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. Author manuscript; available in PMC: 2020 Sep 18.
Published in final edited form as: Blood Cancer Discov. 2020 Jul;1(1):32. doi: 10.1158/2643-3230.BCD-19-0028

Fig. 4. Following exposure to an alkylating agent, haploinsufficiency of both Egr1 and Apc promotes development of MDS; loss of these genes together with Trp53 promotes AML development.

Fig. 4.

(A) Kaplan-Meier survival curves of WT recipients transplanted with Egr1+/−, Apcdel/+ bone marrow cells transduced with luc shRNA (EA-luc: black) or Trp53 shRNA (EA-Trp53: red). Both donor and recipient mice were treated with ENU. Disease development is significantly faster in EA-Trp53 mice compared to EA-luc mice (200d vs. 370 d, P=0.0014). (B) Histological classification of diseases shows that most EA-luc mice developed MDS, and none developed AML. (C-F) Mouse genes were collapsed to human gene names; differentially expressed genes in EA-Trp53 AML samples (n=6) vs. EA-luc MDS samples (n=6) were analyzed using the GSEA software. Features, such as a block in myeloid differentiation and upregulation of MYC target genes and WNT/β-catenin signaling recapitulate human t-MN.