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. Author manuscript; available in PMC: 2017 Aug 1.
Published in final edited form as: Cancer Res. 2016 Jun 8;76(15):4470–4480. doi: 10.1158/0008-5472.CAN-15-2949

Figure 1. FLT3 is highly expressed and miR-150 is repressed in AML.

Figure 1

(A–C) The expression patterns of FLT3 across different FAB subtypes (A), cytogenetic subtypes (B) or subtypes with different molecular mutations (C) in the GSE37642 AML cohort. In Figure plots A and B, P-value was shown for the particular AML subtypes in which FLT3 was expressed at a significantly higher or lower level than that in the whole AML set (n=562). In Figure plot C, the P-value was shown for comparison between each individual AML subtype (with a particular type of molecular abnormalities) and the whole AML set (left panel), or between AML cases with and without a particular type of molecular abnormalities (right panel). ND, not determined; complex, complex karyotypes; other, other cytogenetic abnormalities; CN, cytogenetically normal; _Mut, with a particular type of molecular mutations; _Neg, without a particular type of molecular mutations. Note: The expression values were log(2) transformed and normalized by RMA (29). Over 40% of the AML cases with NPM1 mutations also have FLT3-ITD. (D) qPCR analysis of expression of both FLT3 and miR-150 in 23 human primary AML mononuclear (MNC) samples including 3 t(4;11), 1 t(6;11), 9 t(9;11), 1 t(11;19), 3 t(8;21), 1 t(15;17), 3 inv(16), 1 FLT3-ITD, and 1 t(4;11)/FLT3-ITD, along with 5 normal BM cell controls (Ctrl; including 3 MNC and 2 CD34+ samples). The P-values were calculated by two-tailed t-test.

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