DNA Microarray Assay Helps to Identify Functional Genes Specific for Leukemia Stem Cells

Haojian Zhang,Shaoguang Li

doi:10.1155/2013/520285

Abstract

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.

Highlights

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder that originates from an abnormal hematopoietic stem cell (HSC) harboring the Philadelphia chromosome (Ph) [1,2,3]
Developing new strategies to target leukemia stem cells (LSCs) is necessary and critical for curing CML, and the success of this approach requires a full understanding of the biology of LSCs
We present a detailed description about microarray dataset that might make this dataset very useful for any investigator to compare the gene expression profile of normal HSCs and LSCs with or without imatinib treatment

Summary

Introduction

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder that originates from an abnormal hematopoietic stem cell (HSC) harboring the Philadelphia chromosome (Ph) [1,2,3]. 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. increasing evidence demonstrated that CML stem cells utilize signaling pathways that are independent of BCRABL kinase activity for their maintenance and survival [11, 12], the underlying molecular mechanisms remain unclear. Increasing evidence demonstrated that CML stem cells utilize signaling pathways that are independent of BCRABL 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

Methodology

Dataset Description

Findings

Concluding Remarks