Abstract
The obligatory role of specific cytoplasmic receptors as mediators of steroid hormone action is well established. In lymphoid cell culture systems the development or glucocorticoid resistance is almost always due to a mutation to a receptor negative state [1]. Therefore, if the assumption is that glucocorticoid-induced remission in leukemia is by a direct effect on leukemic blast cells, one would predict that the presence of absence of blast cell glucocorticoid receptors would be a major determinant or clinical steroid sensitivity. However, receptor quantization has not correlated with steroid responsiveness [2–5], and in particular, high receptor numbers are not uniformly associated with responsive disease [6].
Supported by Grant CA288818 from the National Institutes of Health and the Irving Mann Medical Oncology Research Endowment Fund
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References
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© 1983 Springer-Verlag Berlin Heidelberg
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Bell, R., Lillquist, A., Cotter, S., Sallan, S., McCaffrey, R. (1983). Dysfunctional Glucocorticoid Receptors in Acute Leukemia. In: Neth, R., Gallo, R.C., Greaves, M.F., Moore, M.A.S., Winkler, K. (eds) Modern Trends in Human Leukemia V. Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, vol 28. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-68761-7_32
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DOI: https://doi.org/10.1007/978-3-642-68761-7_32
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