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. 2015 Feb 1;13:43. doi: 10.1186/s12967-015-0399-y

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© Doudican et al.; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Data for MM patient 4. (A) Rationale for MM patient 4 patient characteristics and predicted effects on the network. This profile exhibited CCND1 trisomy, P53 deletion and extensive aberrations and hyperdiploid clones. The simulation avatar exhibited significant activation of the ERK, AKT and JAK-STAT signaling pathways. The JAK inhibitor tofacitinib, represented in the red box, was predicted to be effective in this profile. Predictive (B) vs. experimental (C) results regarding the effect of tofacitinib on cell proliferation in MM patient 4. (D) Western blot of non-treated (NT) and Tofacitinib (Tofa)-treated cells. The biomarker cleaved PARP was assessed. Actin serves as a loading control.