MECHANISMS OF RESPONSE AND RESISTANCE TO STI571 IN CML

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. We hyothesize that the ability of STI571 to inhibit growth of primary CML progenitors and suppress BCR/ABL tyrosine kinase activity in primary CML progenitors in vitro will correlate with clinical response or lack of response to STI571 therapy. We further hypothesize that refractoriness to standard STI571 treatment may be overcome by ex vitro exposure to high concentrations of STI571 or through the use of combinations of STI571 with other anti-leukemia interventions.