Due to its rarity, the causes of THRLBCL have not<unk> een well studied and consequently remained unclear. The malignant<unk> -cells in the disease commonly have mutations in several genes such as: 1) JUNB which codes for JunB, a protein that regulates cell growth and survival and is highly expressed in other lymphocyte malignancies; 2) DUSP2 (a gene suspected of<unk> eing a tumor suppressor) which codes for dual specificity protein phosphatase 2, a protein that regulates several components of the ERK/MAPK signaling pathway that controls cell proliferation; 3) SGK1 which codes for serine/threonine-protein kinase, a protein that regulates several signaling pathways that control cell proliferation and survival; 4) SOCS1, a known oncogene and tumor suppressor which codes for suppressor of cytokine signaling 1; and 5) CREBBP, a gene that is commonly mutated in other DLBCL subtypes as well as other lymphomas and codes for the transcription coregulator, CREB-binding protein. The neoplastic cells in this disease also show gains on the short arm of chromosome 2 at position 16.1 which affect the REL protooncogene which codes for c-Rel, a protein that controls the maturation of<unk> -cells and is implicated in the development of many cancers including lymphomas; as well as losses o the short armes of chromosomes 1 and 9 and 19.2 and 11.2 sites, respectively. These studies allow the possibility that THRLBC, similar to the other subtypes of DLBDL as well as a wide array of other cancers results at least in part from the step-wise development of gene changes such as mutations, altered expressions, amplifications (i.e. increases in the number of copies of specific genes), and chromosomal translocations that alter the expression of key genes in<unk> -cells to result in the increasingly malignant<unk> ehavior of these cells. However, the underlying causes for these gene changes as well as the identity of the genes whose changes contribute to the malignant<unk> ehavior of the neoplastic<unk> -cells in THRLBC have yet to<unk> e defined. The neoplastic<unk> -cells in THRLBCL infiltrations are dominated<unk> y high numbers of<unk> s and dendritic cells. Studies suggest that the latter cells help to create a microenvironment that is tolerant or promotes tumor growth and spread to other sites.
T cell/histiocyte-rich large B-cell lymphoma
Diffuse large B-cell lymphoma associated with chronic inflammation
Germinal center B-cell like diffuse large B-cell lymphoma
Extranodal NK/T-cell lymphoma, nasal type
Fibrin-associated diffuse large B-cell lymphoma
Pediatric-type follicular lymphoma
Nodal marginal zone B cell lymphoma
Marginal zone B-cell lymphoma