Growth factors can protect B-chronic lymphocytic leukaemia cells against programmed cell death without stimulating proliferation

Jewell, A. P., Lydyard, P. M., Worman, C. P., Giles, F. J. and Goldstone, A. H. (1995) Growth factors can protect B-chronic lymphocytic leukaemia cells against programmed cell death without stimulating proliferation. Leukemia and Lymphoma, 18(1 & 2), pp. 159-162. ISSN (print) 1042-8194

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Abstract

The proliferation and survival of B-chronic lymphocytic leukaemia (B-CLL) cells may be regulated by autocrine growth factor loops. Furthermore, it has been suggested the reduction in lymphocytosis following therapy with interferon-alpha may be associated with the interruption of autocrine growth factor production. We have therefore examined the effects of a number of cytokines on the proliferation of B-CLL cells, and also on the regulation of programmed cell death, and the role of interferon-alpha in these systems. In the ten patients studied, neither interferon-alpha alone or together with either interferon-gamma, IL1, IL4, IL6, TNF, or serum containing high levels of soluble CD23 was able to induce proliferation of B-CLL cells. Incubation with TPA or IL2 resulted in variable proliferative responses. Co-incubation with interferon-alpha enhanced TPA-induced proliferation in 4 cases, but reduced IL2-induced proliferation in all cases studied. In contrast, all the cytokines studied were able to protect B-CLL cells against programmed cell death, both spontaneous and that induced by hydrocortisone, with the exception of TNF. These data suggest a role for interferon-alpha in disrupting autocrine survival pathways rather than inhibiting proliferation.

Item Type: Article
Uncontrolled Keywords: cll, cytokines, apoptosis
Research Area: Cancer studies
Biological sciences
Faculty, School or Research Centre: Faculty of Health and Social Care Sciences
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Depositing User: Automatic Import Agent
Date Deposited: 28 Jun 2010 10:50
Last Modified: 13 Jul 2010 07:51
URI: http://eprints.kingston.ac.uk/id/eprint/14423

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