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. Author manuscript; available in PMC: 2012 Nov 1.
Published in final edited form as: Cancer Sci. 2011 Aug 18;102(11):2022–2028. doi: 10.1111/j.1349-7006.2011.02043.x

Figure 1.

Figure 1

Regression and relapse of 104-R2 xenografts in athymic mice. (A) Castrated mice were injected subcutaneously with 104-R2 P285 cells. After allowing tumors to grow for 7 weeks, mice were separated into control groups (open circle, 7 mice with 11 tumors, no pellet implantation) and treatment group (filled circle and filled rectangular, 18 mice with 33 tumors, implanted with 20 mg testosterone pellets). Tumors in a subgroup of the treated mice (filled circle, 9 tumors from 6 mice) regressed and did not relapse by the end of the experiment (week 17). Tumors in other treated mice (24 tumors from 15 mice) relapsed 5 weeks after androgen treatment (week 12). (B) The relapsed R2Ad tumors were separated into a control group (pellet removed, open circle, 7 mice with 12 tumors) and a treatment group (pellet remained implanted, filled circle, 7 mice with 10 tumors). Points represent mean of tumor volumes; bars represent standard error. Mice carrying LNCaP 104-S tumors (9 weeks after cancer cell injection, 18 mice), 104-R2 tumors without testosterone pellet implant (control group in (A), week 8 and other 104-R2 tumors, 14 mice), 104-R2 tumors implanted with testosterone pellets (treatment group in (A), week 8, 9 mice), R2Ad tumors after testosterone pellet removal (in (B), week 17, 7 mice), and R2Ad tumors with testosterone pellets (in (B), week 17, 7 mice) were assayed for serum PSA (C) or testosterone level (D). Columns represent mean for 3 to 8 serum samples; bars represent standard deviation. AR (E) and PSA (F) protein and mRNA levels were measured in different tumors.β-actin was measured and used as a loading control. Columns represent mean for 3 replicates; bars represent standard deviation.