Genomes and Genes
proto oncogene proteins c myc
Summary: Cellular DNA-binding proteins encoded by the c-myc genes. They are normally involved in nucleic acid metabolism and in mediating the cellular response to growth factors. Elevated and deregulated (constitutive) expression of c-myc proteins can cause tumorigenesis.
Publications286 found, 100 shown here
- Identification of c-MYC as a target of the APC pathwayT C He
Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA
Science 281:1509-12. 1998..These results provide a molecular framework for understanding the previously enigmatic overexpression of c-MYC in colorectal cancers...
- Reflecting on 25 years with MYCNatalie Meyer
Amgen Canada, Inc Mississauga, Ontario, Canada
Nat Rev Cancer 8:976-90. 2008..Here we chronicle the major advances in our understanding of MYC biology, and peer into the future of MYC research...
- Myc's broad reachMartin Eilers
Institute of Molecular Biology and Tumor Research, 35033 Marburg, Germany
Genes Dev 22:2755-66. 2008..This review is focused on two major aspects of Myc: the nature of the genes and pathways that are targeted by Myc, and the role of Myc in stem cell and cancer biology...
- Generation of induced pluripotent stem cells without Myc from mouse and human fibroblastsMasato Nakagawa
Department of Stem Cell Biology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606 8507, Japan
Nat Biotechnol 26:101-6. 2008..The protocol also enabled efficient isolation of iPS cells without drug selection. Furthermore, we generated human iPS cells from adult dermal fibroblasts without MYC...
- 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...
- c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instabilityOmid Vafa
The Salk Institute for Biological Studies, La Jolla, CA 92037, USA
Mol Cell 9:1031-44. 2002..We propose that oncogene activation can induce DNA damage and override damage controls, thereby accelerating tumor progression via genetic instability...
- Modelling Myc inhibition as a cancer therapyLaura Soucek
Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, California 94143 0875, USA
Nature 455:679-83. 2008..Our data demonstrate the feasibility of targeting Myc, a common downstream conduit for many oncogenic signals, as an effective, efficient and tumour-specific cancer therapy...
- Reverse engineering of regulatory networks in human B cellsKatia Basso
Institute for Cancer Genetics, 1300 St Nicholas Avenue, Room 912, New York, New York 10032, USA
Nat Genet 37:382-90. 2005..The newly identified MYC targets include some major hubs. This approach can be generally useful for the analysis of normal and pathologic networks in mammalian cells...
- The Fbw7 tumor suppressor regulates glycogen synthase kinase 3 phosphorylation-dependent c-Myc protein degradationMarkus Welcker
Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
Proc Natl Acad Sci U S A 101:9085-90. 2004..Because Fbw7 mediates the degradation of cyclin E, Notch, and c-Jun, as well as c-Myc, the loss of Fbw7 is likely to elicit profound effects on cell proliferation during tumorigenesis...
- Repression of p15INK4b expression by Myc through association with Miz-1P Staller
Institute of Molecular Biology and Tumour Research, Emil Mannkopff Strabetae 2, 35033 Marburg, Germany
Nat Cell Biol 3:392-9. 2001..Alleles of c-myc that are unable to bind to Miz-1 fail to inhibit accumulation of p15INK4b messenger RNA in primary cells and are, as a consequence, deficient in immortalization...
- 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...
- MYC inactivation uncovers pluripotent differentiation and tumour dormancy in hepatocellular cancerCatherine M Shachaf
Division of Medical Oncology, Department of Medicine, Stanford University, California 94305, USA
Nature 431:1112-7. 2004....
- 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...
- Distinct thresholds govern Myc's biological output in vivoDaniel J Murphy
Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA
Cancer Cell 14:447-57. 2008..The requirement to keep activated oncogenes at a low level to avoid engaging tumor suppression is likely an important selective pressure governing the early stages of tumor microevolution...
- HIF-1alpha induces cell cycle arrest by functionally counteracting MycMinori Koshiji
Laboratory of Human Carcinogenesis, NCI, National Institutes of Health, Bethesda, MD 20892, USA
EMBO J 23:1949-56. 2004..Hence, we propose that Myc is an integral part of a novel HIF-1alpha pathway, which regulates a distinct group of Myc target genes in response to hypoxia...
- Myc deletion rescues Apc deficiency in the small intestineOwen J Sansom
The Beatson Institute, Garscube Estate, Glasgow G61 1BD, UK
Nature 446:676-9. 2007..Array analysis revealed that Myc is required for the majority of Wnt target gene activation following Apc loss. These data establish Myc as the critical mediator of the early stages of neoplasia following Apc loss...
- Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with MycE M Blackwood
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98104
Science 251:1211-7. 1991..These results suggest that Myc family proteins undergo a restricted set of interactions in the cell and may belong to the more general class of eukaryotic DNA-binding transcription factors...
- The beta-catenin/TCF-4 complex imposes a crypt progenitor phenotype on colorectal cancer cellsMarc van de Wetering
Department of Immunology and Center for Biomedical Genetics, University Medical Center, 3584 CX, Utrecht, The Netherlands
Cell 111:241-50. 2002..Thus, the beta-catenin/TCF-4 complex constitutes the master switch that controls proliferation versus differentiation in healthy and malignant intestinal epithelial cells...
- The Myc/Max/Mad network and the transcriptional control of cell behaviorC Grandori
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109 1024, USA
Annu Rev Cell Dev Biol 16:653-99. 2000..Because Myc and Mad proteins are expressed in response to diverse signaling pathways, the network can be viewed as a functional module which acts to convert environmental signals into specific gene-regulatory programs...
- An alternative pathway for gene regulation by MycK Peukert
Hans Knöll Institut für Naturstoff Forschung, Department of Cell and Molecular Biology, Beutenbergstrasse 11, 07745 Jena, Germany
EMBO J 16:5672-86. 1997..Our data suggest a model for how gene repression by Myc may occur in vivo...
- Skp2 regulates Myc protein stability and activitySo Young Kim
Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA
Mol Cell 11:1177-88. 2003..These data suggest that Skp2 functions to connect Myc activity and destruction, and reveal an unexpected oncoprotein connection that may play an important role in controlling cell growth in normal and cancer cells...
