@article {155,
	title = {Crosstalk between Aurora-A and p53: frequent deletion or downregulation of Aurora-A in tumors from p53 null mice.},
	journal = {Cancer Cell},
	volume = {11},
	year = {2007},
	month = {2007 Feb},
	pages = {161-73},
	abstract = {<p>The Aurora-A kinase gene is amplified in a subset of human tumors and in radiation-induced lymphomas from p53 heterozygous mice. Normal tissues from p53-/- mice have increased Aurora-A protein levels, but lymphomas from these mice exhibit heterozygous deletions of Aurora-A and/or reduced protein expression. A similar correlation between low p53 levels and Aurora-A gene deletions and expression is found in human breast cancer cell lines. In vitro studies using mouse embryo fibroblasts demonstrate that inhibition of Aurora-A can have either positive or negative effects on cell growth as a function of p53 status. These data have implications for the design of approaches to targeted cancer therapy involving the crosstalk between Aurora-A kinase and p53 pathways.</p>},
	keywords = {Animals, Apoptosis, Aurora Kinase A, Aurora Kinases, Breast Neoplasms, Cells, Cultured, Down-Regulation, Embryo, Mammalian, Female, Fibroblasts, Gene Deletion, Gene Dosage, Gene Expression Profiling, Genomic Instability, Heterozygote, Lymphoma, Male, Mice, Mice, Knockout, Microarray Analysis, Neoplasms, Radiation-Induced, Protein-Serine-Threonine Kinases, Survival Rate, Thymus Neoplasms, Tumor Suppressor Protein p53, Whole-Body Irradiation},
	issn = {1535-6108},
	doi = {10.1016/j.ccr.2006.11.025},
	author = {Jiang-Hua Mao and Wu, Di and Perez-Losada, Jesus and Jiang, Tao and Li, Qian and Neve, Richard M and Gray, Joe W and Cai, Wei-Wen and Balmain, Allan}
}
