The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
c-Myc Target Genes Involved in Cell Growth, Apoptosis, and Metabolism
Open accessAbstract
The c-myc gene was discovered as the cellular homolog of the retroviral v-myc oncogene 20 years ago (23, 25, 167). The c-myc proto-oncogene was subsequently found to be activated in various animal and human tumors (37, 39, 42). It belongs to the family of myc genes that includes B-myc, L-myc, N-myc, and s-myc; however, only c-myc, L-myc, and N-myc have neoplastic potential (54, 82, 102, 118, 178). Targeted homozygous deletion of the murine c-myc gene results in embryonic lethality, suggesting that it is critical for development (43). Homozygous inactivation of c-myc in rat fibroblasts caused a marked prolongation of cell doubling time, further suggesting a central role for c-myc in regulating cell proliferation (121). The frequency of genetic alterations of c-myc in human cancers (42) has allowed an estimation that approximately 70,000 U.S. cancer deaths per year are associated with changes in the c-myc gene or its expression. Given that c-myc may contribute to one-seventh of U.S. cancer deaths, recent efforts have been directed toward understanding the function of the c-Myc protein in cancer biology with the hope that therapeutic insights will emerge. Past efforts, which have contributed significantly to our current understanding of c-myc, are discussed in a number of excellent reviews (23, 29, 37, 40, 44, 52, 66, 82, 94, 102, 118, 125, 132, 145, 178, 182, 186).
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Cites
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
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“In this role, c-Myc appears to inactivate cellular responses that are normally required for RAS-mediated growth inhibition, thereby switching the gene for RAS into a growth-promoting gene (165).”
BackgroundLi, J., Yen, C., Liaw, D., Podsypanina, K., Bose, S., Wang, S. I., Puc, J., Miliaresis, C., Rodgers, L., McCombie, R., et al. (1997) · Science · doi:10.1126/science.275.5308.1943 · Cited by 4,785
Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes
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Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization
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Nuclear Receptor Repression Mediated by a Complex Containing SMRT, mSin3A, and Histone Deacetylase
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The novel ATM-related protein TRRAP is an essential cofactor for the c-Myc and E2F oncoproteins
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Self-citationBIN1 is a novel MYC–interacting protein with features of a tumour suppressor
Sakamuro, D., Elliott, K. J., Wechsler-Reya, R., & Prendergast, G. C. (1996) · Nature Genetics · doi:10.1038/ng0996-69 · Cited by 387
Cited by
Otto Warburg's contributions to current concepts of cancer metabolism
Koppenol, W. H., Bounds, P. L., & Dang, C. V. (2011) · Nature Reviews Cancer · doi:10.1038/nrc3038 · Cited by 3,427
Self-citationTGFβ Signaling in Growth Control, Cancer, and Heritable Disorders
Massagué, J., Blain, S. W., & Lo, R. S. (2000) · Cell · doi:10.1016/s0092-8674(00)00121-5 · Cited by 2,385
The STATs of cancer — new molecular targets come of age
Yu, H., & Jove, R. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1275 · Cited by 2,278
Wise, D. R., DeBerardinis, R. J., Mancuso, A., Sayed, N., Zhang, X.-Y., Pfeiffer, H. K., Nissim, I., Daikhin, E., Yudkoff, M., McMahon, S. B., et al. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0810199105 · Cited by 2,001
Reflecting on 25 years with MYC
Meyer, N., & Penn, L. Z. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2231 · Cited by 1,575
Metadata
- Authors
- Dang, C. V.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 1999-01-01
- Volume
- 19
- Issue
- 1
- Pages
- 1-11
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2097774235
- Cited by
- 1,715
- References
- 9
- FWCI
- 34.63
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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