James H. Ahn

TL;DR: The results identify Hsp90 as a critical and multimodal target in this most difficult to treat breast cancer subtype and support the use of the Hsp 90 inhibitor PU-H71 for clinical trials involving patients with TNBC.

TL;DR: This work uses PU-H71 affinity capture to design a proteomic approach that, when combined with bioinformatic pathway analysis, identifies dysregulated signaling networks and key oncoproteins in chronic myeloid leukemia and shows that this method can provide global insights into the biology of individual tumors, including primary patient specimens.

TL;DR: In this article, an HSP90 inhibitor, PU-H71, demonstrated efficacy in cell line and mouse models of the MPN polycythemia vera and essential thrombocytosis (ET) by disrupting JAK2 protein stability.

TL;DR: The synthesis of chemical tools for three Hsp90 inhibitor classes will be useful for probing tumor-by-tumor the HSp90 complexes isolated by specific inhibitors, and will lead to better understanding of tumor specific molecular markers to aid in their clinical development.

TL;DR: The data suggest that Hsp90 may execute functions necessary to maintain the malignant phenotype, and experimental evidence is presented for an additional role; that is, to facilitate scaffolding and complex formation of molecules involved in aberrantly activated signaling complexes.