File S1 - Identification of Novel Genomic Aberrations in AML-M5 in a Level of Array CGH

Figure S1, 3q anomaly identified by karyotype and FISH in two of the 69 de novo AMLs. (A)–(F) showed t(3;21) in case with ID 37 and (G)–(I) showed inv(3) in case with ID 65. Arrows indicated the der(3)t(3;21) (A) and der(21)t(3;21) (B) observed by R-banding. FISH with EVI(3q26) probe showed two fusion signals plus an extra red signal (TEL'EVI1) in interphase (C) and translocation of chromosome 3 with a variant breakpoint of EVI gene in metaphase (D). Hybridization with TEL/AML1 probe demonstrated an extra red signal in interphase (E) and translocation of chromosome 21 in metaphase (F). (G) Arrow indicated the derivative inv(3) showed by R-banding. FISH with EVI(3q26) probe showed two fusion signals plus an extra red signal (TEL'EVI1) in interphase (H) and inv(3) with a variant breakpoint of EVI gene in metaphase (I). Figure S2, The comparisons of FOXN3 Levels in health control, ALL and AML. The significantly reduced FOXN3 level was observed between AML and health controls. *: p<0.05. The FOXN3 level was lower in ALL than health control whereas no significantly difference was observed. Figure S3, The comparisons of FOXN3 Levels in health control, M5 and non-M5. No significantly difference was observed on the FOXN3 levels between AML-M5 and non-AML-M5 (p>0.05). Table S1, The results of karyotype and array CGH in 24 AML-M5. Table S2, FAB subtypes, karyotypes and FISH with EVI (3q26) probe analysis on 69 de novo AML patients. Table S3, Clinical information and FOXN3 expression levels of 97 acute leukemia samples and 16 normal controls. Table S4, The clinical characterizations of 24 cases of AML-M5. Table S5, Drug dose and duration of chemotherapy. Table S6, Primers in qRT-PCR for FOXN3.
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