Research Topics
Genomes and GenesSpecies | CHI DANGSummaryAffiliation: Johns Hopkins University Country: USA Publications
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Publications
Therapeutic targeting of Myc-reprogrammed cancer cell metabolismC 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...
An integrated database of genes responsive to the Myc oncogenic transcription factor: identification of direct genomic targetsKaren 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...- Stimulation of Myc transactivation by the TATA binding protein in promoter-reporter assaysJohn F Barrett
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
BMC Biochem 6:7. 2005.... - Rethinking the Warburg effect with Myc micromanaging glutamine metabolismChi 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... 
The great MYC escape in tumorigenesisChi 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...- 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.... - The c-Myc target gene networkChi 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... - PKM2 tyrosine phosphorylation and glutamine metabolism signal a different view of the Warburg effectChi 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... - The interplay between MYC and HIF in cancerChi 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... - Antimalarial therapy prevents Myc-induced lymphomaChi 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... - Therapeutic targeting of cancer cell metabolismChi 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.... - 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... - Have you seen...?: Micro-managing and restraining pluripotent stem cells by MYCChi V Dang
Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
EMBO J 28:3065-6. 2009.... - MYC-induced cancer cell energy metabolism and therapeutic opportunitiesChi 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... - Edging toward new therapeutics with cyclin D1 Egl'ng on cancerChi 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... - Muscle fatigue from losing your PHDChi 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... - Runner's anemiaC 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... - Global mapping of c-Myc binding sites and target gene networks in human B cellsKaren 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.... - c-Myc-regulated microRNAs modulate E2F1 expressionKathryn 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.... - Hypoxia-inducible factor 1 and dysregulated c-Myc cooperatively induce vascular endothelial growth factor and metabolic switches hexokinase 2 and pyruvate dehydrogenase kinase 1Jung 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.... - Widespread microRNA repression by Myc contributes to tumorigenesisTsung 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... - Global regulation of nucleotide biosynthetic genes by c-MycYen Chun Liu
Program in Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
PLoS ONE 3:e2722. 2008.... - HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxiaJung 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... - Myc stimulates nuclearly encoded mitochondrial genes and mitochondrial biogenesisFeng 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... - Evaluation of myc E-box phylogenetic footprints in glycolytic genes by chromatin immunoprecipitation assaysJung 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... - Lin-28B transactivation is necessary for Myc-mediated let-7 repression and proliferationTsung 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... - c-myc overexpression causes anaplasia in medulloblastomaDuncan 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... - Biology and treatment of Burkitt's lymphomaJason 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... - Inhibition of lactate dehydrogenase A induces oxidative stress and inhibits tumor progressionAnne 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.... - HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activityHuafeng 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... - Histopathological and molecular prognostic markers in medulloblastoma: c-myc, N-myc, TrkC, and anaplasiaCharles 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... - Induction of ectopic Myc target gene JAG2 augments hypoxic growth and tumorigenesis in a human B-cell modelJason 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... - c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolismPing 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... - Effects of hypoxia on tumor metabolismJung 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... - Digoxin and other cardiac glycosides inhibit HIF-1alpha synthesis and block tumor growthHuafeng 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.... - The c-Myc target gene PRDX3 is required for mitochondrial homeostasis and neoplastic transformationDiane 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... - hTERT gene amplification and increased mRNA expression in central nervous system embryonal tumorsXing 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... - The Myc target gene JPO1/CDCA7 is frequently overexpressed in human tumors and has limited transforming activity in vivoRebecca 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... - Activation of transferrin receptor 1 by c-Myc enhances cellular proliferation and tumorigenesisKathryn 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... - MYC overexpression induces prostatic intraepithelial neoplasia and loss of Nkx3.1 in mouse luminal epithelial cellsTsuyoshi 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... - Highlights of the National Cancer Institute Workshop on mitochondrial function and cancerMary Ellen Perry
Division of Cancer Biology, National Cancer Institute, NIH, Bethesda, Maryland, USA
Cancer Res 64:7640-4. 2004 - A strategy for identifying transcription factor binding sites reveals two classes of genomic c-Myc target sitesTimothy 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.... - HIF-1 regulates cytochrome oxidase subunits to optimize efficiency of respiration in hypoxic cellsRyo 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... - Role of NADPH oxidase in arsenic-induced reactive oxygen species formation and cytotoxicity in myeloid leukemia cellsWen-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... - Unexpected antitumorigenic effect of fenbendazole when combined with supplementary vitaminsPing 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... - Cancer's molecular sweet tooth and the Warburg effectJung-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... - Discovering robust protein biomarkers for disease from relative expression reversals in 2-D DIGE dataTroy 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... - Multifaceted roles of glycolytic enzymesJung-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... - Isolation of bone marrow-derived stem cells using density-gradient separationTarja 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... - Identification and characterization of the novel centrosome-associated protein CCCAPAndrew 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)... - HIF-dependent antitumorigenic effect of antioxidants in vivoPing 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... - Human-induced pluripotent stem cells from blood cells of healthy donors and patients with acquired blood disordersZhaohui 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... - Development of human protein reference database as an initial platform for approaching systems biology in humansSuraj 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... - Unique conformation of cancer autoantigen B23 in hepatoma: a mechanism for specificity in the autoimmune responseDanielle 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... - Conditional deletion of c-myc does not impair liver regenerationFeng 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... - Anoxic fibroblasts activate a replication checkpoint that is bypassed by E1aLawrence 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.... - In silico identification of transcriptional regulators associated with c-MycRan 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... - Increased expression of TATA-binding protein, the central transcription factor, can contribute to oncogenesisSandra 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... - Arsenic suppresses gene expression in promyelocytic leukemia cells partly through Sp1 oxidationWen 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... - Evidence for involvement of calpain in c-Myc proteolysis in vivoGeorge 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... - The c-Myc target gene Rcl (C6orf108) encodes a novel enzyme, deoxynucleoside 5'-monophosphate N-glycosidaseYoan 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... - Acute promyelocytic leukemia: recent advances in therapy and molecular basis of response to arsenic therapiesWen-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..SUMMARY: Recent advances in the clinical use of arsenic, the mechanism of arsenic-mediated cytotoxicity, and modulations of ATO to increase its efficacy and expand its clinical spectrum are reviewed... - 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/CDK2Debabrita 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 Grants
- C MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERSCHI DANG; Fiscal Year: 2004....
- C-MYC Targets in the Pathogenesis of Human CancerCHI 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. ..
- C-MYC Targets in the Pathogenesis of Human CancerCHI 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. ..
- C MYC--TRANSCRIPTION AND APOPTOSISChi V Dang; Fiscal Year: 2010....
- C-MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERSCHI 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? ..
- C-MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERSCHI 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...
- C MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERSChi 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. ..