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Analyses of epigenetics in classical Hodgkin lymphoma and anaplastic large cell T-cell lymphoma
Classical Hodgkin lymphoma (cHL) and anaplastic large cell T-cell lymphoma (ALCL) share some similarities which separate them from other lymphoma entities: Both express e.g. the surface marker CD30 and their tumor cells lose almost all of the features of its parent cells - cHL tumor cells accordingly have no B-cell characteristics whereas ALCL tumor cells lose all their T-cell characteristics.
In this project we examined the role of epigenetics in the downregulation of the respective cell characteristics. Our previous results suggest that two epigenetic mechanisms are involved in this loss: firstly specific suppressors are activated by DNA demethylation and histone acetylation, which results in an indirect downregulation of parent cell characteristics. On the other hand important transcription factors such as PAX5 in cHL and TCF1, LEF1 and GATA3 in ALCL are silenced by an additional H3K27 trimethylation to prevent the restoration of the parent cell expression program.
Joosten M, Seitz V, Zimmermann K, Sommerfeld A, Berg E, Lenze D, et al. Histone acetylation and DNA demethylation of T-cells result in an anaplastic large cell lymphoma-like phenotype. Haematologica. 2012 Aug 16. PMID:22899583
Ehlers A, Oker E, Bentink S, Lenze D, Stein H, Hummel M. Histone acetylation and DNA demethylation of B cells result in a Hodgkin-like phenotype. Leukemia. 2008 Apr;22(4):835-41. Epub 2008 Feb 7. PMID: 18256685