- Targeted expression of MYCN causes neuroblastoma in transgenic miceW A Weiss
G W Hooper Foundation, and Department of Neurology, University of California, San Francisco 94143 0552, USA
EMBO J 16:2985-95. 1997....
- Manipulation of stem cell proliferation and lineage commitment: visualisation of label-retaining cells in wholemounts of mouse epidermisKristin M Braun
Keratinocyte Laboratory, Cancer Research UK London Research Institute, 44 Lincoln s Inn Fields, London WC2A 3PX, UK
Development 130:5241-55. 2003..We conclude that LRC are more sensitive to some proliferative stimuli than others and that changes in lineage can occur with or without recruitment of LRC into cycle...
- Drosophila myc regulates cellular growth during developmentL A Johnston
Fred Hutchinson Cancer Research Center, Division of Basic Sciences, Seattle, Washington 98109, USA
Cell 98:779-90. 1999..Our results indicate that dMyc links patterning signals to cell division by regulating primary targets involved in cellular growth and metabolism...
- NOTCH1 directly regulates c-MYC and activates a feed-forward-loop transcriptional network promoting leukemic cell growthTeresa Palomero
Institute for Cancer Genetics and Joint Centers for Systems Biology, Columbia University, New York, NY 10032, USA
Proc Natl Acad Sci U S A 103:18261-6. 2006..These results identify c-MYC as an essential mediator of NOTCH1 signaling and integrate NOTCH1 activation with oncogenic signaling pathways upstream of c-MYC...
- TGFbeta influences Myc, Miz-1 and Smad to control the CDK inhibitor p15INK4bJ Seoane
Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
Nat Cell Biol 3:400-8. 2001..Thus, two separate TGFbeta-dependent inputs - Smad-mediated transactivation and relief of repression by Myc - keep tight control over p15INK4b activation...
- c-Myc is essential for vasculogenesis and angiogenesis during development and tumor progressionTroy A Baudino
Department of Biochemistry, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
Genes Dev 16:2530-43. 2002..These findings support the model wherein c-Myc promotes cell growth and transformation, as well as vascular and hematopoietic development, by functioning as a master regulator of angiogenic factors...
- The Myc oncoprotein as a therapeutic target for human cancerMarina Vita
Department of Microbiology, Tumor and Cell Biology MTC, Karolinska Institutet, Stockholm, Sweden
Semin Cancer Biol 16:318-30. 2006..Such therapies could have potential in combination with mechanistically different cytotoxic drugs to combat and eradicate tumors cells...
- N-myc can functionally replace c-myc in murine development, cellular growth, and differentiationB A Malynn
The Center for Blood Research, Boston, Massachusetts 02115 USA
Genes Dev 14:1390-9. 2000..Therefore, the myc gene family must have evolved, to a large extent, to facilitate differential patterns of expression...
- Myc represses the p21(WAF1/CIP1) promoter and interacts with Sp1/Sp3A L Gartel
Department of Molecular Genetics, University of Illinois College of Medicine, Chicago, IL 60607, USA
Proc Natl Acad Sci U S A 98:4510-5. 2001..Repression of the p21 promoter may contribute to the ability of c-Myc to promote cell proliferation...
- Efficient and rapid generation of induced pluripotent stem cells from human keratinocytesTrond Aasen
Center of Regenerative Medicine in Barcelona, Dr Aiguader 88, 08003 Barcelona, Spain
Nat Biotechnol 26:1276-84. 2008..Our findings provide an experimental model for investigating the bases of cellular reprogramming and highlight potential advantages of using keratinocytes to generate patient-specific iPS cells...
- Myc represses differentiation-induced p21CIP1 expression via Miz-1-dependent interaction with the p21 core promoterSiqin Wu
Upsala Genetic Center, Department of Plant Biology, Swedish University of Agricultural Sciences
Oncogene 22:351-60. 2003..In conclusion, repression of differentiation-induced p21 expression through Miz-1 may be an important mechanism by which Myc blocks differentiation...
- MicroRNA let-7a down-regulates MYC and reverts MYC-induced growth in Burkitt lymphoma cellsValerie B Sampson
Department of Molecular Genetics, Cellular and Tissue Transplantation, Alfred I duPont Hospital for Children, Wilmington, Delaware 19803, and Center for Applied Genomics, Public Health Research Institute, UMDNJ New Jersey Medical School, Newark, USA
Cancer Res 67:9762-70. 2007....
- 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....
- HIF and c-Myc: sibling rivals for control of cancer cell metabolism and proliferationJohn D Gordan
Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Cancer Cell 12:108-13. 2007..However, acting in concert these transcription factors reprogram metabolism, protein synthesis, and cell cycle progression, to "fine tune" adaptive responses to hypoxic environments...
- Myc represses transcription through recruitment of DNA methyltransferase corepressorCarmen Brenner
Free University of Brussels, Faculty of Medicine, Laboratory of Molecular Virology, Brussels, Belgium
EMBO J 24:336-46. 2005..Furthermore, these findings suggest that targeting of DNA methyltransferases by transcription factors is a wide and general mechanism for the generation of specific DNA methylation patterns within a cell...
- Genomic targets of the human c-Myc proteinPaula C Fernandez
DNAX Research Institute, Palo Alto, California 94304, USA
Genes Dev 17:1115-29. 2003..Myc further enhanced histone acetylation, with or without accompanying induction of mRNA expression. Our findings point to a high regulatory and biological diversity among Myc-target genes...
- 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....
- p53-Dependent transcriptional repression of c-myc is required for G1 cell cycle arrestJenny S L Ho
Ontario Cancer Institute, Prince Margaret Hospital, Toronto, Canada
Mol Cell Biol 25:7423-31. 2005..These data suggest that p53 represses c-myc transcription through a mechanism that involves histone deacetylation...
- Control of cell proliferation by MycC Bouchard
Institute for Molecular Biology and Tumour Research, University of Marburg, Germany
Trends Cell Biol 8:202-6. 1998..This review summarizes recent progress in understanding how Myc stimulates cell proliferation and how this might contribute to cellular transformation and tumorigenesis...
