Despite improvements in the treatment of patients with Ewing family tumors (EFT), the prognosis for patients with advanced disease is still unsatisfactory. Recently, we identified lipase I as an EFT-associated gene that might be interesting for the development of new immunological or pharmacological treatment strategies. Lipase I is a member of the large protein superfamilies of alpha/beta hydrolases and serine hydrolases. In the present paper we describe high expression of another member of these superfamilies in EFT. By DNA microarray data base mining we found exceptional high expression of alpha/beta hydrolase domain containing 6 (ABHD6) in EFT but not in other sarcomas. Expression of ABHD6 in EFT correlated with expression of another EFT-associated gene, aristaless. Analysis of ABHD6-associated GGAA microsatellites revealed shorter microsatellites in EFT with lack of ABHD6 expression. ABHD6 homologues were found in varying chordata but not in other animal species. Based on homology modeling we predicted the 3D-structure of ABHD6, which shows high similarity with bacterial homoserine transacetylases. High expression of ABHD6 in EFT in comparison to normal tissues and other tumors suggests that ABHD6 might be an interesting new diagnostic or therapeutic target for EFT. However, knock down of ABHD6 in EFT cells did not inhibit tumor cell growth.
Human antigen presenting cells commonly express CD4 but the significance of this phenomenon has not been clarified. We analyzed a panel of Epstein–Barr virus‐immortalized B cells (so called lymphoblastoid cell lines, LCL) by using flow cytometry, DNA‐microarray analysis, and reverse transcriptase‐polymerase chain reaction (RT‐PCR). The number of CD4+ cells varied from cell line to cell line but expression of CD4 was detected by flow cytometry and RT‐PCR in all investigated cell lines. To characterize CD4 expressing LCL in more detail, we separated CD4+ and CD4− cells from single cell lines by using immunomagnetic beads. When we cultured sorted CD4+ and CD4− cells, we observed that CD4 expression was stable for several passages. However, the number of CD4+ cells decreased with time in culture. We never observed that CD4− cell lines returned back to a CD4+ phenotype. DNA‐microarray analysis of isolated CD4+ and CD4− cells indicated that the overall gene expression profile of both cell populations was highly similar. In addition, CD4+ and CD4− cells showed the same allostimulatory capacity. CD4+ LCL showed a slightly increased interleukin‐16 induced chemotaxis. Differences in the gene expression profile of CD4+ and CD4− cell lines suggested that loss of CD4 expression occurred during a differentiation step involving achaete–scute complex homolog‐like 1.
Abstract:In the present paper we review the translocation network involving TET and ETS family members with special focus on the Ewing family of tumors. FUS (fusion, involved in t(12;16) in malignant liposarcoma = TLS, Translocated in liposarcoma), EWSR1 (Ewing sarcoma breakpoint region 1) and TAF15 (TATA box-binding protein-associated factor, 68-KD) are the three human members of the TET family of RNA binding proteins. In addition, two EWSR1 pseudogenes are present in the human genome. TET family members are involved in several oncogenic gene fusions. Five of the 18 known fusion partners belong to the E26 (E twenty-six, ETS) family of transcription factors. Gene fusions between TET or ETS family members and other fusion partners link these gene fusions to a large network of oncogenic gene rearrangements.
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