Skip to main content

Table 1 Tumor regression and progression under endocrine therapy in the MCF7L-shPTEN xenograft model with PTEN-WT (-Dox) or -KD (+Dox)

From: Overcoming endocrine resistance due to reduced PTEN levels in estrogen receptor-positive breast cancer by co-targeting mammalian target of rapamycin, protein kinase B, or mitogen-activated protein kinase kinase

Treatment TRa(%) TTRb(95% CI) P e TP470c(%) TTPd(95% CI) P
E2-Dox 0 NAf (NA-NA) 1 100 8 (5–12) 0.671
E2 + Dox 0 NA (NA-NA)   100 10 (6–13)  
ED-Dox 100 25 (6–39) 0.011 13 NA (223-NA) 0.098
ED + Dox 64 108 (30-NA)   43 NA (41-NA)  
Tam-Dox 71 24 (9-NA) 0.002 71 86 (73-NA) 0.022
Tam + Dox 24 NA (43-NA)   94 54 (36–71)  
Ful-Dox 100 17 (6–24) <0.001 14 NA (462-NA) 0.107
Ful + Dox 73 107 (38–198)   47 NA (101-NA)  
  1. aTR is the fraction of mice achieving tumor regression, defined by the tumor size halving since the randomization; bTTR is the median time to tumor regression with 95% confidence interval; cTP470 is the fraction of mice experiencing tumor progression within 470 days after treatment, defined by the tumor size doubling since the randomization; dTTP is the median time to tumor progression with 95% confidence interval; eP value is based on the generalized Wilcoxon test comparing the -/+Dox groups in each endocrine treatment arm; fNA = not-achieved. PTEN, phosphatase and tensin homolog; WT, wild-type; Dox, doxycycline; KD, knockdown; TTR, time to tumor regression; TTP, time to tumor progression; E2, β-estradiol; ED, estrogen deprivation; Tam, tamoxifen; Ful, fulvestrant.