- c-Myc associates with ribosomal DNA and activates RNA polymerase I transcriptionAzadeh Arabi
Södertörns högskola, S 141 89 Huddinge, Sweden
Nat Cell Biol 7:303-10. 2005..These results suggest that c-Myc coordinates the activity of all three nuclear RNA polymerases, and thereby plays a key role in regulating ribosome biogenesis and cell growth...
- Myc is a Notch1 transcriptional target and a requisite for Notch1-induced mammary tumorigenesis in miceApostolos Klinakis
Department of Genetics and Development, Columbia University, 1150 St Nicholas Avenue, New York, NY 10032, USA
Proc Natl Acad Sci U S A 103:9262-7. 2006..Consistent with this mechanistic link, Notch1 and Myc expression is positively correlated by immunostaining in 38% of examined human breast carcinomas...
- Transcriptional regulation and transformation by Myc proteinsSovana Adhikary
Institute for Molecular Biology and Tumour Research, University of Marburg, Emil Mannkopff Strasse 2, 35033 Marburg, Germany
Nat Rev Mol Cell Biol 6:635-45. 2005..Recently, a wealth of data has shed new light on the biochemical functions of Myc proteins and on the mechanisms through which they function in cellular transformation...
- PIM1-dependent phosphorylation of histone H3 at serine 10 is required for MYC-dependent transcriptional activation and oncogenic transformationAlessio Zippo
Dipartimento di Biologia Molecolare Università di Siena, Via Fiorentina 1, 53100 Siena, Italy
Nat Cell Biol 9:932-44. 2007....
- Phosphorylation-dependent degradation of c-Myc is mediated by the F-box protein Fbw7Masayoshi Yada
Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, Maidashi, Higashi ku, Fukuoka, Fukuoka, Japan
EMBO J 23:2116-25. 2004..Accumulation of c-Myc was also apparent in mouse Fbw7-/- embryonic stem cells. These observations suggest that two F-box proteins, Fbw7 and Skp2, differentially regulate c-Myc stability by targeting MB1 and MB2, respectively...
- The novel ATM-related protein TRRAP is an essential cofactor for the c-Myc and E2F oncoproteinsS B McMahon
Department of Molecular Biology, Princeton University, New Jersey 08544 1014, USA
Cell 94:363-74. 1998..These data suggest that TRRAP is an essential cofactor for both the c-Myc and E1A/E2F oncogenic transcription factor pathways...
- Sp1 cooperates with c-Myc to activate transcription of the human telomerase reverse transcriptase gene (hTERT)S Kyo
Department of Obstetrics and Gynecology, Kanazawa University, School of Medicine, 13 1 Takaramachi, Kanazawa, Ishikawa 920 0934, Japan
Nucleic Acids Res 28:669-77. 2000..These findings suggest that c-Myc and Sp1 cooperatively function as the major determinants of hTERT expression, and that the switching functions of Myc/Max and Mad/Max might also play roles in telomerase regulation...
- The ubiquitin ligase HectH9 regulates transcriptional activation by Myc and is essential for tumor cell proliferationSovana Adhikary
Institute for Molecular Biology and Tumor Research, University of Marburg, Emil Mannkopff Str 2, 35033 Marburg, Germany
Cell 123:409-21. 2005..Our results suggest that site-specific ubiquitination regulates the switch between an activating and a repressive state of the Myc protein, and they suggest a strategy to interfere with Myc function in vivo...
- The basic region/helix-loop-helix/leucine zipper domain of Myc proto-oncoproteins: function and regulationB Luscher
Institut fur Molekularbiologie, Medizinische Hochschule Hannover, Germany
Oncogene 18:2955-66. 1999..Importantly this domain together with the N-terminal transactivation domain is essential for Myc biology. Here we have summarized the structural, functional, and regulatory aspects of the bHLHZip domain of Myc proteins...
- The many faces of c-MYCStella Pelengaris
Molecular Medicine, Biomedical Research Institute, University of Warwick, Coventry CV4 7AL, UK
Arch Biochem Biophys 416:129-36. 2003..Although still in its infancy, encouraging results have been reported for several approaches using gene targeting to interfere with c-MYC expression or activity both in vitro and in vivo...
- The F-box protein Skp2 participates in c-Myc proteosomal degradation and acts as a cofactor for c-Myc-regulated transcriptionNatalie von der Lehr
Department of Plant Biology and Forest Genetics, Swedish University of Agricultural Sciences, 750 07 Uppsala, Sweden
Mol Cell 11:1189-200. 2003..The results suggest that Skp2 is a transcriptional cofactor for c-Myc and indicates a close relationship between transcription activation and transcription factor ubiquitination...
- Physical and functional interactions between Pim-1 kinase and Cdc25A phosphatase. Implications for the Pim-1-mediated activation of the c-Myc signaling pathwayT Mochizuki
Biophysics Division, National Cancer Center Research Institute, 5 1 1 Tsukiji, Chuo Ku, Tokyo 104 0045, Japan
J Biol Chem 274:18659-66. 1999..Our results indicate that Cdc25A might be a key molecule that links Pim-1 and c-Myc and that also ties Pim-1-mediated mitogenic signals to cell cycle machinery...
- A small-molecule c-Myc inhibitor, 10058-F4, induces cell-cycle arrest, apoptosis, and myeloid differentiation of human acute myeloid leukemiaMing Jer Huang
Department of Medicine, Mackay Memorial Hospital, Taipei, Taiwan
Exp Hematol 34:1480-9. 2006..Inhibition of the c-Myc/Max heterodimerization by the recently identified small-molecule compound, 10058-F4, might be a novel antileukemic strategy...
- Direct reprogramming of genetically unmodified fibroblasts into pluripotent stem cellsAlexander Meissner
Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge Massachusetts 02142, USA
Nat Biotechnol 25:1177-81. 2007..Here we demonstrate that reprogrammed pluripotent cells can be isolated from genetically unmodified somatic donor cells solely based upon morphological criteria...
- Induction of Mxi1-SR alpha by FOXO3a contributes to repression of Myc-dependent gene expressionOona Delpuech
Gene Expression Analysis Laboratory, Cancer Research UK London Research Institute, 44 Lincoln s Inn Fields, London WC2A 3PX, United Kingdom
Mol Cell Biol 27:4917-30. 2007..Our results provide evidence of direct regulation of Mxi1 by FOXO3a and imply an additional mechanism through which the PI3-kinase/Akt/FOXO pathway can modulate Myc function...
