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. 2016 Dec 19;36(23):3263–3273. doi: 10.1038/onc.2016.471

Figure 2.

Figure 2

Relapsed NRI AMLs are resistant to doxycycline (Dox)-mediated suppression of NRAS(V12) expression and do not re-express oncogenic NRAS protein. (a) NRI1 or NRI2 AML cells were transplanted in secondary SCID beige recipient mice. NRI AMLs continued to grow in secondary recipients despite Dox treatment, and mice rapidly succumbed to progressive leukemia. (b) NRI1 or NRI2 AML cells harvested from the spleens of leukemic mice were treated ex vivo with 1 μg/ml Dox for 48 h and then plated in leukemia colony-forming cell (L-CFC) assays. Results are presented as L-CFC in Dox-treated relative to control treated AML cells (n=3 independent experiments, error bars=1 s.d., *P<0.001). (c) Western blotting for NRAS protein in splenocytes harvested from mice with NRD and NRI AMLs in the presence or absence of Dox as indicated. NRI AMLs were generated and maintained in the presence of Dox to prevent re-expression of NRAS(V12) or re-emergence of NRD AML, so were not evaluated in the absence of Dox.