypassed by E1a
    Lawrence B Gardner
    Division of Hematology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Mol Cell Biol 23:9032-45. 2003
    ....
  57. pmc In silico identification of transcriptional regulators associated with c-Myc
    Ran Elkon
    The David and Inez Myers Laboratory for Genetic Research, Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Israel
    Nucleic Acids Res 32:4955-61. 2004
    ..The approach applied here is general and demonstrates how computational analysis of functional genomics experiments can identify novel modules in complex networks of transcriptional regulation...
  58. pmc Increased expression of TATA-binding protein, the central transcription factor, can contribute to oncogenesis
    Sandra A S Johnson
    Department of Biochemistry and Molecular Biology, Keck School of Medicine and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, California 90033, USA
    Mol Cell Biol 23:3043-51. 2003
    ..We conclude that TBP may be a critical component in dysregulated signaling that occurs downstream of genetic lesions that cause tumors...
  59. pmc Arsenic suppresses gene expression in promyelocytic leukemia cells partly through Sp1 oxidation
    Wen Chien Chou
    Department of Laboratory Medicine, National Taiwan University Hospital
    Blood 106:304-10. 2005
    ..We conclude that ROS contributed partly to arsenic-mediated gene regulation and that Sp1 oxidation contributed to gene suppression by arsenic-induced ROS...
  60. ncbi request reprint Evidence for involvement of calpain in c-Myc proteolysis in vivo
    George W Small
    The Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    Arch Biochem Biophys 400:151-61. 2002
    ..These studies support a role for calpain in the control of c-Myc levels in vivo, and suggest that mutations impacting on sensitivity to calpain may contribute to c-Myc-mediated tumorigenesis...
  61. ncbi request reprint The c-Myc target gene Rcl (C6orf108) encodes a novel enzyme, deoxynucleoside 5'-monophosphate N-glycosidase
    Yoan Konto Ghiorghi
    Unite de Chimie Organique, CNRS Unité de Recherche Associée 2128, Institut Pasteur, 25 28 Rue du Dr Roux, 75724 Paris Cedex 15, France
    J Biol Chem 282:8150-6. 2007
    ..The reaction products of this novel enzyme activity have been implicated in purine or pyrimidine salvage, glycolysis, and angiogenesis, and hence are all highly relevant for tumorigenesis...
  62. ncbi request reprint Acute promyelocytic leukemia: recent advances in therapy and molecular basis of response to arsenic therapies
    Wen Chien Chou
    Department of Laboratory Medicine and Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan
    Curr Opin Hematol 12:1-6. 2005
    ..This paper reviews recent findings that reveal why a traditional poison has become a magical potion for a major type of APL, which is characterized by a balanced chromosomal translocation t(15;17)...
  63. ncbi request reprint MYC can enforce cell cycle transit from G1 to S and G2 to S, but not mitotic cellular division, independent of p27-mediated inihibition of cyclin E/CDK2
    Debabrita Deb-Basu
    Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, California, USA
    Cell Cycle 5:1348-55. 2006
    ..Our results have implications for the mechanisms by which MYC overexpression dysregulates cell cycle transit, causes genomic destabilization and is restrained from causing tumorigenesis...

Research Grants25

  1. C MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERS
    CHI DANG; Fiscal Year: 2004
    ....
  2. C-MYC Targets in the Pathogenesis of Human Cancer
    CHI DANG; Fiscal Year: 2007
    ..Aim 4. To determine the molecular mechanisms by which Myc collaborates with the hypoxia inducible transcription factor, HIF1, in regulating hypoxia-responsive genes vital for tumor survival such as those encoding glycolytic enzymes. ..
  3. C-MYC Targets in the Pathogenesis of Human Cancer
    CHI DANG; Fiscal Year: 2009
    ..Aim 4. To determine the molecular mechanisms by which Myc collaborates with the hypoxia inducible transcription factor, HIF1, in regulating hypoxia-responsive genes vital for tumor survival such as those encoding glycolytic enzymes. ..
  4. C MYC--TRANSCRIPTION AND APOPTOSIS
    Chi V Dang; Fiscal Year: 2010
    ....
  5. C-MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERS
    CHI DANG; Fiscal Year: 1999
    ..in neoplasia? 3) What are the effects of Mxi-1 on the expression of c-Myc target genes? and 4) Which c-Myc target genes predispose fibroblasts to lymphotoxin-mediated apoptosis, and is this pathway exploitable for therapeutic purposes? ..
  6. C-MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERS
    CHI DANG; Fiscal Year: 1993
    ..In addition, it is hoped that the understanding of these mechanisms will provide a rational molecular approach to potential cancer therapeutics...
  7. C MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERS
    Chi V Dang; Fiscal Year: 2010
    ..We will use a new way of retrieving subpopulations of cancer cells from tumors and determine their sensitivities to specific therapies, informing strategic combination therapy targeting metabolism. ..