Characterization of EBV‐genome negative “null” and “T” cell lines derived from children with acute lymphoblastic leukemia and leukemic transformed non‐Hodgkin lymphoma

Abstract

Sixty-two explants from peripheral blood, bone marrow and cerebral fluid of children with acute lymphoblastic leukemia (ALL) and leukemic transformed non-Hodgkin lymphoma (NHL) were cultivated for at least 8 weeks. Although lymphatic cells persisted up to 16 weeks in tissue culture, no proliferation was observed in 54 cultures. From the remaining cultures, eight permanently growing cell lines were obtained. Five of these were EBNA (Epstein-Barr virus-specific nuclear antigen)-positive. Three, however, were ENBA-negative and lacked Epstein-Barr virus genomes. Two cell lines (KM-3 and SH-2) expressed neither B nor T cell characteristics. One line (JM) expressed T cell characteristics and complement receptors. The growing lymphatic cells represented leukemic cells, since the pattern of cytochemical staining and that of membrane receptors of lymphoblasts from the same donor prior to cultivation were identical. All leukemic cell lines were derived from patients in relapse. In contrast, no proliferation of leukemic cells occurred in explains from patients revealing the first manifestation of the disease. These results suggest enhanced growth potential of lymphoblasts resisting antileukemic therapy.

The Modulatory Effects of the Polymorphisms in GLA 5′-Untranslated Region Upon Gene Expression Are Cell-Type Specific

“…Experimental data (Samac et al 1998) have shown that sequence changes that increase the affinity of the GLA 5 0 UTR MDBP binding site for its cognate ligands exert a strong repressive effect upon gene expression. Furthermore, a C>T transition in the third nucleotide position of a MDBP binding site in the human cytomegalovirus significantly increased ligand binding, resulting in 10-fold reduction of reporter gene expression (Schneider et al 1977). However, to the best of our knowledge, no EMSA studies have ever been performed with the human GLA 5 0 UTR MDBP binding site, to assess the relative affinities of the c.-10(C > T) alleles.…”

“…The diverse embryological lineages of HEK-293 (Shaw et al 2002), HeLa (Macville et al 1999), HDMEC (Richard et al 1999), and Jurkat (Schneider et al 1977) cells are a logical explanation for this finding, as the GLA gene may be under different constitutive expression regulation on different cells.…”

“…The pGL3-Control Vector contains a cDNA encoding a modified firefly luciferase (luc+) under the control of the Simian virus 40 (SV40) promoter. The recombinant pGL3 vectors were transiently transfected into each of four human cell lines of different embryological origin: (1) human embryonic kidney, HEK-293 (Shaw et al 2002); (2) human cervical carcinoma, HeLa (Macville et al 1999); (3) human dermal microvascular endothelial cells, HDMEC (Richard et al 1999); and (4) human T cell lymphoblast-like, Jurkat (Schneider et al 1977). A plasmid (pCDNA3.3-LacZ; Invitrogen, Life Technologies, Carlsbad, CA, USA) containing the Escherichia coli (E. coli) b-galactosidase gene (pGAL) was used as an internal control for transfection efficiency.…”

Inhibition of BCL11B expression leads to apoptosis of malignant but not normal mature T cells

“…Assuming the profound role of Bcl-xL and TRAIL in BCL11B-RNAi mediated cell death, one should expect a lack of apoptosis induction in non-transformed mature T cells upon Bcl11b suppression, as demonstrated here. Notably, as Jurkat is derived from immature (Schneider et al, 1977) and huT-78 (Gootenberg et al, 1981) from fully differentiated T cells, the selective apoptogenic effect of the BCL11B suppression seems to be not only a property of the differentiation status (DN thymocytes vs mature T cells) but also of the transformed phenotype (malignant vs normal T cells).…”

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

“…We also used an IL-2-independent human T-cell line, Jurkat, which originated from human acute lymphocytic leukemia. 22 CTLL-2 cell clones permanently expressing wild-type and mutant Tax were established as described previously. 19 LLnL and Bay 11-7082 were purchased from Sigma-Aldrich (Tokyo, Japan) and Calbiochem (La Jolla, CA), respectively.…”