- Concomitant MYC and microRNA cluster miR-17-92 (C13orf25) amplification in human mantle cell lymphomaAndrea Rinaldi
Leuk Lymphoma 48:410-2. 2007
- Phosphorylation by Cdk2 is required for Myc to repress Ras-induced senescence in cotransformationPer Hydbring
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE 171 77 Stockholm, Sweden
Proc Natl Acad Sci U S A 107:58-63. 2010..Finally, our findings highlight that pharmacological inhibition of Cdk2 activity is a potential therapeutical principle for cancer therapy, in particular for tumors with activated Myc or Ras...
- Human NM23/nucleoside diphosphate kinase regulates gene expression through DNA binding to nuclease-hypersensitive transcriptional elementsE H Postel
Department of Molecular Biology, Princeton University, New Jersey 08544, USA
J Bioenerg Biomembr 32:277-84. 2000..These data support a model in which NM23/NDP kinase modulates gene expression through DNA binding and subsequent structural transactions...
- Myc-induced proliferation and transformation require Akt-mediated phosphorylation of FoxO proteinsCaroline Bouchard
Institute for Molecular Biology and Tumor Research, Marburg, Germany
EMBO J 23:2830-40. 2004..We suggest that the cooperativity between Myc and Ras is at least in part due to the fact that Myc and FoxO proteins control distinct steps in the activation of an overlapping set of critical target genes...
- Overexpression of the c-Myc oncoprotein blocks the growth-inhibitory response but is required for the mitogenic effects of transforming growth factor beta 1M G Alexandrow
Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
Proc Natl Acad Sci U S A 92:3239-43. 1995..Addition of estradiol late in G1 had no suppressive effect on TGF beta 1-induced growth inhibition...
- A signalling pathway controlling c-Myc degradation that impacts oncogenic transformation of human cellsElizabeth Yeh
Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
Nat Cell Biol 6:308-18. 2004..Thus, Ras-dependent signalling cascades ensure transient and self-limiting accumulation of c-Myc, disruption of which contributes to human cell oncogenesis...
- Non-transcriptional control of DNA replication by c-MycDavid Dominguez-Sola
Institute for Cancer Genetics, Department of Genetics and Development and Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York 10032, USA
Nature 448:445-51. 2007..These findings identify a critical function of c-Myc in DNA replication and suggest a novel mechanism for its normal and oncogenic functions...
- The many roles of c-Myc in apoptosisE B Thompson
Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston 77555 0645, USA
Annu Rev Physiol 60:575-600. 1998..Hypotheses of the mechanisms by which expression and repression of c-myc lead to apoptosis are discussed...
- Dissection of transcriptional programmes in response to serum and c-Myc in a human B-cell lineIsabel Schlosser
GSF Research Centre, Institute of Clinical Molecular Biology and Tumour Genetics, Marchioninistr 25, D 81377 Munich, Germany
Oncogene 24:520-4. 2005..The data support our current notion that Myc is essential for the regulation of a large number of growth-related genes in B cells, and cannot be replaced by other serum-induced factors...
- Overexpression of an mRNA-binding protein in human colorectal cancerJ Ross
McArdle Laboratory for Cancer Research, Department of Oncology, University of Wisconsin Madison, 1400 University Avenue, Madison, WI 53706, USA
Oncogene 20:6544-50. 2001..c-myc mRNA levels appeared to be elevated in tumor specimens. We conclude that the CRD-BP is scarce or absent from normal colon but is overexpressed in colorectal cancer. The CRD-BP might be a novel human tumor marker...
- Integration of estrogen and Wnt signaling circuits by the polycomb group protein EZH2 in breast cancer cellsBin Shi
Department of Biochemistry and Molecular Biology, Peking University Health Science Center, 38 Xue Yuan Road, Beijing 100083, China
Mol Cell Biol 27:5105-19. 2007..Our experiments indicated that EZH2 is a dual function transcription regulator with a dynamic activity, and we provide a mechanism for EZH2 in tumorigenesis...
- Myc-binding-site recognition in the human genome is determined by chromatin contextErnesto Guccione
Department of Experimental Oncology, European Institute of Oncology, IFOM IEO Campus, Milan 20139, Italy
Nat Cell Biol 8:764-70. 2006..These data imply that tethering of a transcription factor to restricted chromatin domains is rate-limiting for sequence-specific DNA binding in vivo...
- Mnt loss triggers Myc transcription targets, proliferation, apoptosis, and transformationJonas A Nilsson
Department of Biochemistry, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
Mol Cell Biol 24:1560-9. 2004..Therefore, Mnt behaves as a tumor suppressor. These findings support a model where Mnt represses Myc target genes and Myc functions as an oncogene by relieving Mnt-mediated repression...
- Smad pathway-specific transcriptional regulation of the cell cycle inhibitor p21(WAF1/Cip1)Katerina Pardali
Ludwig Institute for Cancer Research, Uppsala, Sweden
J Cell Physiol 204:260-72. 2005..Thus, p21 is a common target of all TGF-beta superfamily pathways. However, the ability of TGF-beta superfamily members to induce cell growth arrest depends on the regulation of additional gene targets...
- Repression of transcription of the p27(Kip1) cyclin-dependent kinase inhibitor gene by c-MycW Yang
Department of Biochemistry, Boston University Medical School, Boston, Maryland, MA 02118, USA
Oncogene 20:1688-702. 2001..Overall, these studies identify the p27 CKI gene as a new target whereby c-Myc can control cell proliferation, survival and neoplastic transformation...
- Stimulation of c-MYC transcriptional activity and acetylation by recruitment of the cofactor CBPJörg Vervoorts
Institut fur Molekularbiologie, Medizinische Hochschule Hannover, Carl Neuberg Strasse 1, 30625 Hannover, Germany
EMBO Rep 4:484-90. 2003..Functionally, this results in a decrease in ubiquitination and stabilization of c-MYC proteins. Thus, CBP and p300 are novel functional binding partners of c-MYC...
