Figure 4.
Comparative analysis between the SAA-CNL and SCN-AML patients regarding mutations and transcriptional profile. (A) Mutational spectrum observed in the SCN-AML patient and the SAA-CNL patient. The bold genes are overlapping (SUZ12 and EZH2 together form the polycomb-repressive complex 2). (B-C) GSEA comparing nonleukemic CD34high cells from 3 healthy controls with CD34high cells obtained from the SAA-CNL patient (B), CD34high cells from 3 healthy controls with CD34high cells obtained from the SCN patient (SCN phase before AML became clinically overt) (C), both showing increased IFN-related signaling. (D) Expression levels (in transcript per million [TPM]) of various IFN-inducible genes, which are significantly increased in both the SAA-CNL and the SCN stage. *P < .05. ES, enrichment score; FDR, false discovery rate; NES, normalized enrichment score.

Comparative analysis between the SAA-CNL and SCN-AML patients regarding mutations and transcriptional profile. (A) Mutational spectrum observed in the SCN-AML patient and the SAA-CNL patient. The bold genes are overlapping (SUZ12 and EZH2 together form the polycomb-repressive complex 2). (B-C) GSEA comparing nonleukemic CD34high cells from 3 healthy controls with CD34high cells obtained from the SAA-CNL patient (B), CD34high cells from 3 healthy controls with CD34high cells obtained from the SCN patient (SCN phase before AML became clinically overt) (C), both showing increased IFN-related signaling. (D) Expression levels (in transcript per million [TPM]) of various IFN-inducible genes, which are significantly increased in both the SAA-CNL and the SCN stage. *P < .05. ES, enrichment score; FDR, false discovery rate; NES, normalized enrichment score.

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