Lymphoma cell

Steinberg, R. A. A kinase-negative mutant of s49 mouse lymphoma cells is defective in posttranslational maturation of catalytic subunitof cyclic amp-dependent protein kinase. Mol. Cell Biol. 11 (1991) 705-712. 

The multidrug resistance (mdr) reversing effect of the new phenothiazine complexes were tested on mouse T cell lymphoma cell lines. Trifluoperazine (TFP) was much more effective at the same concentration than verapamil. The efficacy of some metal coordination complexes [TFP-Cu(ll) and TFP-V(IV)] exceeded the action of TFP alone. Chlorpromazine (CPZ) or CPZ-Pt(ll) complex had the same or less effect than verapamil or promethazine (Pz) used as a control. 

McGregor DB, Brown A, Cattanach P, et al. 1988. Responses of the L5178Y tk+/tk- mouse lymphoma cell forward mutation assay III. 72 coded chemicals. Environ Mol Mutagen 12 85-154. 

B and T cells can undergo neoplastic transformation that is governed by specific mutations in their chromosomes that result in populations of malignant lymphoma cells. 

Hematopathology evaluation of biopsy specimen-morphologic inspection, immunohistochemistry for cell-surface antigens to characterize lymphoma cells, cytogenetic analysis... 

Myhr B, Bowers L, Caspary WJ. 1985. Assays for the induction of gene mutations at the thymidine kinase locus in L5178Y mouse lymphoma cells in culture. In Ashby J, de Serres FJ, et al., eds. Progress in mutation research. Vol. 5. Evaluation of short-term tests for carcinogens. Amsterdam, The Netherlands Elsevier Science Publishers, 555-568. 

Hurwitz, E., Kashi, R., Burowsky, D., Arnon, R., and Haimovich, J. (1983b) Site-directed chemotherapy with a drug bound to antiidiotypic antibody to a lymphoma cell-surface IgM. Int. J. Cancer 31, 745. 

Amacher, D.E., S C Pail lei. G.N.Tumer, V.A.Ray, and D.S.Salsburg. 1980. Point mutations at the thymidine kinase locus in L5178Y mouse lymphoma cells. II. Test validation and interpretation. Mutat. Res. 72 447-474. 

McGregor, D.B., A.G.Brown, S.Howgate, D.McBride, C.Riach, and W.J.Caspary. 1991. Responses of the L5178Y mouse lymphoma cell forward mutation assay. V. 27 coded chemicals. Environ. Mol. Mutagen. 17 196-219. 

Matheson et al. (1978) reported the results of a battery of in vivo and in vitro assays to assess the genotoxicity of 1,1-dimethylhydrazine. Included were the Ames Salmonella microsome assay, a microbial suspension assay, mutation induction at the TK locus in L5178Y mouse lymphoma cells, stimulation of UDS in WI-38 cells, and a dominant lethal assay in mice. 1,1-Dimethylhydrazine was active in all of the tests except the dominant lethal assay. 

In a study using cultured L5178Y mouse lymphoma cells, Rogers and Back (1981) reported that both 1,1-dimethylhydrazine and 1,2-dimethylhydrazine induced forward mutations at the thymidine kinase level in the absence of an extraneous metabolic activation system. The investigators also noted that the two dimethylhydrazines appeared to have different modes of action under these conditions. 

Rogers, A.M., and K.C.Back. 1981. Comparative mutagenicity of hydrazine and 3 methylated derivatives in L5178Y mouse lymphoma cells. Mutat. Res. 89 321-328. 

The IL-2 portion of the fusion protein facilitates product interaction with cells displaying cell surface IL-2 receptors, found in high levels on some leukaemia and lymphoma cells, including CTCL cells. Binding appears to trigger internalization of the receptor-fusion protein complex (Figure 9.B1). Sufficient quantities of the latter escape immediate cellular destruction to allow diphtheria toxin-mediated inhibition of cellular protein synthesis. Cell death usually results within hours. 

Watson, P., Krupinski, J., Kempinski, A. M. and Frankenfield, C. D. Molecular cloning and characterization of the type VII isoform of mammalian adenylyl cyclase expressed widely in mouse tissues and in S49 lymphoma cells. /. Biol. Chem. 269 28893-28898,1994. 

In mice, nickel chloride produces a dose-dependent increase in abnormal lymphoma cells (WHO 1991). Mice given high concentrations of nickel in drinking water, equivalent to 23 mg Ni/kg BW daily and higher, have an increased incidence of micronuclei in bone marrow (USPHS 1993). However, mice injected once with 50 mg Ni/kg BW as nickel chloride show no evidence of mutagenicity (USPHS 1977). 

The mouse lymphoma forward mutation test at the thymidine kinase locus (detects mutations to a nonfunctional thymidine kinase in a line of culture mouse lymphoma cells). 

Levitsky, H.I. et al., Immunization with granulocyte-macrophage colony-stimulating factor- transduced, but not B7-l-transduced, lymphoma cells primes idiotype-specific T cells and generates potent systemic antitumor immunity, J Immunol, 156, 3858, 1996. 

Joseph, D.B. and Bidlack, J.M., The kappa-opioid receptor expressed on the mouse lymphoma cell line Rl.l contains a sulfhydryl group at the binding site, Fur J. Pharmacol., 267, 1, 1994. 

In a battery of mutagenicity and genotoxicity studies, PGDN tested negative except in L5178Y mouse lymphoma cells where it induced mutations at... 

The TK+/ fine was originally isolated as a spontaneously arising revertant clone from a UV-induced TK / clone. The parental TK+/+ cell and the heterozygote were then the only TK-competent mouse lymphoma cells that could be maintained in THMG medium (3 pg ml-1 thymidine, 5 pg ml-1 hypoxanthine, 0.1 pg ml-1 methotrexate and 7.5 pg ml-1 glycine) (Clive, 1987). Thus, like most established lines, these cells are remote from wild-type cells. The karyotype of the TK+/ —3.7.2C line has a modal chromosome number of 40 like wild-type, but has a variety of chromosomal rearrangements and centromeric heteromorphisms (Blazak et al., 1986). 

When metabolic activation is used, S9 mix should not exceed 1-10 percent of the culture medium by volume. It has been shown that the S9 mix is clastogenic in CHO cells and mouse lymphoma cells (Cifone et al., 1987 Kirkland et al., 1989) but not in human lymphocytes, where blood components can inactivate active oxygen species which could cause chromosome damage. When S9 mix from animals treated with other enzyme-inducing agents such as phenobarbitone/beta-naphtho-flavone, is used, clastogenesis may be minimized (Kirkland et al., 1989). 

Applegate, M.L., Moore, M.M., Broder, C.B. et al. (1990). Molecular dissection of mutations at the heterozygous thymidine canise locus in mouse lymphoma cells. Proc. Nat. Acad. Sci. U.S.A. 87 51-55. 

Blazak, W.E, Steward, B.E., Galperin, I., Allen, K.L., Rudd, C.J., Mitchell, A.D. and Caspary, W.J. (1986). Chromosome analysis of triflourothymidine-resistant L5178Y mouse lymphoma cells colonies. Environ. Mutagen. 8 229-240. 

Clive, D., Flamm, W.G. and Patterson, J.B. (1972). A mutational assay system using the thymidine kinase locus in mouse lymphoma cells. Mutation Res. 16 77-87. 

Evans, H.H., Mencl, J., Homg, M.F., Ricanti, M., Sanchez, D. and Hozier, J. (1986). Lucus specificity in the mutability of L5178Y mouse lymphoma cells the role of multilocus lesions. Proc. Nat. Acad. Sci. U.S.A. 83 4379-4385. 

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