Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2138239 | Leukemia Research | 2010 | 6 Pages |
Abstract
Glucocorticoids (GCs) cause apoptosis and cell cycle arrest in lymphoid cells and are used in the therapy of lymphoid malignancies. SLA (Src-like-adaptor), an inhibitor of T- and B-cell receptor signaling, is a promising candidate derived from expression profiling analyses in children with acute lymphoblastic leukemia (ALL). Over-expression and knock-down experiments in ALL in vitro model revealed that transgenic SLA alone had no effect on survival or cell cycle progression, nor did it affect sensitivity to, or kinetics of, GC-induced apoptosis. Although SLA is a prominent GC response gene, it does not seem to contribute to the anti-leukemic effects of GC.
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Authors
Muhammad Mansha, Michela Carlet, Christian Ploner, Georg Gruber, Muhammad Wasim, Gerrit Jan Wiegers, Johannes Rainer, Stephan Geley, Reinhard Kofler,