Growth Factors Can Protect B-Chronic Lymphocytic Leukaemia Cells Against Programmed Cell Death Without Stimulating Proliferation
| Autor: | Andrew P. Jewell, C. P. Worman, F. J. Giles, Peter M. Lydyard, Ah Goldstone |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Cancer Research
Programmed cell death Lymphocytosis Apoptosis Biology Tritium immune system diseases hemic and lymphatic diseases medicine Humans Autocrine signalling Interleukin 4 Hydrocortisone CD23 DNA Neoplasm Hematology Leukemia Lymphocytic Chronic B-Cell Recombinant Proteins Stimulation Chemical Cell biology Oncology Interferon Type I Cytokines Tumor necrosis factor alpha medicine.symptom Cell Division Thymidine medicine.drug |
| Zdroj: | Leukemia & Lymphoma. 18:159-162 |
| ISSN: | 1029-2403 1042-8194 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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