Bcl-2 is an attractive therapeutic target. It is overexpressed in a wide variety of malignancies including acute leukemia, and its overexpression is often associated with clinical treatment failures. Most intriguing, the temporary inhibition of Bcl-2 may not be toxic to normal cells. Bcl-2 knock-out mice survive until birth with no histologic abnormalities in the brain, skin, intestines, or bone marrow hematopoetic precursors. Beginning one week after birth, however, these mice begin to develop renal dysfunction similar to polycystic kidney disease. By 4 weeks after birth, the mice become lymphopenic primarily due to the death of mature T cells. Inhibition of Bcl-2 does not automatically induce a compensatory up-regulation of other antiapoptotic proteins.
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