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Human leukaemia

XU K and thornalley p j (2000) Studies on the mechanism of the inhihition of human leukaemia cell growth hy dietary isothiocyanates and their cysteine adducts in vitro , Biochem Pharmacol, 60 221-31. [Pg.63]

Longhurst TJ, O Neill GM, Harvie RM, Davey RA. The anthracycline resistance-associated (ara) gene, a novel gene associated with multidrug resistance in a human leukaemia cell line. Br J Cancer 1996 74(9) 1331—1335. [Pg.209]

Popovich, D. G., and Kitts, D. D. (2002). Structure-function relationship exists for ginsenosides in reducing cell proliferation and inducing apoptosis in the human leukaemia (THP-1) cell line. Arch. Biochem. Biophys. 406,1-8. [Pg.92]

Annexin V binding has been used to investigate the induction of apoptosis by a variety of factors. Induction of apoptosis in the human leukaemia cell hne, HL60, by photosensitizer dyes (Purpurin-18) administered in low doses after exposure to visible light, for example, has been monitored by annexin V binding to the cell surface (Di Stefano et al., 2001). It was found that when higher doses of the drug was employed necrosis of the cells resulted. [Pg.43]

Chloropurine, as its ribonucleotide, is active against a number of animal neoplasms [444] and human leukaemias [363], but is less effective than the purinethiones, which it resembles in its action. [Pg.108]

Catechol (approx. 10 mol/L) inhibited the growth of bone-marrow cells from female C57BL/6 x DBA/2 mice (Seidel et al., 1991) and from male C57 and SW mice (Neun et al., 1992). Catechol (25, 50, 75 or 100 mg/kg bw, single intraperitoneal administration) decreased the incorporation of Fe to erythrocytes in a dose-dependent fashion in female Swiss mice, when administered with phenol (50 mg/kg bw, single intraperitoneal administration) (Snyder et al., 1989). Catechol induced apoptosis in the human leukaemia cell line HL60 at concentrations (50 pmol/L) at which necrosis was not observed (Moran et al., 1996). On the other hand, catechol (> 0.5 pmol/L) prevented elimination by apoptosis of G418-resistant, transformed Swiss 3T3 M X Cll cells by co-cultured TGF-P-treated C3H I OT A cells (Schaeffer et al., 1995). [Pg.441]

On the other hand, hydroquinone (3 pmol/L) prevented the staurosporine-induced apoptosis of HL-60 and the IL-3-dependent murine myeloblastic (32D) cell line it also prevented apoptosis of the 32D cells observed in the absence of IL-3. The myeloperoxidase inhibitor indomethacin opposed the effect of hydroquinone on staurosporine-induced apoptosis of HL-60 cells (Hazel et al., 1995, 1996b). Pretreatment of human leukaemia cells ML-1 with buthionine sulfoximine (100 pmol/L for 24 h), in order to decrease their glutathione content, increased the susceptibility of these cells to hydroquinone-induced inhibition of differentiation caused by phorbol acetate pretreatment with l,2-dithiole-3-thione, which induces reduced glutathione synthesis, prevented the differentiation inhibition of hydroquinone. Treatment of DBA/2 mice with 1,2-dithiole-3-thione, which increased the activity of quinone reductase of bone-marrow stromal cells by 50%, decreased the susceptibility of these cells towards hydroquinone (Trush et al., 1996). [Pg.701]

Hydroquinone (1-10 (.miol/L) induced fluorescence from 2. 7 -dichlorofluorcscin acetate in HL-60 human leukaemia cells this was interpreted to indicate intracellular generation of hydrogen peroxide and other peroxides (Hiraku Kawanishi, 1996). Hydroquinone (200 mg/kg bw, as a single oral dose) administered to male Sprague-Dawley rats induced a three-fold increase in urinary excretion of malonaldehyde, increased hepatic ornithine decarboxylase activity from a control value of 16.8 pmol/mg/h... [Pg.701]

Gewirtz, A.M. (1997) Oligonucleotide therapeutics for human leukaemia. In D.J.Chadwick and G.Cardew (eds) Oligonucleotides as Therapeutic Agents. Ciba Foundation Symposium 209, Wiley, Chichester, pp. 169-194. [Pg.47]

Mammalian cells can spend variable times in the G1 phase of the cell division cycle. Time spent in this phase varies considerable with cell type, some terminally differentiated cells dividing only rarely (e.g. liver) or not at all (e.g. heart muscle, nerve). Because of the ability of HNE to reduce cell proliferation, its effect on cell differentiation has also recently been explored. When HL60 human leukaemia cells are exposed to 1 iM HNE their proliferation is inhibited, but significantly without loss of viability. Perhaps more importantly it appears that such treatment progressively induces them to differentiate terminally into either monocyte/macrophage-like cells or granulocytes [33]. [Pg.162]

