Additional file 3: Figure S2. of GEP analysis validates high risk MDS and acute myeloid leukemia post MDS mice models and highlights novel dysregulated pathways

In a preliminary work, mRAS-BCL2 (referred in this study as MRP8[NRASD12/ hBCL-2], AML post MDS mice) transgenic mice Sca1+ spleen cells genes were analyzed on Affimetrix 430A mouse arrays. Compared to normal FVB/N Sca1+ spleen cells, (A) DAVID analysis, (B) Principal component analysis (PCA), and hierarchical clustering, were performed with R software (http://www.R-project.org) and Partek Genomics Suite (http://www.partek.com). Each sphere represents a single GEP from a given transgenic mouse: mRas (referred in this study as MRP8NRASD12 transgenic mice), mBCL2 transgenic mice (referred in this study as MRP8hBCL-2 transgenic mice), mRAS-BCL2 transgenic mice (referred in this study as MRP8[NRASD12/ hBCL-2] or AML post MDS transgenic mice), (C) Gene spring single gene analysis identified significant up-regulation of ADA, KRTCAP2, SSR4, CKAP4 and ATPG3 genes in mRAS-BCL2 transgenic mice (referred in this study as MRP8[NRASD12/ hBCL-2] or AML post MDS transgenic mice). (D). In this study; ADA and KRTCAP2 were up dysregulated in MRP8hBCL2 (mBCL2), AML post MDS (mRAS-BCL2) and HR-MDS transgenic mice Sca1+ spleen cells; SSR4 in AML post MDS (mRAS-BCL2) and HR-MDS transgenic mice Sca1+ spleen cells and; CKAP4 and ATPG3 in AML post MDS (mRAS-BCL2) transgenic mice Sca1+ spleen cells. (TIF 30355 kb