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Unrestricted cell cycling and cancer

Recent data suggest that deregulation of the restriction point in the cell-cycle G1 phase appears to be required for the development of neoplasias.

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References

  1. Pardee, A.B. G1 events and regulation of cell proliferation. Science 246, 603–608 (1989).

    Article  CAS  Google Scholar 

  2. Pardee, A.B. A restriction point for control of normal animal cell proliferation. Proc. natn. Acad. Sci. U.S.A. 71, 1286–1290 (1974).

    Article  CAS  Google Scholar 

  3. Weinberg, R.A. The retinoblastoma protein and cell cycle control. Cell 81, 323–330 (1995).

    Article  CAS  Google Scholar 

  4. Sherr, C.J. & Roberts, J.M. Inhibitors of mammalian G1 cyclin-dependent kinases. Genes Dev. 9, 1149–1163 (1995).

    Article  CAS  Google Scholar 

  5. Baldin, V., Lukas, J., Marcote, M.J., Pagano, M. & Draetta, G. Cyclin D1 is a nuclear protein required for cell cycle progression in G1. Genes Dev. 7, 812–821 (1993).

    Article  CAS  Google Scholar 

  6. Lukas, J., Bartkova, J., Rohde, M., Strauss, M. & Bartek, J. Cyclin D1 is dispensable for G1 control in retinoblastoma gene-deficient cells independently of cdk4 activity. Molec. Cell. Biol. 15, 2600–2611 (1995).

    Article  CAS  Google Scholar 

  7. Lukas, J. et al. Retinoblastoma-protein-dependent cell-cycle inhibition by the tumor suppressor p16. Nature 375, 503–506 (1995).

    Article  CAS  Google Scholar 

  8. Koh, J., Enders, G.H., Dynlacht, B. & Harlow, E. Tumour-derived p16 alleles encoding proteins defective in cell-cycle inhibition. Nature 375, 506–510 (1995).

    Article  CAS  Google Scholar 

  9. Matsushime, H. et al. Identification and properties of an atypical catalytic subunit (p34PSKJ3/cdk4) for mammalian D type G1 cyclins. Cell 71, 323–334 (1992)

    Article  CAS  Google Scholar 

  10. Bates, S. & Peters, G. Cyclin D1 as a cellular protooncogene. Sem. Cancer Biol. 6, 73–82 (1995).

    Article  CAS  Google Scholar 

  11. Schmidt, E.E., Ichimura, K., Reifenberger, G. & Collins, V.P. CDKN2 (p16/MTS1) gene deletion or CDK4 amplification occurs in the majority of gliobiastoma. Cancer Res. 54, 6321–6324 (1994).

    CAS  Google Scholar 

  12. Wölfel, T. et al. A pl6INK4a-insensitive CDK4 mutant targeted by cytolytic T lymphocytes in a human melanoma. Science 269, 1281–1284 (1995).

    Article  Google Scholar 

  13. Merlo, A. et al. 5′ CpG island methylation is associated with transcriptional silencing of the tumor suppressor p16/CDKN2/MTSl in human cancers. Nature Med. 1, 686–692 (1995).

    Article  CAS  Google Scholar 

  14. Lukas, J., Aagaard, L., Strauss, M. & Bartek, J. Oncogenic aberrations of p16INK4/CDKN2 and cyclin D1 cooperate to deregulate G1 control. Cancer Res. 55, 4818–4823 (1995).

    CAS  PubMed  Google Scholar 

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Strauss, M., Lukas, J. & Bartek, J. Unrestricted cell cycling and cancer. Nat Med 1, 1245–1246 (1995). https://doi.org/10.1038/nm1295-1245

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