Chunk #8 — Introduction — MiR-15/16 and DLEU7 at 13q14: a unique collaboration of coding and noncoding genes in indolent CLL — DLEU7, a second tumor suppressor at 13q14
Recent studies of CLL animal models as well as mechanistic studies demonstrated the importance of the NF-kB pathway in the pathogenesis of CLL CLL (reviewed in [21]). For instance, transgenic expression of a proliferation-inducing TNF ligand (APRIL), a member of the tumor necrosis factor (TNF) superfamily involved in NF-kB activation resulted in the development of a disease very similar to CLL (see below) [22]. In our recent report we found that Tcl1 activation caused CLL by activation of NF-kB pathway and inhibition of AP-1 [23]. Since these studies suggested a significant role for the NF-kB pathway in the pathogenesis of CLL [21], we investigated whether Dleu7 might function as an inhibitor of NF-kB, in particular in the pathway involving APRIL.
