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. Author manuscript; available in PMC: 2009 Aug 23.
Published in final edited form as: Cancer Cell. 2007 Feb;11(2):161–173. doi: 10.1016/j.ccr.2006.11.025

Figure 2. Gene Copy Number Changes at the Aurora-A Locus in Tumors.

Figure 2

(A) Frequency of somatic gain/loss of Aurora-A in lymphomas as a function of p53 status.

(B–D) Representative BAC array profiles of chromosome 2 in tumors from p53+/− mice. The arrows indicate the position of the Aurora-A gene, which is frequently gained in tumors from p53+/− mice.

(E and F) Loss of the Aurora-A gene in tumors from p53−/− mice.

(G) Detection of Aurora-A genetic alterations in radiation-induced tumors from p53 heterozygous mice (HR) by TaqMan assay.

(H) Detection of Aurora-A protein levels in radiation-induced tumors from p53 heterozygous mice (HR) by western blotting. The first four lanes show levels of Aurora-A in normal thymus from unirradiated p53+/− mice. Tumors in lanes labeled HR 1–20 correspond to those labeled HR1–HR20 in (G).

(I) Detection of Aurora-A genetic alterations in radiation-induced tumors from p53 null mice (NR) by TaqMan assay.

(J) Detection of Aurora-A protein levels in radiation-induced tumors from p53 null mice (NR) by western blotting. The first four lanes show levels of Aurora-A in normal thymus from unirradiated p53−/− mice. These are consistently higher than in corresponding p53+/− mice (H). Tumors in lanes labeled NR 1–20 correspond to those labeled NR1–NR20 in (I).