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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.