%0 Journal Article
%T DNA Microarray Assay Helps to Identify Functional Genes Specific for Leukemia Stem Cells
%A Haojian Zhang
%A Shaoguang Li
%J Dataset Papers in Science
%D 2013
%R 10.1155/2013/520285
%X Chronic myeloid leukemia (CML) is a myeloproliferative disease derived from an abnormal hematopoietic stem cell (HSC) and is consistently associated with the formation of Philadelphia (Ph) chromosome. Tyrosine kinase inhibitors (TKIs) are highly effective in treating chronic phase CML but do not eliminate leukemia stem cells (LSCs), which are believed to be related to disease relapse. Therefore, one major challenge in the current CML research is to understand the biology of LSCs and to identify the molecular difference between LSCs and its normal stem cell counterparts. Comparing the gene expression profiles between LSCs and normal HSCs by DNA microarray assay is a systematic and unbiased approach to address this issue. In this paper, we present a DNA microarray dataset for CML LSCs and normal HSCs to show that the microarray assay will benefit the current and future studies of the biology of CML stem cells. 1. Introduction Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder that originates from an abnormal hematopoietic stem cell (HSC) harboring the Philadelphia chromosome (Ph) [1¨C3]. The Ph is caused by a reciprocal translocation between chromosomes 9 and 22 (t(9; 22)(q34; q11)), resulting in the formation of the chimeric BCR-ABL protein [1, 4]. As a result, the BCR-ABL oncogene is formed. BCR-ABL is a constitutively active tyrosine kinase, which has provided the molecular basis for designing therapeutic drugs. Imatinib is the first tyrosine kinase inhibitor (TKI) found to be highly effective in CML treatment through inhibiting BCR-ABL kinase activity [5¨C7]. Targeted therapy with TKIs induces a complete hematologic and cytogenetic response in more than 90% of chronic phase CML patients [8]. However, TKIs cannot efficiently eradicate leukemia stem cells (LSCs) of CML due to the insensitivity of LSCs to TKIs [9, 10]. Therefore, developing new strategies to target LSC is necessary and critical for curing CML, and the success of this approach requires a full understanding of the biology of LSCs. Although increasing evidence demonstrated that CML stem cells utilize signaling pathways that are independent of BCR-ABL kinase activity for their maintenance and survival [11, 12], the underlying molecular mechanisms remain unclear. To address these challenging issues, we performed a DNA microarray assay to compare the gene expression profiles between LSCs and normal HSCs. Here, we present the entire microarray dataset in open access format to demonstrate the usefulness of the microarray data in studying LSCs in CML. 2. Methodology Our previous
%U http://www.hindawi.com/journals/dpis/2013/520285/