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. 2009 Mar 20;100(5):813–820. doi: 10.1111/j.1349-7006.2009.01120.x

Figure 1.

Figure 1

Immunohistochemical localization of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and phospho‐PTEN in association with glutathione S‐transferase placental form (GST‐P)‐positive liver cell foci after promotion for 6 weeks. (a) Lack of PTEN expression (right) in a GST‐P‐positive focus (left) in the liver of a rat promoted with 3600 p.p.m. fenbendazole (FB) after N‐diethylnitrosamine (DEN) initiation. Bar = 500 µm. The graph shows concordance ratios (%) of PTEN negativity with GST‐P‐positive foci generated after promotion with FB, piperonyl butoxide (PBO), or thioacetamide (TAA). *, **: P < 0.05, 0.01 versus DEN‐alone group (χ2‐test). (b) Lack of phospho‐PTEN expression (right) in a GST‐P‐positive focus (left) in the liver of a rat promoted with 3600 p.p.m. FB after DEN initiation. Bar = 500 µm. The graph shows concordance ratios (%) of phospho‐PTEN negativity with GST‐P‐positive foci generated after promotion with FB, PBO, or TAA. *, **: P < 0.05, 0.01 versus DEN‐alone group (χ2‐test).