MECHANISMS OF RESPONSE AND RESISTANCE TO STI571 IN CML

这个子项目是许多利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 我们推测STI 571在体外抑制原代CML祖细胞生长和抑制原代CML祖细胞中BCR/ABL酪氨酸激酶活性的能力将与对STI 571治疗的临床反应或缺乏反应相关。 我们进一步假设，标准STI 571治疗的难治性可以通过体外暴露于高浓度的STI 571或通过使用STI 571与其他抗白血病干预的组合来克服。

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.