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Cancer Stem Cells
Article first published online: 12 FEB 2013
Copyright © 2012 AlphaMed Press
Volume 31, Issue 2, pages 236–247, February 2013
How to Cite
Tsuzuki, S. and Seto, M. (2013), TEL (ETV6)-AML1 (RUNX1) Initiates Self-Renewing Fetal Pro-B Cells in Association with a Transcriptional Program Shared with Embryonic Stem Cells in Mice. STEM CELLS, 31: 236–247. doi: 10.1002/stem.1277
Author contributions: S.T.: conception and design, collection of data, data analysis and interpretation, manuscript writing; M.S.: administrative support, data analysis and interpretation.
Disclosure of potential conflicts of interest is found at the end of this article.
First published online in STEM CELLSEXPRESS November 8, 2012.
- Issue published online: 12 FEB 2013
- Article first published online: 12 FEB 2013
- Accepted manuscript online: 8 NOV 2012 06:54AM EST
- Manuscript Accepted: 9 OCT 2012
- Manuscript Received: 13 AUG 2012
- Second Term Comprehensive 10-Year Strategy for Cancer Control from the Ministry of Health and Welfare
- The Ministry of Education, Culture, Sports, Science and Technology
- Japan Society for the Promotion of Science
- Research Grant of the Princess Takamatsu Cancer Research Fund. Grant Number: 11-24307
Additional Supporting Information may be found in the online version of this article.
|sc-12-0743_sm_SupplFigure1.TIF||60K||Supplemental Figure 1. Western blot analysis of TEL-AML1 expression of fetal pro-B cells infected with TEL-AML1“low” and TEL-AML1“high” viruses. Anti-myc and anti-tubulin blots are presented, along with relative cell numbers used for the analysis.|
|sc-12-0743_sm_SupplFigure2.TIF||49K||Supplemental Figure 2. Analyses of colony-forming activities of TEL-AML1-expressing pro-B cells. Fetal pro-B cells were isolated from e18 mouse fetal liver, infected with the indicated virus, sorted for GFP, and assayed for replating potential in semi-solid media under the Bcell condition. Note that only TEL-AML1“low”-infected cells efficiently yielded colonies at the 3rd plating. Typical data of three experiments conducted in triplicate are presented.|
|sc-12-0743_sm_SupplFigure3.TIF||130K||Supplemental Figure 3. Analysis for differentiation of GFP+/N-RASG12D+ and TEL-AML1+/ N-RASG12D+ cells in transplanted mice. Mice described in the legend to Figure 5C were analyzed for expression of the indicated molecules. Typical data of 4 mice are presented.|
|sc-12-0743_sm_SupplFigure4.TIF||209K||Supplemental Figure 4. GSEA for genes with transcription or chromatin annotations. Gene expression data presented in Figure 6 are analyzed for the enrichment of genes with transcription or chromatin annotation in ES_EXPRESSED_1 and ES_EXPRESSED_2 . Enrichment plot and heat map of the leading edge are presented along with NES and nominal p-value. Genes marked with asterisks were included in the analysis conducted in Figure 6.|
|sc-12-0743_sm_SupplFigure5.TIF||94K||Supplemental Figure 5. Differentiation of spleen B cells in vitro. TEL-AML1+ B220+ B cells were flow-sorted from spleen of mice that received a transplant with pro-B cells infected with TEL-AML1“low” virus, and cultured in the condition that allows differentiation in vitro. Flow-cytometric analyses of B cells before and after the differentiation induction are presented. Note that IgG1+ B cells and B220-CD138+ plasma cells emerged after the induction.|
|sc-12-0743_sm_SupplFigure6.TIF||66K||Supplemental Figure 6. Effects of shRNA-mediated silencing of genes on growth of TEL-AML1cell lines, Reh and KOPN41. (A) Cell number versus time elapsed. Reh and KOPN41 cells were infected with lentivirus vector encoding shRNA for the indicated gene. Infected cells were then selected with puromycin-resistance, and monitored for cell growth. (B) Efficiencies of respective shRNAs on gene expression, as assessed by quantitative PCR, in Reh. Relative levels of transcripts of cells infected with shRNA for the indicated gene are presented, as compared with those in cells infected with shRNA for luciferase.|
|sc-12-0743_sm_SupplFigure7.TIF||66K||Supplemental Figure 7. Expression of MYBL2, TGIF2, HMGB3, PIM2 and its related PIM1 genes in childhood ALL cases. (A) Expression of the indicated genes according to subgroups of childhood ALL: TEL-AML1 (n=34), E2A-PBX1 (n=16), MLL-rearranged (n=13), BCR-ABL (n=20), hyperdiploid (n=27), hyperdiploid with <50 chromosomes (n=16), hypodiploid (n=8), and pseudodiploid (n=16). Box plots show the range of gene expression. Median expression is shown by the horizontal line, the size of the box represents the borders that contain 50% of the values, and the error bars represent the upper and the lower quartile of the values. Data were obtained from Affymetrix gene arrays (GSE12995)  with the use of a BioConductor program with RMA correction, and normalized values are presented. The statistical significance comparing values of TEL-AML1 samples and those of any one group was calculated using Mann-Whitney U-test. * <0.05, ** <0.01, NS: not significant.|
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