- The miR-17/92 polycistron is up-regulated in sonic hedgehog-driven medulloblastomas and induced by N-myc in sonic hedgehog-treated cerebellar neural precursorsPaul A Northcott
Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre, Program in Developmental and Stem Cell Biology, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada
Cancer Res 69:3249-55. 2009..We conclude that miR-17/92 is a positive effector of Shh-mediated proliferation and that aberrant expression/amplification of this miR confers a growth advantage to medulloblastomas...
- Down-regulation of c-Myc following MEK/ERK inhibition halts the expression of malignant phenotype in rhabdomyosarcoma and in non muscle-derived human tumorsFrancesco Marampon
Department of Experimental Medicine, University of L Aquila, L Aquila, Italy
Mol Cancer 5:31. 2006....
- AID-dependent activation of a MYC transgene induces multiple myeloma in a conditional mouse model of post-germinal center malignanciesMarta Chesi
Comprehensive Cancer Center, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ 85259, USA
Cancer Cell 13:167-80. 2008....
- Fbw7 and Usp28 regulate myc protein stability in response to DNA damageNikita Popov
Institute of Molecular Biology and Tumor Research, Emil Mannkopff Str 2, Marburg, Germany
Cell Cycle 6:2327-31. 2007..Our data extend previous observations that link Myc function to the cellular response to DNA damage...
- c-Myc phosphorylation is required for cellular response to oxidative stressBarbara Benassi
Experimental Chemotherapy Laboratory, Experimental Research Center, Regina Elena Cancer Institute, Rome, Italy
Mol Cell 21:509-19. 2006..Thus, the c-Myc phosphorylation-dependent activation of the GSH-directed survival pathway can contribute to oxidative stress resistance in tumor cells, which generally exhibit deregulated c-Myc expression...
- Molecular determinants of Akt-induced keratinocyte transformationC Segrelles
Department of Cell and Molecular Biology, CIEMAT, Madrid, Spain
Oncogene 25:1174-85. 2006..Collectively, these results demonstrate that Akt is able to transform keratinocytes by specific mechanisms involving transcriptional and post-transcriptional processes...
- Function of the c-Myc oncogenic transcription factorC V Dang
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, 21205, USA
Exp Cell Res 253:63-77. 1999..From this perspective, c-Myc emerges as an oncogenic transcription factor that integrates the cell cycle machinery with cell adhesion, cellular metabolism, and the apoptotic pathways...
- Stat3 and c-Myc genome-wide promoter occupancy in embryonic stem cellsBenjamin L Kidder
EMD Serono Research Institute, Inc, Rockland, Massachusetts, United States of America
PLoS ONE 3:e3932. 2008..Altogether, we reveal transcriptional targets of two key pluripotency-related genes in ES cells--Stat3 and c-Myc, thus providing further insight into the ES cell transcriptional network...
- Suppression of Myc-induced apoptosis in beta cells exposes multiple oncogenic properties of Myc and triggers carcinogenic progressionStella Pelengaris
Molecular Medicine Research Center, Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, United Kingdom
Cell 109:321-34. 2002..Our data indicate that highly complex neoplastic lesions can be both induced and maintained in vivo by a simple combination of two interlocking molecular lesions...
- gamma-catenin is regulated by the APC tumor suppressor and its oncogenic activity is distinct from that of beta-cateninF T Kolligs
Division of Medical Genetics and the Cancer Center, University of Michigan School of Medicine, Ann Arbor, Michigan 48109 USA
Genes Dev 14:1319-31. 2000..Furthermore, the data imply beta- and gamma-catenin may have distinct roles in Wnt signaling and cancer via differential effects on downstream target genes...
- Nuclear MYC protein overexpression is an early alteration in human prostate carcinogenesisBora Gurel
Department of Pathology, The Johns Hopkins University, School of Medicine, Baltimore, MD 21231, USA
Mod Pathol 21:1156-67. 2008....
- HIF-2alpha promotes hypoxic cell proliferation by enhancing c-myc transcriptional activityJohn D Gordan
Abramson Family Cancer Research Institute, School of Medicine, University of Pennsylvania, 421 Curie Boulevard, Philadelphia, PA 19104, USA
Cancer Cell 11:335-47. 2007..Enhanced c-Myc activity likely contributes to HIF-2alpha-mediated neoplastic progression following loss of the VHL tumor suppressor and influences the behavior of hypoxic tumor cells...
- Targeting ornithine decarboxylase in Myc-induced lymphomagenesis prevents tumor formationJonas A Nilsson
Department of Biochemistry, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
Cancer Cell 7:433-44. 2005..Therefore, Odc is a critical Myc transcription target that regulates checkpoints that guard against tumorigenesis and is an effective target for cancer chemoprevention...
- Myc goes global: new tricks for an old oncogenePaul S Knoepfler
Department of Cell Biology and Human Anatomy, Institute of Pediatric Regenerative Medicine, Shriners Hospital for Children Northern California, University of California Davis School of Medicine, Davis, California 95616, USA
Cancer Res 67:5061-3. 2007..These findings suggest actions for Myc that extend beyond the traditional concept of a targeted gene regulator...
- Inhibition of CDK1 as a potential therapy for tumors over-expressing MYCAndrei Goga
Department of Medicine, Division of Hematology Oncology, University of California, San Francisco, San Francisco, California 94143 0552, USA
Nat Med 13:820-7. 2007..As there are no effective small-molecule inhibitors that selectively target the MYC pathway, we propose that CDK1 inhibition might therefore be useful in the treatment of human malignancies that overexpress MYC...
- p53 represses c-Myc through induction of the tumor suppressor miR-145Mohit Sachdeva
Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL 62794, USA
Proc Natl Acad Sci U S A 106:3207-12. 2009....
- Bim is a suppressor of Myc-induced mouse B cell leukemiaAlexander Egle
The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Melbourne, Victoria 3050, Australia
Proc Natl Acad Sci U S A 101:6164-9. 2004..Whereas the p19Arf/p53 pathway is frequently mutated in tumors arising in Bim(+/+) Emicro-Myc mice, it was unaffected in most Bim-deficient tumors, indicating that Bim reduction is an effective alternative to loss of p53 function...
