File S1 - Identification of Novel Genomic Aberrations in AML-M5 in a Level of Array CGH ZhangRui LeeJi-Yun WangXianfu XuWeihong HuXiaoxia LuXianglan NiuYimeng TangRurong LiShibo LiYan 2014 <p>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 <i>EVI</i> 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 <i>EVI</i> gene in metaphase (I). Figure S2, The comparisons of <i>FOXN3</i> Levels in health control, ALL and AML. The significantly reduced <i>FOXN3</i> level was observed between AML and health controls. *: p<0.05. The <i>FOXN3</i> level was lower in ALL than health control whereas no significantly difference was observed. Figure S3, The comparisons of <i>FOXN3</i> Levels in health control, M5 and non-M5. No significantly difference was observed on the <i>FOXN3</i> 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 <i>FOXN3</i> 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 <i>FOXN3</i>.</p> <p>(7Z)</p>