PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 200333

Human leukemic "null" cell line (NALL-1).

S Hiraki·I Miyoshi·I Kubonishi·Y Matsuda·T Nakayama·H Kishimoto·H Masuji
View original source ↗Export metadata ↓

Abstract

A human lymphoblast cell line, NALL-1, was established from the peripheral blood of a patient with acute lymphoblastic leukemia (ALL). NALL-1 cells had neither properties of T and B cells nor Epstein-Barr virus (EBV). Many characteristics of the NALL-1 line were distinct from those of numerous EBV-positive lymphoblastoid cell lines previously reported. NALL-1 cells are considered to have originated from the donor's leukemic cells on the basis of their cytogenetic, morphologic and functional features. The NALL-1 line is the first human leukemic "null" cell line derived from ALL. The significance of this cell line is disscussed.

Explore related subjects

B-LymphocytesCell LineChromosomes, HumanHerpesvirus 4, HumanHumansLeukemia, LymphoidT-LymphocytesJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S Hiraki, I Miyoshi, I Kubonishi, Y Matsuda, T Nakayama, H Kishimoto, H Masuji. 1977. Human leukemic "null" cell line (NALL-1).. https://doi.org/10.1002/1097-0142(197711)40%3A5%3C2131%3A%3Aaid-cncr2820400523%3E3.0.co%3B2-v

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1992

A mutation generating a stop codon in the alpha-L-fucosidase gene of a fucosidosis patient.

Fucosidosis is an autosomal recessive, lysosomal storage disease featured by deficient activity of alpha-L-fucosidase. Lymphoid cell lines from a fucosidosis patient (JT) and a healthy individual (control) contained alpha-L-fucosidase mRNA of the same size, 2.3 Kb, as determined by Northern blot analysis. cDNA was prepared from alpha-L-fucosidase mRNA of JT and control cells and each cDNA was amplified by the polymerase chain reaction. Direct DNA sequencing of the amplified products revealed a single mutation in JT, a G1141-->T transition. This changed the codon (GAA) for Glu-375 to a stop codon (UAA). Amplification and sequencing of the area containing the G1141-->T transition in genomic DNA of JT and control cells demonstrated that the mutation was homozygous in JT. Analysis of cDNA and genomic DNA derived from lymphoid cells of mother JT revealed her to be heterozygous (G and T) at position 1141. The G1141-->T mutation is probably responsible for disease in JT.

B-Lymphocytes↗
PubMed1992

Transcription of the tumor necrosis factor alpha gene is rapidly induced by anti-immunoglobulin and blocked by cyclosporin A and FK506 in human B cells.

The human tumor necrosis factor alpha (TNF-alpha) gene encodes a cytokine whose activities have been implicated in many immunopathological processes, including the activation and differentiation of lymphocytes. Originally identified as a monocyte factor, our studies and those of others have demonstrated that B and T lymphocytes produce TNF-alpha when stimulated by a variety of inducers. We report here that TNF-alpha gene transcription is rapidly and highly induced in three independently derived human Burkitt lymphoma cell lines, as well as in freshly isolated human splenic B cells, activated by antibodies to surface immunoglobulin. This burst in TNF-alpha gene transcription is associated with an induction of TNF-alpha bioactivity in the culture supernatants from stimulated splenic B cells. Moreover, induction of TNF-alpha gene transcription by anti-immunoglobulin was blocked by the immunosuppressants cyclosporin A and FK506. These studies demonstrate that TNF-alpha production is an early event in B-cell activation and they establish the efficacy of using immunosuppressants as probes in dissecting transcriptional activation pathways in human B cells.

B-Lymphocytes↗
PubMed1992

Epstein-Barr virus-transformed B lymphocytes produce low molecular mass molecules with autocrine growth factor and competence factor activity.

A human Epstein-Barr virus (EBV)-positive lymphoblastoid B cell line, named BA-D10-4, produces a factor of a molecular mass less than 10 kDa that promotes cell proliferation of both BA-D10-4 cells and other human T or B lymphoid cell lines, either EBV-positive or -negative. The factor synergizes with higher molecular mass autocrine growth factors and makes both BA-D10-4 cells and B cell lines from Burkitt's lymphoma, but not cells from T cell leukemia, more responsive to interleukin-1 and interleukin-6. Therefore, this low molecular mass factor seems to be an autocrine growth factor per se and to have the characteristics of a competence factor.

B-Lymphocytes↗