- Analysis of Myc-induced histone modifications on target chromatinFrancesca Martinato
Department of Experimental Oncology, European Institute of Oncology IEO, IFOM IEO Campus, Milan, Italy
PLoS ONE 3:e3650. 2008..Our data are also consistent with the additive and redundant role of multiple acetylation events in transcriptional activation...
- Deficiency in glutamine but not glucose induces MYC-dependent apoptosis in human cellsMariia Yuneva
Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
J Cell Biol 178:93-105. 2007....
- c-Myc mediates activation of the cad promoter via a post-RNA polymerase II recruitment mechanismS R Eberhardy
University of Wisconsin Medical School, Madison, Wisconsin 53706, USA
J Biol Chem 276:48562-71. 2001..In summary, our results suggest that c-Myc activates transcription of cad by stimulating promoter clearance and elongation, perhaps via recruitment of P-TEFb...
- A non-transgenic mouse model for B-cell lymphoma: in vivo infection of p53-null bone marrow progenitors by a Myc retrovirus is sufficient for tumorigenesisDuonan Yu
Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania, PA 19104 6051, USA
Oncogene 21:1922-7. 2002..Our model would also be instrumental in assessing the transforming potential of Myc mutants and in studying cooperation between Myc and other oncogenes...
- A non-AUG translational initiation in c-myc exon 1 generates an N-terminally distinct protein whose synthesis is disrupted in Burkitt's lymphomasS R Hann
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104
Cell 52:185-95. 1988..In Burkitt's lymphomas, the removal or specific mutation of exon 1 in c-myc translocations correlates with suppression of synthesis of the larger protein, and thus may contribute to the oncogenic activation of c-myc...
- Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-mycVishva Mitra Sharma
Department of Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA
Mol Cell Biol 26:8022-31. 2006..These studies define the Notch1 molecular signature in mouse T-ALL and importantly provide mechanistic insight as to how Notch1 contributes to human T-ALL...
- The Oscar-worthy role of Myc in apoptosisNatalie Meyer
Division of Cancer Genomics and Proteomics, Ontario Cancer Institute Princess Margaret Hospital, Department of Medical Biophysics, University of Toronto, Toronto, Ont, Canada
Semin Cancer Biol 16:275-87. 2006..In this review, we will discuss established data, recent advances and future objectives regarding the regulatory processes and the functional cooperators that effect and abrogate apoptosis induced by Myc...
- Deregulated Wnt/beta-catenin program in high-risk neuroblastomas without MYCN amplificationX Liu
Division of Oncology, The Children s Hospital of Philadelphia, Philadelphia, PA 19104 4318, USA
Oncogene 27:1478-88. 2008..Thus, high-risk NBs without MYCN amplification may deregulate MYC and other oncogenic genes via altered beta-catenin signaling providing a potential candidate pathway for therapeutic inhibition...
- Reversible lymphomagenesis in conditionally c-MYC expressing miceDragan Marinkovic
Department of Physiological Chemistry, Ulm University, Ulm, Germany
Int J Cancer 110:336-42. 2004..The main observation was a gain of genomic material that corresponded to chromosome 15 in several T-cell tumors, which could be identified as trisomy...
- N-myc alters the fate of preneoplastic cells in a mouse model of medulloblastomaJessica D Kessler
Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
Genes Dev 23:157-70. 2009..These studies provide the first direct evidence that PNCs can give rise to tumors, and demonstrate that identification of genetic changes that promote tumor progression is critical for designing effective therapies for cancer...
- TMPRSS2-ERG fusion, a common genomic alteration in prostate cancer activates C-MYC and abrogates prostate epithelial differentiationC Sun
Department of Surgery, Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Rockville, MD 20852, USA
Oncogene 27:5348-53. 2008....
- N-Myc regulates a widespread euchromatic program in the human genome partially independent of its role as a classical transcription factorRebecca Cotterman
Department of Cell Biology, University of California Davis School of Medicine, Davis, California 95616, USA
Cancer Res 68:9654-62. 2008..These findings support a new dual model for Myc chromatin function with important implications for the role of Myc in cancer and stem cell biology, including that of induced pluripotent stem cells...
- Miz1 is required for early embryonic development during gastrulationSovana Adhikary
Institute for Molecular Biology and Tumor Research Institute for Cytobiology and Cytopathology, University of Marburg, 35033 Marburg, Germany
Mol Cell Biol 23:7648-57. 2003..Miz1(-/-) embryos succumb to massive apoptosis of ectodermal cells around day 7.5 of embryonic development. Our results show that Miz1 is required for early embryonic development during gastrulation...
- FUNCTION OF A DUAL SPECIFICITY TRANSCRIPTION FACTORPeter Hurlin; Fiscal Year: 2003..Finally, gene targeting in the mouse will be used to study the biological activities of Mga and the individual roles of its bHLHZip domain and T-domain. ..
- Myc Antagonism and Tumor Suppression by MntPeter Hurlin; Fiscal Year: 2008..abstract_text> ..
- Antisense Morpholino Oligomers to Treat RetinopathyGayathri Devi; Fiscal Year: 2003..The primary goal of this grant is to identify the optimal antisense alphav PMO, dose and schedule that maximally decreases alpha V expression and inhibits retinopathy of prematurity. ..
- P21 transcriptional inhibitors as proapoptotic compoundsAndrei Gartel; Fiscal Year: 2003..This study may improve treatment of cancer by leading to the identification of new compounds that will increase the efficiency of cell death promoting anticancer drugs for cancer treatment. ..
- Inhibition of Androgen Receptor to treat Prostate CancerGayathri Devi; Fiscal Year: 2003..Based on these data, future pharmacokinetic and toxicology animal studies will allow proceeding to human phase I testing in a timely and efficient manner. ..
- FUNCTIONS OF CYCLIN D1 IN BREAST CANCEREmmett Schmidt; Fiscal Year: 2007..These candidate genes involved in neoplastic progression will be validated by analysis of human cancers, in functional assays, and by assessment of their regulatory controls. ..
- GENES REGULATED BY C MYCEmmett Schmidt; Fiscal Year: 2004..Biological functions of the 4ERFs in growth regulation will be analyzed and their potential regulation by c-myc tested. ..
