Glucocorticoid‐induced lymphocytolysis: State of the genetic analysis

Abstract

The glucocorticoid-induced lysis of lymphoid cell lines offers a genetic approach to steroid hormone action because unresponsive variants can easily be selected as resistant to this lytic effect. The present state of analysis of lymphocytolysis in two murine cell lines, the S49 T-lymphoma and the W7 thymoma, is reviewed. All glucocorticoid-resistant variants isolated so far result from various defects in the glucocorticoid receptor. The absence of variants blocked at another step of the lytic mechanism is discussed. The observed hemizygosity of the glucocorticoid receptor locus in the S49 line and the instability of cell hybrids illustrate some of the potential problems encountered in somatic cell genetics.

Glucocorticoids, oxysterols, and cAMP with glucocorticoids each cause apoptosis of CEM cells and suppress c-myc

“…It should be mentioned that this general kind of time course, with a prolonged interval preceding apoptosis after the addition of drug, is observed in most glucocorticoid sensitive transformed cell lines of mouse or human origin. For example, it has been seen in the mouse lines P1798, S49 and WEHI-7 [9][10][11]. Such a time course has been seen in Jurkat cells (when they are transfected with an expression vector carrying an active glucocorticoid receptor) [12].…”