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P. Fenaux, G. J. Mufti, E. Hellstrom-Lindberg, V. Santini, N. Gattermann, U. Germing, G. Sanz, A. F. List, S. Gore, J. F. Seymour, H. Dombret, J. Backstrom, L. Zimmerman, D. McKenzie, C. L. Beach and L. R. Silverman, “Azacitidine Prolongs Overall Survival Compared with Conventional Care Regimens in Elderly Patients with Low Bone Marrow Blast Count Acute Myeloid Leukemia,” Journal of Clinical Oncology, Vol. 28, No. 4, 2009, pp. 562-569. doi:10.1200/JCO.2009.23.8329

has been cited by the following article:

• TITLE: Gene Expression Profiling of Human Myeloid Leukemic MV4-11 Cells Treated with 5-Aza-2’-deoxycytidine

  AUTHORS: Kyu-Tae Kim, David Mossman, Donald Small, Rodney J. Scott

  KEYWORDS: 5-Aza-2’-deoxycytidine; Gene Expression Profile; HOX; CD9; RGS2

  JOURNAL NAME: Journal of Cancer Therapy, Vol.3 No.3, June 20, 2012

  ABSTRACT: The pyrimidine analog, 5-aza-2’-deoxycytidine (5-aza-dC) is a DNA methyltransferase inhibitor that triggers DNA demethylation leading to the reactivation of epigenetically silenced tumor suppressor genes. To understand the shift in gene expression which mediates the beneficial 5-aza-dC effects in leukemia, we have treated human myeloid derived leukemic cells with 5-aza-dC. Target genes were identified first in MV4-11 cells using a genome-wide gene expression profiling assay to detect differences in treated and untreated cells. From this analysis six genes were identified (HOXA4, HOXD4, HOXA8, HOXD12, CD9 and RGS2) as being significantly different expressed after treatment. To validate microarray data, we performed quantitative PCR on these genes from multiple leukemic cells. The results suggest that these genes are epigenetically regulated indicating that dysregulation of HOXA4, HOXD4, HOXA8, HOXD12, CD9 and RGS2 expression may play an important role in establishing the malignant phenotype in AML.