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There are two distinct forms of HL, known as classical Hodgkin lymphoma (cHL) and nodular lymphocyte- predominant Hodgkin lymphoma (NLPHL), that are separated on the basis of morphologic, immunophenotypic, and clinical differences.
The striking epidemiological differences between EBV-positive and -negative paediatric HL (Weinreb et al, 1996; Glaser et al, 1997) Flavell et al, 2000) have been used to support the view that these two forms of HL are aetiologically distinct.
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Epidemiologic studies suggest there are three forms of cHL: pediatric HL (EBV-positive, mixed cellularity type), HL of young adults (EBV-negative, nodular sclerosis type), and HL of older adults (EBV-positive, mixed cellularity type) [20], [21].
In conclusion, although HL with extranodal involvement is not common, it should be considered a unique form of HL.
Although HL with extranodal involvement is rare, it should be considered as a unique form of HL.
Our results also provide further evidence for aetiological differences between the EBV-positive and -negative forms of paediatric HL.
The precise nature of disturbances in the cellular signaling, caused by the other two non functional forms, i.e. the membrane bound monomer and the non-lytic pre-pore forms of α-HL are still not clear.
Verifying this, C/EBPβ knockdown significantly restored the colony forming capacity of HL-60 cells as repressed by JMJD3 overexpression (Fig. 6j, l).
Mixed cellularity and lymphocyte depleted form of classical HL are the predominant pathologic subtypes and bone marrow involvement is found in about half of patients.
All these observations suggest that the induction of apoptosis by α-HL was due to the presence of the monomeric form of α-HL.
In contrast, W179C, a mutant form of α-HL (which has a mutation in Cav-1 binding motif) did not affect the caveolae dynamics (Video S5).
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