Overexpression of Cytokine Receptor-Like Factor 2 (CRLF2) has been shown to occur in Acute Lymphoblastic Leukaemia (ALL), particularly that associated with Down Syndrome (DS-ALL)1,2.
Overexpression of this protein has been associated with activation of the JAK/STAT5 pathway in transduced primary B-cell progenitors1,3 and various groups have attempted to characterise the biochemical consequences of these genetic lesions, with the goal of identifying targets for new therapies2,3.
CRLF2 overexpression has been shown to be caused by chromosomal rearrangements including the t(X;14) or t(Y;14) translocations or interstitial deletions of the pseudoautosomal region 1 (PAR1) of chromosomes X and Y. These place CRLF2 under control of an IGH enhancer1 or juxtapose the first non-coding exon of P2RY8 to the coding region of CRLF22, respectively. All of these CRLF2 rearrangements are cytogenetically cryptic and cannot be detected by conventional G-banded analysis1, making FISH a powerful detection tool for these abnormalities and an aid to furthering this research. Our CRLF2 Breakapart probe will detect rearrangements of the CRLF2 gene, whilst the P2RY8 Deletion probe allows detection of deletions between CRLF2 and P2RY8, causing the fusion gene.
1. Russell et al., Blood. 2009 Sep 24;114(13)2688-98
2. Mullighan et al., Nat Genet 2009; 41(11): 1243-6
3. Tasian et al., Blood 2012; 120(4):833-842
- Area of Interest*
For research use only, not for use in diagnostic procedures.
*Disease information supported by the literature and is not a reflection of the intended purpose of this product.