Two oncogenic mechanisms that appear to<unk> e active in GCB DLBCL are the prevention of apoptosis and the<unk> locking of<unk>  differentiation. Preventing apoptosis Normal<unk><unk> <unk> -cells appear to<unk> e poised for apoptosis unless they are selected to progress to the next stage of differentiation. Most normal<unk><unk> <unk> -cells express low levels of anti-apoptotic proteins such as<unk> cl-2. In GBC DLBCLs, the T(14,18) translocation can result in an increase of the<unk> cl-2 protein, which may reduce the number of cells that undergo apoptosis.<unk> locking differentiation<unk> locking the differentiation of<unk><unk> <unk>  cells is dangerous<unk> ecause the cells are programmed to divide rapidly at this stage. The SHM that occurs in the<unk><unk>  can also target non-immunoglobulin loci and may<unk> e responsible for translocation of the<unk> CL-6 gene.<unk> CL-6 genes are involved in several cell processes that can affect the ability of the<unk> -cell to differentiate and proliferate.<unk> CL-6 genes produce<unk> CL-6 proteins. These proteins work with other transcription factors <unk> LIMP1, PAX5, XBP1) to form a regulatory circuit that controls the progression of<unk><unk> <unk>  cells to plasma cells.<unk> CL-6 proteins repress genes involved in<unk>  differentiation and promote proliferation<unk> y<unk> locking expression of a cell-cycle inhibitor (p27KIP1).<unk> CL-6 is also an inhibitor of cellular senescence. Cellular senescence is a programmed response that prevents a cell from dividing after some number of cell divisions.
Germinal center B-cell like diffuse large B-cell lymphoma
Diffuse large B-cell lymphoma associated with chronic inflammation
Epstein–Barr virus positive diffuse large B-cell lymphoma, not otherwise specified
T cell/histiocyte-rich large B-cell lymphoma
Nodular lymphocyte predominant Hodgkin lymphoma
Extranodal NK/T-cell lymphoma, nasal type
Large B-cell lymphoma arising in HHV8-associated multicentric Castleman's disease
Pediatric-type follicular lymphoma