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. 2010 Nov 3;102(21):1663–1675. doi: 10.1093/jnci/djq392

Figure 5.

Figure 5

Susceptibility of C57BL/6.glutathione S-transferase α4 deficient (Gsta4−/−) vs wild-type mice to tumor promotion by TPA. Groups of at least 24 mice of each strain were initiated by topical application of 100 nmol 7,12-dimethylbenz(a)anthracene to the shaved dorsal skin and promoted twice weekly with 3.4 nmol TPA for 38 weeks. Tumors were counted weekly by palpation and tumor multiplicity was determined by dividing the total number of tumors by the number of mice at risk when the first tumor was observed. Two independent experiments were performed with similar results; therefore, the data have been combined (C57BL/6.Gsta4−/−, n = 62; C57BL/6.Gsta4+/+, n = 53). A) Time course of tumor development in Gsta4-deficient and wild-type mice. Tumor multiplicity was statistically significantly higher in Gsta4-deficient mice than in wild-type mice at 38 weeks (P = .007, one-tailed Mann–Whitney U test). The mean and 95% confidence interval for tumor multiplicity at 36 and 38 weeks are presented. B) Tumor latency in Gsta4-deficient and wild-type mice. Tumor latency was decreased in Gsta4-deficient mice (P = .006, Gehan–Breslow–Wilcoxon). The number of mice at risk for weeks 0, 20, and 38 were 53, 53, 36 for wild-type and 62, 54, and 31 for Gsta4-deficient mice.