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. Author manuscript; available in PMC: 2017 May 31.
Published in final edited form as: Science. 2016 May 20;352(6288):aad3018. doi: 10.1126/science.aad3018

Figure 3. Resistance to CSF-1R inhibition is mediated by the microenvironment and rebound TAMs are alternatively activated.

Figure 3

(A) Quantification of bioluminescent imaging (BLI) from intracranially transplanted 52Reb cells into naïve mice. Results show that 52Reb cells, isolated from a recurrent PDG tumor that developed resistance to BLZ945 treatment in vivo, reestablish sensitivity to BLZ945 in the naïve setting (Student’s t-test d15, P<0.05, n=10 mice). Representative BLI images at d15 are shown. (B) Left: H&E of a rebound tumor (T) adjacent to glial scarring (S). Scale bar = 500 μm. Right: Representative regions of calcification (top), reactive astrocytic barrier (middle), and recurrent tumor (bottom). Scale bars = 50 μm. (C) H&E, Von Kossa and GFAP staining on rebound tissue. Scale bars = 200 μm, except GFAP 20× = 50 μm as indicated. (D) Allred score for the astrocyte marker GFAP, showing a higher intensity and proportion of GFAP+ staining in Reb tissues (n=8 mice) compared to other treatment groups (n=5 mice per group). (E) Flow cytometry of TAMs (CD45+CD11b+Gr1−) in Veh, 28d, EP and Reb tumors (n=5–7). Data were analyzed by a one-way ANOVA and Tukey’s multiple comparisons test. (F) Heatmap showing RNA-seq expression changes of M2-like associated genes in Veh, EP and Reb TAMs (n=5–6 per group). Wound-associated genes are indicated in bold with asterisks.