Dataset: Histone acetylation and DNA demethylation of T-cells result in an anaplastic large cell lymphoma-like phenotype.

A characteristic feature of anaplastic large cell lymphoma (ALCL) is the significant reduction of the T-cell expression program despite its T-cell origin, a finding very similar to the loss of B-cell identity of classical Hodgkin lymphoma (cHL). Previously we demonstrated that epigenetic mechanisms are active in cHL to induce this peculiar phenotype. The results show that combined DNA demethylation and histone acetylation of T-cell lines induce an almost complete extinction of the T-cell phenotype, including the down-regulation of essential T-cell receptor signalling pathway genes such as CD3, LCK and ZAP70, as well as an up-regulation of ALCL-characteristic genes. In contrast, combined DNA demethylation and histone acetylation of ALCL cells is not able to reconstitute their T-cell phenotype. This clearly demonstrates that similar epigenetic mechanisms are active in ALCL and cHL which are responsible for the extinction of their cell type characteristic phenotype. We subjected T-cell lymphoma/leukemia cell lines and ALCL cell lines (n=4, each) to epigenetic modifiers to evoke DNA demethylation and the histone acetylation. Global gene expression profiling (Affymetrix) was performed from treated and untreated cell lines which were evaluated by real-time RT-PCR and Western Blot analysis.

Species:

human

Samples:

16

Source:

E-GEOD-26101

PubMed:

22899583

Updated:

Dec.12, 2014

Registered:

Jun.18, 2014