The role of cytosolic tyrosine kinases in the pathogenesis of human leukaemia has made them a target for drugs. The so-called Tyrphostins , developed by A. Levitzki and... [Pg.272]

Another event causing overexpression of transcription factors is juxtaposition of these genes to a gene locus for antigen receptors in T lymphocytes. Nearly half of the genes that are translocated to antigen receptor loci in human leukaemia cells, notably in T-cell acute lymphoblastic leukaemia (T-ALL), encode helix-loop-helix (HLH) transcription factors (such as Max and MAD) (see Chapter 10 and 17). [Pg.274]

M. L. Cleary. Transcr mon fectors in human leukaemias. Oncogenes in the development of leukaemia. hnperkd Cancer Research Fund. Cancer surv, 15, 89—104,1992. [Pg.282]

Rothem L, Ifergan I, Kaufman Y, Priest DG, Jansen G, Assaraf YG. Resistance to multiple novel antifolates is mediated via defective drug transport resulting from clustered mutations in the reduced folate carrier gene in human leukaemia cell lines. Biochem J 2002 367 741-50. [Pg.224]

Figure 3.X The methyl region of a 270 MHz HNMR spectrum of human leukaemia lysozyme (5 mM, 55°C). The upper trace is the normal spectrum, the lower trace (a) is a convolution difference spectrum. Note the additional fine structure present in (a) which aids... Figure 3.X The methyl region of a 270 MHz HNMR spectrum of human leukaemia lysozyme (5 mM, 55°C). The upper trace is the normal spectrum, the lower trace (a) is a convolution difference spectrum. Note the additional fine structure present in (a) which aids...
Martin SJ Cotter TG (1991) Ultraviolet B irradiation of human leukaemia HL-60 cells in vitro induces apoptosis. International Journal of Radiation Biology 59 1001-1016. [Pg.185]

Resveratrol [2], 3,4 ,5-trihydroxy-rra/ A-stilbene, is a phytoalexin found in grapes and other plants, that exhibits a variety of biological activities, including antileukemic, antibacterial, antifungal, anti antiplatelet aggregation, coronary vasodilator. Recently, it has been shown to induce apoptosis and decrease expression of Bcl-2 in the human leukaemia HL-60 cell line. [Pg.77]

Mollinedo F, Lopez-Perez R, Gajate C (2008) Differential gene expression patterns coupled to commitment and acquisition of phenotypic hallmarks during neutrophil differentiation of human leukaemia HL-60 cells. Gene 419 16-26... [Pg.42]

James, S.Y. et al. (1997) The role ofvitamin D derivatives and retinoids in the differentiation of human leukaemia cells. Biochemical Pharmacology, 54, 625-634. [Pg.358]

F. F. Becker, X-B. Wang, Y. Huang, R. Pethig, J. Vykoukal and P. R. C. Gascoyne, The removal of human leukaemia cells from blood using interdigitated microelectrodes, J. Phys. D Appl. Phys. 27,2659-2662 (1994). [Pg.504]

Tang G, Wang J, Zhuang Z (1997) Cytotoxicity and genotoxicity of methyl tert-butyl ether and its metabolite in human leukaemia cells. Clin J Prev Med 31 334-337... [Pg.399]

Finally, quinones from the benzoquinone group have also been reported to be antitumor agents against several tumoral cell lines, such as prostatic cancer [84] and human leukaemia K 562 cells [85],... [Pg.315]

Smith, D.K., Treutlein, H.R., Maurer, T., Owczarek, C.M., Layton, M.J., Nicola, N.A. and Norton, R.S. (1994) Homology modelling and IHNMR studies of human leukaemia inhibitory factor. FEBS Lett. 350 275-280. [Pg.290]


See other pages where Human leukaemia is mentioned: [Pg.356]    [Pg.234]    [Pg.154]    [Pg.293]    [Pg.391]    [Pg.1336]    [Pg.1336]    [Pg.271]    [Pg.808]    [Pg.354]    [Pg.831]    [Pg.192]    [Pg.176]    [Pg.271]    [Pg.115]    [Pg.990]    [Pg.121]    [Pg.831]   
See also in sourсe #XX -- [ Pg.271 ]

See also in sourсe #XX -- [ Pg.271 ]




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