Subtypes of diffuse large B-cell lymphoma
DLBCL subtypes have been sorted into groups based on their distinctive morphology or immunophenotype, distinctive clinical issues, and distinctive virus-driven etiology. The prognoses and treatment of these subtypes varies with their severity. Most subtypes are aggressive diseases and consequently treated in a manner similar to DLBCL,NOS. Further details on these subtypes, including their treatments, can be found in their respective main article linkages. DLBCL with a distinctive morphology or immunophenotype
T cell/histiocyte-rich large B-cell lymphoma
T-cell/histiocyte-rich large B-cell lymphoma (THRLBCL) is a DLBCL in which tumors containing small numbers of usually large neoplastic B-cells embedded in a background of reactive T-cells and histiocytes develop in the liver, spleen, bone marrow and/or, rarely other sites. Patients usually present with advanced disease; their overall 3 year survival rates in different studies range between 46% and 72%. ALK+ large B-cell lymphoma
ALK+ large B-cell lymphoma (ALK+ LBCL) is a DLBCL in which neoplastic lymphocytes that express the ALK tyrosine kinase receptor protein infiltrate lymph nodes as well as extranodal sites, e.g. the mediastinum, bones, bone marrow, nasopharynx, tongue, stomach, liver, spleen, and skin. About 60% of these individuals present with advanced disease. ALK+ LBCL has an overall 5 year survival rate of ~34%. Plasmablastic lymphoma
Plasmablastic lymphoma (PBL) is a DLBCL in which neoplastic immunoblastic or plasmablastic cells embedded in a background of other cell types infiltrate the oral/nasal cavity or much less often the gastrointestinal tract. Some 70% of individuals with PBL are infected with EBV and/or (particularly those with oral/nasal cavity disease) human immunodeficiency virus (HIV).
Causes
It is possible that facial clefts are caused by a disorder in the migration of neural crest cells.Another theory is that facial clefts are caused by failure of the fusion process and failure of inwards growth of the mesoderm. Other theories are that genetics play a part in the development of facial clefts or that they are caused by amniotic bands. Genetics
Overview
Around one in 700 individuals are born with craniofacial clefts. There are multiple genetic and environmental factors which contribute to craniofacial development. Within craniofacial disorders and abnormalities, orofacial clefts, and specifically cleft lip (CL) and cleft palate (CP) are the most common in humans. Occurrences of CL/P are most often (around seventy percent of cases) isolated and nonsyndromic, meaning they are not associated with a syndrome or inherited genetic conditions. Around thirty percent occur with other structural variances, and over 500 syndromes have been identified in which clefting is a principal feature. Clefting can result from teratogens, an agent that disrupts embryo development such as, radiation, maternal infection, chemicals, or drugs. Chromosomal abnormalities or mutations at single gene loci have also contributed to clefting development. Genetic causes are linked with most craniofacial syndromes, and CL/P and other orofacial clefts are recognized as heterogeneous disorders, meaning there are multiple recognized causes. Orofacial clefts have great phenotypic diversity, and their associated genetic environments have called for vast research and investigation.