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Fig. 5. Pharmacological JAK2 inhibition in vivo abrogates tumor-initiating potential after chemotherapy. Pharmacological JAK2 inhibition in vivo abrogates.

Published bySudirman Hartono Modified over 6 years ago

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Presentation on theme: "Fig. 5. Pharmacological JAK2 inhibition in vivo abrogates tumor-initiating potential after chemotherapy. Pharmacological JAK2 inhibition in vivo abrogates."— Presentation transcript:

1 Fig. 5. Pharmacological JAK2 inhibition in vivo abrogates tumor-initiating potential after chemotherapy. Pharmacological JAK2 inhibition in vivo abrogates tumor-initiating potential after chemotherapy. (A and B) Female athymic mice were injected with MDA-436 or HCC-38 cells in the no. 4 mammary fat pad. Mice bearing tumors ≥150 mm3 were randomized to treatment with vehicle, paclitaxel [20 mg/kg per day × 4 doses intraperitoneally (i.p.)], or paclitaxel (20 mg/kg per day × 4 doses i.p.) + BSK805 [100 mg/kg per day orally (p.o.)]. Paclitaxel doses are represented by arrows. Tumor volumes were measured twice weekly. Two complete responses to dual therapy were achieved in mice bearing HCC-38 tumors. Bars represent means ± SEM. Differences were analyzed by one-way analysis of variance (ANOVA) with Tukey’s contrasts. (C) Representative images of mammospheres from treated tumors in (A) and (B). Scale bars, 200 μm. (D) Quantification of mammospheres from tumors harvested at the end of treatment. Bars represent means + SEM for n = 9 measurements. (E) Severe combined immunodeficient (SCID)/beige mice implanted with PDX model PDX4013 were randomized to treatment with vehicle (intraperitoneal saline and oral gavage with oral suspension agent), paclitaxel (20 mg/kg per day × 4 doses i.p.), BSK805 (80 mg/kg per day p.o.), or paclitaxel (20 mg/kg per day × 4 doses i.p.) + BSK805 (80 mg/kg per day p.o.). Tumor volumes were measured twice weekly. (F) Image of JAK2-FISH in the PDX4013 model demonstrating gene amplification. Scale bar, 20 μm. Justin M. Balko et al., Sci Transl Med 2016;8:334ra53 Published by AAAS

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