Glucocorticoid receptors in subpopulations of childhood acute lymphocytic leukemia.

In view of the known differences in sensitivity to glucocorticoids among functional subcategories of lympocytes in the mouse and the awareness that different subcategories of acute lymphocytic leukemia may represent proliferation of different clones of lymphoblasts, we examined lymphoblast populations with known surface markers for differences in specific cytoplasmic glucocorticoid receptor activity. Lymphoblasts were divided into those that formed sheep erythrocyte rosettes (T-lymphoblasts) and those that lacked all surface markers (null lymphoblasts). The latter were further subdivided by their ability to stimulate allogeneic donors in mixed lymphocyte culture (MLC). Lack of stimulation in MLC is a characteristic of mature T-cells. Eighteen patients had null lymphoblasts that did stimulate in MLC, and glucocorticoid binding sites in these ranged from 4,096 to 21,869 sites/cell (median, 7,571). Eighteen patients with T-lymphoblasts had binding sites ranging from 0 to 5,887 sites/cell (median, 2,173). This difference in specific glucocorticoid receptor levels is highly significant ( p < 0.001). Nine patients whose lymphoblasts lacked identifiable surface markers but failed to stimulate in MLC had intermediate values for receptor sites. Thus it appears that null lymphoblasts are more likely to have higher numbers of specific glucocorticoid receptor than T-lymphoblasts. The differential capacity of lymphoblasts to bind steroid may prove useful in designing therapeutic regimens for the different subcategories of acute lymphocytic leukemia.