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. 2002 Jan 29;99(3):1455–1460. doi: 10.1073/pnas.022632099

Figure 2.

Figure 2

Collaboration of Pten and Ink4a/Arf deficiency in vivo and status of the Ink4a/Arf locus and Pten gene in pheochromocytomas. (A) Kaplan–Meier survival analysis of Ink4a/Arf+/−Pten+/+, Ink4a/Arf−/−Pten+/+, Ink4a/Arf+/+Pten+/−, and Ink4a/Arf and Pten compound mutant mice. Statistically significant differences for pairwise comparison (P < 0.001) were detected between cohorts Ink4a/Arf−/−Pten+/− vs. Ink4a/Arf−/−Pten+/+ and Ink4a/Arf+/−Pten+/− vs. Ink4a/Arf+/+Pten+/−. (B) Southern blot analysis of the Pten gene in pheochromocytomas. Ink4a/Arf+/+Pten+/− mouse tail genomic DNA digested with SacI was the control. The sizes of wt and mutant Pten alleles are 12 and 6.8 kb, respectively. (C) Southern blot of PstI-digested genomic DNA of pheochromocytomas derived from Ink4a/Arf+/−Pten+/− mice or control Ink4a/Arf+/−Pten+/+ mouse tails. The sizes of wt and mutant Ink4a/Arf alleles are 9.2 and 6.0 kb, respectively.