IGH/MAF Translocation, Dual Fusion
The translocation t(14;16)(q32.3;q23) involving MAF and IGH is present in 25% of myeloma cell lines1, in 5% of primary Multiple Myeloma samples2,3 and results in high levels of MAF expression. Patients harbouring the t(14;16) appear to have a worse outcome3,4. The majority of the breakpoints are dispersed over a region of approximately 500kb, centromeric to the MAF proto-oncogene at 16q23. Another breakpoint, has been observed that is telomeric to MAF1. Translocations with the centromeric breakpoints place MAF under the control of strong 3' IGH enhancers. Recent gene expression profiling of myeloma cell lines revealed that MAF caused transactivation of cyclin D2 (a promoter of cell cycle progression), thus enhancing proliferation of myeloma cells4.Within or near to the MAF/IGH breakpoint region lies the putative tumour suppressor gene, WWOX, which spans the common chromosomal fragile site 16D (FRA16D) at chromosome 16q23.3-24.1 - a region that is a frequent target for both loss of heterozygosity and chromosomal rearrangements in ovarian, breast, hepatocellular and prostate carcinomas as well as other neoplasias5.
1. Chesi M et al., Blood 1998;91(12):4457-632.
2. Avet-Loiseau H et al., Blood 2002;99(6):2185-913.
3. Fonseca R et al., Blood 2003;101(11):4569-754.
4. Chang H et al., Leukemia 2007;21:1572-45.
5. Nunez MI et al., BMC Cancer 2005;5:64
- Area of Interest*
This product is intended to be used on Carnoy’s solution (3:1 methanol/acetic acid) fixed haematological samples.
*Disease information supported by the literature and is not a reflection of the intended purpose of this product.