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. Author manuscript; available in PMC: 2010 Aug 15.
Published in final edited form as: Cancer Res. 2009 Aug 4;69(16):6546–6555. doi: 10.1158/0008-5472.CAN-09-0605

Figure 5. FoxO3a, TRAIL, and BIM are suppressed in a BCR-ABL-induced CML mouse model, with bortezomib treatment abrogating these effects.

Figure 5

a) 2 mice were analyzed from each treatment group through all the immunohistochemistry experiments and the same results were received for both within each group. Immunohistochemical (IHC) staining for FoxO3a using a FoxO3a-specific antibody on spleen sections from vehicle or bortezomib-treated vector control and BCR-ABL-transduced mice. Original magnification 400x. Note presence of myeloperoxidase on H&E stained spleen section from vehicle-treated BCR-ABL-transduced mice. Original magnification 400x. b) IHC staining for FoxO3a on marrow sections from vehicle or bortezomib-treated vector control and BCR-ABL-transduced mice showing a similar FoxO3a expression pattern as in a. Original magnification 1000x. c) IHC staining for phospho-FoxO3a (Thr32)/FoxO1 (Thr24) on spleen sections from vehicle or bortezomib-treated vector control and BCRABL-transduced mice. Original magnification 400x. d) Western blot of mononuclear cells from CML patients (P1-P3) and a Ph+ positive ALL patient (P4) and healthy individuals (N) demonstrates a loss of FoxO3a and FoxO1 expression in CML and ALL patients.