geneMAP™ WT1 Expression Analysis Kit (WT1-24)

FEATURES

  • Fast and Easy to Use with Multiplex Realtime PCR Technology
  • Accurate expression analysis with TaqMan Probe technology
  • Compatible with FAM, VIC/HEX two Colors Real-Time PCR Instruments
  • RUO

WT1 is an important regulatory molecule involved in cell growth and development. It has been found that WT1 can either enhance or repress the expression of specific target genes, depending on the levels of WT1 expression, the isoforms, the location of the transcriptional start site, and the cell type in which the experiment was performed. In human hematopoietic cells, WT1 appears to behave as a tumor suppressor gene as the overexpression of WT1 in early human bone marrow (BM) cells leads to growth arrest and reduced colony formation. Indeed, in normal human BM, WT1 is expressed at extremely low levels and is confined to the primitive CD34+ population of cells. Besides, WT1 is highly overexpressed in the BM or peripheral blood (PB) of a variety of leukemias, and these evidences support the role of WT1 as an oncogene in this subset. Increased levels of WT1 expression can be found in both acute lymphoblastic and acute myeloid leukemia (AML) although more frequently in AML (frequencies varying from 73% to 91%. Following the discovery of overexpression of WT1, there has been growing evidence that the WT1 expression levels may have a prognostic role in AML.

Many studies have shown that the assessment of MRD may prove useful to better stratify high-risk patients and address treatment intensity in AML. The most sensitive method for this strategy involves the detection of fusion genes derived from chromosome translocations, such as PML-RARa, AML-ETO1, and CBFb-MYH11 and more recently gene mutations such as NPM1. Besides, more than 50% of AML lack known genetic lesions or clonality markers suitable for MRD monitoring. Thus, alternative markers for MRD are highly sought, and WT1 gene has been suggested as a candidate.

Quick Contact Form

    error: Content is protected !!