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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 532))

Abstract

Normal cells possess mechanisms that protect them from the action of oncogenes. Thus, normal primary cells are not affected by neoplastic transformations, whereas the majority of immortal cells used in laboratory cultures have acquired mutations during the immortalization process and are susceptible to being transformed. Our main interest is the study of the molecular mechanisms which signal anti-tumor responses as well as the impact these anti-tumor responses have upon the cell cycle.

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References

  • Brotherton, D. H., Dhanaraj, V., Wick, S., Brizuela, L., Domaille, P. J., Volyanik, E., Xu, X., Parisini, E., Smith, B. O., Archer, S. J., Serrano, M., Brenner, S. L., Blundell, T. L., and Laue, E. D. (1998). Crystal structure of the complex of the cyclin D-dependent kinase Cdk6 bound to the cell-cycle inhibitor p19INK4d.Nature395, 244–250

    Article  PubMed  CAS  Google Scholar 

  • Palmero, I., Pantoja, C., and Serrano, M. (1998). P19`ßlinks the tumour suppressor p53 to Ras.Nature 395,125–126

    Article  PubMed  CAS  Google Scholar 

  • Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., and Lowe, S. W. (1997). Oncogenicrasprovokes premature cell senescence associated with accumulation of p53 and p16INK4aCell 88, 593–602

    Google Scholar 

  • Serrano, M., Lee, H.-W., Chin, L., Cordon-Cardo, C., Beach, D. and DePinho, R. A. (1996). Role of theINK4alocus in tumor suppression and cell mortality.Cell,85, 27–37

    Article  PubMed  CAS  Google Scholar 

  • Serrano, M., Hannon, G. and Beach, D. (1993). A New Regulatory Motif in Cell-cycle Control Causing Specific Inhibition of Cyclin D/CDK4.Nature 336704–707

    Article  Google Scholar 

  • Serrano, M. (1997). The Tumor Suppressor Protein pl61NK4a . Exp. Cell Res. 2377–13.

    Article  PubMed  CAS  Google Scholar 

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© 2003 Springer Science+Business Media New York

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Serrano, M. (2003). Proliferation: The Cell Cycle. In: Llombart-Bosch, A., Felipo, V. (eds) New Trends in Cancer for the 21st Century. Advances in Experimental Medicine and Biology, vol 532. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0081-0_2

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  • DOI: https://doi.org/10.1007/978-1-4615-0081-0_2

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-4914-3

  • Online ISBN: 978-1-4615-0081-0

  • eBook Packages: Springer Book Archive

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