p16INK4A and p19ARF act in overlapping pathways in cellular immortalization (original) (raw)

• Hayflick, L. & Moorhead, P. S. The serial cultivation of human diploid cell strains. Exp. Cell Res. 25, 585–621 (1961).
  Article CAS Google Scholar
• Campisi, J. The biology of replicative senescence. Eur. J. Cancer 33, 703–709 (1997).
  Article CAS Google Scholar
• Bodnar, A. G. et al. Extension of life-span by introduction of telomerase into normal human cells. Science 279, 349– 352 (1998).
  Article CAS Google Scholar
• Wang, J., Xie, L. Y., Allan, S., Beach, D. & Hannon, G. J. Myc activates telomerase. Genes Dev. 12, 1769–1774 (1998).
  Article CAS Google Scholar
• Blasco, M. A. et al. Telomere shortening and tumor formation by mouse cells lacking telomerase RNA. Cell 91, 25– 34 (1997).
  Article CAS Google Scholar
• Kamb, A. Cyclin-dependent kinase inhibitors and human cancer. Curr. Top. Microbiol. Immunol. 227, 139–148 ( 1998).
  CAS PubMed Google Scholar
• Ruas, R. & Peters, G. The p16INK4A/CDKN2A tumor suppressor and its relatives. Biochem. Biophys. Acta 1378, 115–177 (1998).
  Google Scholar
• Sherr, C. J. Tumour surveillance via the ARF-p53 pathway. Genes Dev. 12, 2984–2991 (1998).
  Article Google Scholar
• Kamijo, T. et al. Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF. Cell 91 , 649–659 (1997).
  Article CAS Google Scholar
• Serrano, M. et al.. Role of the INK4a locus in tumor suppression and cell mortality . Cell 85, 27–37 (1996).
  Article CAS Google Scholar
• Alcorta, D. A. et al. Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblasts. Proc. Natl Acad. Sci. USA 93, 13742–13747 (1996).
  Article CAS Google Scholar
• Zindy, F., Quelle, D. E., Roussel, M. F. & Sherr, C. J. Expression of the p16INK4A tumor suppressor versus other INK4 family members during mouse development and aging. Oncogene 15, 203–211 (1997).
  Article CAS Google Scholar
• Kiyono, T. et al. Both Rb/p16INK4A inactivation and telomerase activity are required to immortalize human epithelial cells. Nature 396, 84–88 ( 1998)
  Article CAS Google Scholar
• Noble, J. R. et al. Association of extended in vitro proliferative potential with loss of p16INK4 expression. Oncogene 13, 1259–1268 (1996).
  CAS PubMed Google Scholar
• Chin, L., Pomerantz, J. & DePinho, R. A. The INK4a/ARF tumor suppressor: one gene — two products — two pathways. Trends Biochem. Sci. 23, 291–296 (1998).
  Article CAS Google Scholar
• Hannon, G. J. et al. Genetics in mammalian cells. Science 283, 1129–1130 (1999).
  Article CAS Google Scholar
• Serrano, M., Gomez-Lahoz, E., DePinho, R. A., Beach, D. & Bar-Sagi, D. Inhibition of ras-induced proliferation and cellular transformation by p16INK4. Science 267, 249–252 ( 1995).
  Article CAS Google Scholar
• Lukas, J. et al. Retinoblastoma-protein-dependent cell-cycle inhibition by the tumour suppressor p16. Nature 375, 503– 506 (1995)
  Article CAS Google Scholar
• Medema, R. H., Herrera, R. E., Lam, F. & Weinberg, R. A. Growth suppression by p16ink4 requires functional retinoblastoma protein. Proc. Natl Acad. Sci. USA 92, 6289– 6293 (1995).
  Article CAS Google Scholar
• Zhang, Y., Xiong, Y. & Yarbrough, W. G. ARF promotes MDM2 degradation and stabilizes p53: ARF-INK4a locus deletion impairs both the Rb and p53 tumor suppression pathways . Cell 92, 725–734 (1998).
  Article CAS Google Scholar
• Pomerantz, J. et al. The Ink 4a tumor suppressor gene product, p19ARF, interacts with MDM2 and neutralizes MDM2’s inhibition of p53. Cell 92, 713–723 ( 1998).
  Article CAS Google Scholar
• Kamijo, T. et al. Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2. Proc. Natl Acad. Sci. USA 95, 8292–8297 (1998).
  Article CAS Google Scholar
• Xiao, Z. X. et al. Interaction between the retinoblastoma protein and the oncoprotein MDM2. Nature 375, 694–698 (1995).
  Article CAS Google Scholar
• Sun, P. Q., Dong, P., Dai, K., Hannon, G. J. & Beach, D. H. p53-independent function of MDM2 may contribute to TGFβ resistance in tumors. Science 282, 2270–2272 (1998).
  Article CAS Google Scholar
• Macleod, K. pRb and E2F-1 in mouse development and tumorigenesis. Curr. Opin. Genet. Dev. 9, 31–39 ( 1999)
  Article CAS Google Scholar
• Johnson, D. G. & Schneider-Broussard, R. Role of E2F in cell cycle control and cancer. Frontiers Biosci. 3, 447–448 (1998).
  Article Google Scholar
• Qin, X. Q., Livingston, D. M., Kaelin, W. G. Jr & Adams, P. D. Deregulated transcription factor E2F-1 expression leads to S-phase entry and p53-mediated apoptosis. Proc. Natl Acad. Sci. USA 91 , 10918–10922 (1994).
  Article CAS Google Scholar
• Hiebert, S. W. et al. E2F-1:DP-1 induces p53 and overrides survival factors to trigger apoptosis. Mol. Cell. Biol. 15, 6864– 6874 (1995)
  Article CAS Google Scholar
• Pan, H. et al. Key roles for E2F1 in signaling p53-dependent apoptosis and in cell division within developing tumors. Mol. Cell 2, 283–292 (1998).
  Article CAS Google Scholar
• Nevins, J. R., Leone, G., DeGregori, J. & Jakoi, L. Role of the Rb/E2F pathway in cell growth control. J. Cell Physiol. 173 , 233–236 (1997)
  Article CAS Google Scholar
• Weinberg, R. A. The retinoblastoma protein and cell cycle control. Cell 81, 323–330 (1995).
  Article CAS Google Scholar
• Rittling, S. R. & Denhardt, D. T. p53 mutations in spontaneously immortalized 3T12 but not 3T3 mouse embryo cells. Oncogene 7, 935–942 ( 1992)
  CAS PubMed Google Scholar
• Iravani, M., Dhat, R. & Price, C. M. Methylation of the multi tumor suppressor gene-2 (MTS2,CDKN1, p15INK4B) in childhood acute lymphoblasticleukemia. Oncogene 15, 2609–2614 ( 1997).
  Article CAS Google Scholar