- Stability of prolactin receptor and prolactin signalingSerge Y Fuchs; Fiscal Year: 2010....
- DIRECT TARGET GENES OF THE MYC ONCOPROTEINCarla Grandori; Fiscal Year: 2002..These studies will provide several pieces of the puzzle necessary to understand how Myc functions as an oncogene. ..
- Role of RecQ Helicases to Prevent Senescence By c-MycCarla Grandori; Fiscal Year: 2010..If so, drug inhibitors of WRN function could be proposed for the treatment of cancer. ..
- Regulation of interferon receptor by Leishmania kinaseSERGE FUCHS; Fiscal Year: 2008..unreadable] [unreadable] [unreadable]..
- Chemopreventive properties of aryl hydrocarbon receptor antagonistsHollie Swanson; Fiscal Year: 2007..2) Determine whether apigenin inhibits cigarette smoke condensate-induced malignant transformation of human lung epithelial cells in vivo. [unreadable] [unreadable] [unreadable]..
- Extramural Research Facilities Construction. UCLA Yip C*No Hee Park; Fiscal Year: 2009..The long-term goal is to elevate and enhance the UCLA oral/head &neck oncology research program to be the premier research center and research training program in the country with significant level of NIH research support. ..
- MECHANISMS OF GENOMIC IMPRINTINGAndrew Hoffman; Fiscal Year: 2007..Ultimately, it will be possible to develop a comprehensive chromatin/DNA model of imprinting. [unreadable] [unreadable]..
- Cell Growth Inhibiton and Estrogen ActionBarry Markaverich; Fiscal Year: 2004..The proposed studies should precisely define specific effects of MeHPLA and bioflavonoids on chromatin structure and function, growth related gene transcription and cellular proliferation in normal and malignant cells. ..
- CELLULAR REGULATION OF PROSTAGLANDIN SYNTHESISAndrey Sorokin; Fiscal Year: 2009....
- Control of SnoN Activity by SUMO modificationXia Lin; Fiscal Year: 2006..Finally, the results may also provide a foundation for the rational design of novel therapeutic approaches for prevention and treatment of cancer and musculoskeletal diseases. [unreadable] [unreadable]..
- Regulation of NK Cell Function by Vav-family ProteinsWojciech Swat; Fiscal Year: 2006..ITAM-containing adaptors. Here, we propose to use several in vitro and in vivo approaches to determine Vav mechanism in NK cell function and development of natural cytotoxicity against virally-infected and tumor cells. ..
- Phenotypic Plasticity in Human NeuroblastomaRobert Ross; Fiscal Year: 2008..abstract_text> ..
- Topoisomerase II Site-Directed Alkylation of DNALaurence Hurley; Fiscal Year: 2006..A variety of techniques, including solution and parallel synthesis, in vitro cytotoxicity assays, DNA chip array analysis, gel electrophoresis, promoter assays, and LM-PCR, will be used to carry out these objectives. ..
- Myc Signaling in MedulloblastomasCharles Eberhart; Fiscal Year: 2006..Finally, in Specific Aim 4 we propose developing a novel medulloblastoma transgenic model by overexpressing c-Myc in the cerebellum of transgenic mice. ..
- A flexible somatic and sporadic mouse model for pancreatic ductal adenocarcinomaBrian Lewis; Fiscal Year: 2007..Such an advance would benefit public health by reducing the mortality associated with this disease. [unreadable] [unreadable] [unreadable]..
- Molecular and Cellular Basis of Oncogene AddictionDean W Felsher; Fiscal Year: 2010..The results of our proposed experiments will have important implications for the mechanisms by which the MYC oncogene maintains tumorigenesis and the development of new therapies for the treatment of cancer. ..
- MECHANISMS OF MYC FUNCTION IN GROWTH AND CARCINOGENESISSTEPHEN HANN; Fiscal Year: 2005....
- TRANSCRIPTIONAL REGULATION AND TUMORIGENESIS BY MMTVJAQUELIN DUDLEY; Fiscal Year: 2002..Finally, mutations of Cux and SATB1 binding sites and MMTV Sag will be introduced into a full-length infectious MMTV provirus in order to evaluate the role of these elements in the induction of T-cell lymphoma. ..
- STEM CELLS IN TRANSGENIC MOUSE MAMMARY TUMORIGENESISRobert Dickson; Fiscal Year: 2002....
- EXPRESSION AND IN VIVO ROLE OF TROPHININ IN MICEMichiko Fukuda; Fiscal Year: 2002....
- MATERNAL IMMUNE TOLERANCE TO THE ALLOGENEIC FETUSAdrian Erlebacher; Fiscal Year: 2003..Genes will be isolated by cDNA representational difference analysis and DNA microchip array analysis. and will be functionally evaluated by their ability to modulate tumor immunogenicity in vivo. ..
- B-MYC REGULATION AND FUNCTIONSTEPHEN HANN; Fiscal Year: 2003..The interaction of B-Myc with critical c-Myc binding proteins will be investigated. ..
- PROTEIN PHOSPHATASE 2A IN CELLULAR SIGNALINGMarc Mumby; Fiscal Year: 2001..C subunit domains required for interaction with the A subunit will be identified by chemical crosslinking and deletional and site-directed mutagenesis. ..
- Mechanism of MMP gene induction in osteoarthritisBIMAL RAY; Fiscal Year: 2004..abstract_text> ..
- Development of tissue-specific cell lines in DrosophilaAmanda Simcox; Fiscal Year: 2009..Subsequent use of the cell lines by individual investigators to study diverse biological problems is expected to impact our understanding of human disease. ..
- Novel Approaches to Niemann-Pick Type C DiseaseROBERT MAUE; Fiscal Year: 2004....
- Fostriecin and Related Protein Phosphatase InhibitorsDale Boger; Fiscal Year: 2005....
- COX-2 and p53 interactions and cancer preventionM Sheikh; Fiscal Year: 2004..abstract_text> ..
- Control of c-Myc Function by the Tumor Suppressor p19ARFSTEPHEN HANN; Fiscal Year: 2008..Finally, the inhibition of c-Myc-induced transformation and enhancement of c-Myc-induced apoptosis by ARF has direct therapeutic significance for cancer treatment. ..
