Journal article
Integrative analysis of RUNX1 downstream pathways and target genes
J Michaud, KM Simpson, R Escher, K Buchet-Poyau, T Beissbarth, C Carmichael, ME Ritchie, F Schütz, P Cannon, M Liu, X Shen, Y Ito, WH Raskind, MS Horwitz, M Osato, DR Turner, TP Speed, M Kavallaris, GK Smyth, HS Scott
BMC Genomics | BMC | Published : 2008
Open access
Abstract
Background: The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification. It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML). The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia. We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia. Results: Here wereport genes regulated either directly or indirectly by RUNX1 based on the study..
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Awarded by National Institutes of Health
Funding Acknowledgements
We thank Dr. S. Brenz Verca and Prof S. Rusconi for providing the adenoviral backbone, transfer vector (pScot) and the HER911 packaging cell line. We thank Prof. S. E. Antonarakis for his support during the adenovirus production. This project was supported by grants from the Ligue Genevoise Contre le Cancer, the Fondation Pour la Lutte Contre le Cancer, the Fondation Dr Henri Dubois-Ferriere Dinu Lipatti, the Nossal Leadership Fellowship from the Walter and Eliza Hall Institute of Medical Research, NHMRC Grants (257501, 257529) and NHMRC fellowship 171601 to HSS; International Postgraduate Research (Australian government) and Melbourne International Research scholarships to JAM and FS, an Australian postgraduate award to MER, an NHMRC Dora Lush Postgraduate Award (305552) to CC, a Swiss National Science Foundation and Bernische Krebsliga fellowships to RE, NIH (DK58161 and HL079507), to MH and NHMRC Career Development Award 300580 to MK.