IGH/CCND3 Plus Translocation, Dual Fusion
Approximately 40-60% of Multiple Myeloma cases are associated with translocations involving the IgH locus at chromosome 14q32 and one of several partners including CCND1, WHSC1 (MMSET), CCND3, MAF or MAFB. Cases lacking an IgH translocation are associated with a hyperdiploid phenotype1.
The CCND3/IGH translocation, t(6;14)(p21;q32), has been reported in 4% of multiple myeloma tumours2. However, it is also characteristic of a variety of other B-cell malignancies, including plasma cell leukaemia, diffuse large B-cell non-Hodgkin lymphoma (DLBCL) and Splenic Lymphomas with Villous Lymphocytes (SLVLs)3. CCND3 has been identified as a putative oncogene that is dysregulated as a consequence of the translocation2. The translocation appears to be mediated by an error in IgH switch recombination as it has been shown that in KMM-1 cell lines, the translocation disrupts a switch sequence in this region and results in juxtaposition of CCND3 with the IGH promoter, thus elevating the levels of CCND3 expression2. It is thought that this mechanism is similar in all cases of IgH translocation. Most breakpoints appear to be clustered in a region that is fewer than 200kb centromeric to CCND32 and this region is flanked by the Cytocell probe.
1. Fonseca et al., Cancer Res 2004;64:1546-58
2. Shaughnessy et al., Blood 2001;98(1):217-233.
3. Soniki et al., Blood 2001;98(9):2837-44
- 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.