Neil P. Shah

Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop

Roumiantsev, Sergei, Shah, Neil P., Gorre, Mercedes E., Nicoll, John, Brasher, Bradley B., Sawyers, Charles L., ...

The Abl tyrosine kinase inhibitor STI-571 is effective therapy for stable phase chronic myeloid leukemia (CML) patients, but the majority of CML blast-crisis patients that respond to STI-571 relapse...

Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance

Burgess, Michael R., Skaggs, Brian J., Shah, Neil P., Lee, Francis Y., Sawyers, Charles L.

Structural studies suggest that most point mutations in the BCR-ABL kinase domain cause resistance to the ABL kinase inhibitor imatinib by impairing the flexibility of the kinase domain, restricting...

Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases

Carter, Todd A., Wodicka, Lisa M., Shah, Neil P., Velasco, Anne Marie, Fabian, Miles A., Treiber, Daniel K., ...

To realize the full potential of targeted protein kinase inhibitors for the treatment of cancer, it is important to address the emergence of drug resistance in treated patients. Mutant forms of...

Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop

Roumiantsev, Sergei, Shah, Neil P., Gorre, Mercedes E., Nicoll, John, Brasher, Bradley B., Sawyers, Charles L., ...

The Abl tyrosine kinase inhibitor STI-571 is effective therapy for stable phase chronic myeloid leukemia (CML) patients, but the majority of CML blast-crisis patients that respond to STI-571 relapse...

Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance

Burgess, Michael R., Skaggs, Brian J., Shah, Neil P., Lee, Francis Y., Sawyers, Charles L.

Structural studies suggest that most point mutations in the BCR-ABL kinase domain cause resistance to the ABL kinase inhibitor imatinib by impairing the flexibility of the kinase domain, restricting...

Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases

Carter, Todd A., Wodicka, Lisa M., Shah, Neil P., Velasco, Anne Marie, Fabian, Miles A., Treiber, Daniel K., ...

To realize the full potential of targeted protein kinase inhibitors for the treatment of cancer, it is important to address the emergence of drug resistance in treated patients. Mutant forms of...

Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency

Shah, Neil P., Skaggs, Brian J., Branford, Susan, Hughes, Timothy P., Nicoll, John M., Paquette, Ronald L., ...

Molecularly targeted kinase inhibitor cancer therapies are currently administered sequentially rather than simultaneously. We addressed the potential long-term impact of this strategy in patients...