- Colon Cell Differentiation: NAB and MUC2 Gene ExpressionAnna Velcich; Fiscal Year: 2009..5. Finally, we will extend our use of microarray technology to determine how NaB perturbs profiles of gene expression that define lineage specific differentiation (Velcich et al., submitted). ..
- CONTROL OF VASCULAR SMOOTH MUSCLE CELL PHENOTYPE BY CGMPThomas Lincoln; Fiscal Year: 2009....
- Regulation of SMAD2 Signaling by SMP1 PhosphataseXia Lin; Fiscal Year: 2008..The results will be pertinent towards development for a foundation for the rational design of novel therapeutic approaches for prevention and treatment of human cancers and other diseases. ..
- G-Quadruplexes as Targets for Drug DesignLaurence Hurley; Fiscal Year: 2007..In vitro and in vivo evaluation will be carried out to evaluate these leads prior to preclinical development and phase 1 clinical trials carried out in collaboration with Cylene Pharmaceuticals. ..
- Role of an RNA-Binding Protein in Mammary CarcinogenesisJeffrey Ross; Fiscal Year: 2009..By investigating the oncogenic properties of the CRD-BP, the RNAs it affects in vivo, and its interactions with tumor-inducing genetic and environmental factors, we hope to uncover novel tumorigenesis pathways. ..
- Hypoxia-Inducible Factor 1 and Oxygen HomeostasisGregg Semenza; Fiscal Year: 2009....
- Firefly Shared Instrument GrantDean Felsher; Fiscal Year: 2008..David Hirschberg. A vital additional component of our program involves the integration of data through support from Bioinformatics [see Letter, Amar Das]. [unreadable] [unreadable] [unreadable]..
- Novel Probe for Quantitative Imaging of Gene ExpressionAndrew Tsourkas; Fiscal Year: 2007..It is envisioned that the approach proposed here will allow significant advancements in our[unreadable] understanding of human health and disease and could potentially prove to be a powerful diagnostic tool. ..
- Inactivation of the Muc2 gene and colorectal cancerAnna Velcich; Fiscal Year: 2005....
- APOPTOSIS IN COLON CANCER CHEMOPREVENTIONEugene Gerner; Fiscal Year: 2005..abstract_text> ..
- Molecular basis of glutamate receptor field formationDavid Featherstone; Fiscal Year: 2006..drug targets that could be important for understanding and treating neurological conditions such as epilepsy, schizophrenia, damage due to stroke, learning disorders, spinal cord regeneration, or drug addiction [unreadable] [unreadable]..
- Role of MUC1 in Repair of Injured AirwaysERIK LILLEHOJ; Fiscal Year: 2006..We expect that future therapies for respiratory diseases, particularly those related to toxicant inhalation, will be developed based upon clinical modulation of MUC1 expression. [unreadable] [unreadable]..
- Transcriptional Repression by the Myc Antagonist MxilNicole Schreiber Agus; Fiscal Year: 2006..Moreover, a better understanding of the molecular functions of the Myc antagonists (e.g., Mxi1) may suggest new therapeutic approaches for the plethora of cancer types in which MYC is disregulated. ..
- CONVERGENCE OF TCDD GENE ACTIVATION WITH OTHER PATHWAYSHollie Swanson; Fiscal Year: 2006..We will then determine whether ARNT is present within DNA binding complexes at the p53 promoter (Aim 4) and identify the protein(s) that interact with ARNT to elicit its synergistic effect on Myc transactivation (Aim 5). ..
- C-MYC INDUCED TUMORIGENESIS AND GENOMIC INSTABILITYDean Felsher; Fiscal Year: 2002....
- Targeting Akt/NF-kappa beta for Pancreatic Cancer TherapyFazlul Sarkar; Fiscal Year: 2007..These results will provide mechanistic as well as pre-clinical data in support of our hypotheses and may open new and novel avenues for the treatment of human pancreatic cancer. ..
- Protein Tyrosine Kinases in Leiomyomata UteriJean Wang; Fiscal Year: 2007..Information gathered from the proposed research may therefore lead to the development of new therapeutics to control the growth of fibroids. ..
- MECHANISM OF SERUM AMYLOID A PROTEIN SYNTHESISBIMAL RAY; Fiscal Year: 2003..abstract_text> ..
- Relationship between diet and sex of offspringRobert Roberts; Fiscal Year: 2008..abstract_text> ..
- INTERACTION BETWEEN BLASTOCYST AND UTERINE ENDOMETRIUMROBERT MICHAEL ROBERTS; Fiscal Year: 2010..Together these studies are expected to provide information on two key events in early pregnancy, the formation of an early placenta and immediate maternal responses to the presence of a tiny embryo attaching to her uterine wall. ..
- MECHANISM OF SERUM AMYLOID A PROTEIN SYNTHESISBIMAL RAY; Fiscal Year: 2005..Results of these studies will improve understanding of the basic mechanisms of cellular response to inflammation and help in the development of a therapeutic regimen to control harmful effects of chronic inflammation. ..
- Transcription Factors in Trophectoderm DifferentiationRobert Roberts; Fiscal Year: 2007..The studies are expected to reveal mechanisms underpinning the transition of embryonic stem cells to trophectoderm, a developmental event that immediately precedes implantation and a time when expression of hCG begins. ..
- Cytokine signal transduction in immune systemHodaka Fujii; Fiscal Year: 2007..Detailed information gained from the proposed experiments will be valuable for elucidation of molecular mechanisms of oncogenesis and autoimmune diseases caused by dysregulation of cytokine signaling. ..
- ISOLATION OF THE NEUROBLASTOMA PREDISPOSITION GENEJohn Maris; Fiscal Year: 2006..Ultimately, these experiments should lead to the identification of a common pathway to neuroblastoma tumorigenesis that will be an outstanding target for rationally designed therapeutics. ..
- HOXB4 Is An Activator of HSC Self-RenewalGuy Sauvageau; Fiscal Year: 2009..This aim combines cell purification of newly characterized HSC populations with microarray analysis from small cell numbers and preliminary target gene validation. ..