Carcinogenesis, Vol. 21, No. 5, 865-869,
May 2000
© 2000 Oxford University Press
Commentaries |
The INK4a/ARF locus in murine tumorigenesis
Department of Immunology and Oncology, Centro Nacional de Biotecnología, Campus de Cantoblanco, Madrid E-28049, Spain Email: mserrano{at}cnb.uam.es
Abstract
The INK4a/ARF locus is regarded as one of the most important anti-tumoral defenses that mammalian organisms possess. The characterization of its two gene products, p16INK4a and p19ARF, has provided a great insight on the functioning of the tumor suppressors Rb and p53, respectively. Present evidence indicates that the INK4a/ARF locus is transcriptionally activated by oncogenic stresses, resulting in cell-cycle arrest or apoptosis. Here, I review the evidence accumulated on the involvement of the INK4a/ARF locus in murine tumorigenesis. Also, I summarize the phenotype of the different transgenic mouse models based on the inactivation of the INK4a/ARF locus.
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