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. Author manuscript; available in PMC: 2015 Oct 15.
Published in final edited form as: Clin Cancer Res. 2012 Feb 28;18(8):2210–2219. doi: 10.1158/1078-0432.CCR-11-2413

Figure 5. Re-activation of cell cycle regulators and anti-apoptosis is a mechanism of resistance to MVabrogated by MVR therapy.

Figure 5

Figure 5

Figure 5

Figure 5

(A). Tumor sizes of 3 mice per cohort sacrificed 3h after end of the last treatment are shown for control, MR, MV and MVR therapy. (B). Gene expression profiling identified unique and common gene ontologies repressed by individual drug treatments compared to control and each other (Venn diagram and list of repressed functionalities). (C). Protein was isolated from the tumors 3h after the end of last treatment as indicated and at relapse (MV2). Western blotting analysis demonstrated that Proliferating cell nuclear antigen (PCNA), Aurora B, cyclin B1 cyclin D1 and Bcl-2 were inhibited by MV1 (tumor regression phase) and MVR but not MR and MV2 (tumor relapse phase). (D). PCNA was evaluated by immunohistochemistry from tumors 3h after the end of last treatment for control, MR, MV1, MVR and MV2 (at relapse).