MECHANISMS OF RESPONSE AND RESISTANCE TO STI571 IN CML

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 我们推测，STI571在体外抑制原代CML祖细胞生长和抑制BCR/ABL酪氨酸激酶活性的能力将与STI571治疗的临床反应或缺乏反应有关。我们进一步假设，标准STI571治疗的难治性可以通过体外暴露于高浓度的STI571或通过使用STI571与其他抗白血病干预措施的组合来克服。

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.