Figure 7.
Enobosarm Does Not Inhibit Growth of an ER-negative AR-positive HCI-9 PDX
(A) AR-positive, but ER-negative, HCI-9 PDX was surgically implanted as 1 mm3 fragments under the mammary fat pad in intact NSG mice (n = 8–10/group). Once the tumors reached 100–200 mm3, the mice were randomized and treated with vehicle (DMSO:PEG-300 (15%:85%)) or enobosarm (10 mpk p.o.). Tumor volume was measured thrice weekly.
(B) AR Western blot was performed from the tumor specimens shown on the left. Densitometric quantification of the bands is provided at the bottom of the blot.
(C) HCI-9 tumors were formalin-fixed and immunostained with the indicated antibodies. Representative images of n = 4–5/group/stain are shown. Ki-67 staining was quantified and represented as bar graph (n = 5/group). Scale is provided in one of the images (50 μm).
(D) Table showing the percent of stromal and epithelial cells in the xenografts.
(E) Enobosarm increases AR-target genes. HCI-9 tumor fragments from vehicle- or enobosarm-treated samples (n = 4/group) were homogenized and RNA isolated. Expression of AR-target genes was measured by real-time PCR and normalized to GAPDH expression. Data are represented as fold change from vehicle-treated samples.