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Advances in Brief

Identification of c-Myc Responsive Genes Using Rat cDNA Microarray

Qingbin M. Guo, Renae L. Malek, Sunkyu Kim, Chia Chiao, Mei He, Mauro Ruffy, Krishna Sanka, Norman H. Lee, Chi V. Dang and Edison T. Liu
Qingbin M. Guo
Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
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Renae L. Malek
Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
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Sunkyu Kim
Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
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Chia Chiao
Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
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Mei He
Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
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Mauro Ruffy
Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
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Krishna Sanka
Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
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Norman H. Lee
Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
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Chi V. Dang
Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
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Edison T. Liu
Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
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DOI:  Published November 2000
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Abstract

c-Myc functions through direct activation or repression of transcription. Using cDNA microarray analysis, we have identified c-Myc-responsive genes by comparing gene expression profiles between c-myc null and c-myc wild-type rat fibroblast cells and between c-myc null and c-myc null cells reconstituted with c-myc. From a panel of 4400 cDNA elements, we found 198 genes responsive to c-myc when comparing wild-type or reconstituted cells with the null cells. The plurality of the named c-Myc-responsive genes that were up-regulated, including 30 ribosomal protein genes, are involved in macromolecular synthesis and metabolism, suggesting a major role of c-Myc in the regulation of protein synthetic and metabolic pathways. When ectopically overexpressed, c-Myc induced a different and smaller set of c-Myc-responsive genes as compared with the physiologically expressed c-Myc condition. Thus, these results from expression profiling suggest a new primary function for c-Myc and raise the possibility that the physiological and transforming functions of c-myc may be separable.

  • Received June 6, 2000.
  • Accepted September 15, 2000.
  • ©2000 American Association for Cancer Research.
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Volume 60, Issue 21
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Identification of c-Myc Responsive Genes Using Rat cDNA Microarray
Qingbin M. Guo, Renae L. Malek, Sunkyu Kim, Chia Chiao, Mei He, Mauro Ruffy, Krishna Sanka, Norman H. Lee, Chi V. Dang and Edison T. Liu
Cancer Res November 1 2000 (60) (21) 5922-5928;

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Identification of c-Myc Responsive Genes Using Rat cDNA Microarray
Qingbin M. Guo, Renae L. Malek, Sunkyu Kim, Chia Chiao, Mei He, Mauro Ruffy, Krishna Sanka, Norman H. Lee, Chi V. Dang and Edison T. Liu
Cancer Res November 1 2000 (60) (21) 5922-5928;
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