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Immunochemical Differences between Glucocorticoid Receptors from Corticoid-sensitive and -resistant Malignant Lymphocytes¹

Research Institute and Department of Medicine, Joint Diseases North General Hospital, Mount Sinai School of Medicine, New York, New York 10035, and Developmental Pharmacology Branch, National Institute of Child Health and Human Development, NIH, Bethesda, Maryland 20205

We have explored the possibility of using antibodies against purified rat liver glucocorticoid receptors to study the immunochemical properties of glucocorticoid receptors from murine and human malignant lymphocytes. For this purpose, purified immune immunoglobulin G was covalently linked to Sepharose CL-4B. We then examined the ability of the affinity gel to recognize cytosolic [³H]triamcinolone acetonide-receptor complexes from the corticoid-sensitive (CS) and -resistant strains of mouse lymphoma P1798, from CS lymphocytes of patients with chronic lymphatic leukemia, and from a CS clone of human leukemic lymphoblasts in tissue culture (CH6). Mouse thymus was used as a source of glucocorticoid receptor from normal CS lymphocytes. Whereas the immunoaffinity column retained 70 to 84% of the 58- to 62-Å (Stokes radius) [³H]triamcinolone acetonide-receptor complexes characteristic of the CS mouse and human lymphocytes, it failed to recognize the 27- to 28-Å (Stokes radius) glucocorticoid receptor present in corticoid-resistant mouse lymphoma P1798 cells. Therefore, under appropriate experimental conditions, it was possible to demonstrate cross-reactivity between the antiserum against rat liver glucocorticoid receptor and the 58- to 62-Å (Stokes radius) glucocorticoid receptor from species as diverse as mouse and humans.

¹ Supported by NIH Grants CA 14987 and P 30 14194, by American Cancer Society Grant BC-327, and by funds from the Dworetz-Wolf Foundation for Leukemia Research.

² Scholar of the Leukemia Society of America, Inc. To whom requests for reprints should be addressed.

Received 6/16/80. Accepted 10/ 2/80.