Zhang, Rui Lee, Ji-Yun Wang, Xianfu Xu, Weihong Hu, Xiaoxia Lu, Xianglan Niu, Yimeng Tang, Rurong Li, Shibo Li, Yan File S1 - Identification of Novel Genomic Aberrations in AML-M5 in a Level of Array CGH <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> FOXN 3;CR;13 q 31.3;2A;candidate AML-M 5;3 q 21q abnormality;tumor suppressor gene;CDKN;tumor suppressor genes;oligonucelotide array CGH;14 q 32. Amplication;AML-M 5;AML-M 5 subtype;3 q 26.2-qter;copy number alterations;MLL;CNA;AML-M 5.;Novel Genomic Aberrations;myeloid leukemia-M 5 2014-04-11
    https://plos.figshare.com/articles/dataset/_Identification_of_Novel_Genomic_Aberrations_in_AML_M5_in_a_Level_of_Array_CGH_/996712
10.1371/journal.pone.0087637.s001