Hillary E. Mulvey

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Tyrosine kinase inhibitors are effective treatments for non-small-cell lung cancers (NSCLCs) with epidermal growth factor receptor (EGFR) mutations. However, relapse typically occurs after an average of 1 year of continuous treatment. A fundamental histological transformation from NSCLC to small-cell lung cancer (SCLC) is observed in a subset of the(More)
PURPOSE A secondary EGFR mutation, T790M, is the most common resistance mechanism in EGFR-mutant adenocarcinomas that have progressed on erlotinib. Third-generation EGFR inhibitors capable of inhibiting mutant EGFR with T790M produce responses in nearly two thirds of patients. However, acquired resistance mechanisms in patients treated with these drugs are(More)
Although mechanisms of acquired resistance of epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancers to EGFR inhibitors have been identified, little is known about how resistant clones evolve during drug therapy. Here we observe that acquired resistance caused by the EGFR(T790M) gatekeeper mutation can occur either by selection of(More)
UNLABELLED Rociletinib is a third-generation EGFR inhibitor active in lung cancers with T790M, the gatekeeper mutation underlying most first-generation EGFR drug resistance. We biopsied patients at rociletinib progression to explore resistance mechanisms. Among 12 patients with T790M-positive cancers at rociletinib initiation, six had T790-wild-type(More)
Rociletinib is a third-generation EGFR inhibitor active in lung cancers with T790M, the gatekeeper mutation underlying most fi rst-generation EGFR drug resistance. We biopsied patients at rociletinib progression to explore resistance mechanisms. Among 12 patients with T790M-positive cancers at rociletinib initiation, six had T790–wild-type(More)
Zofia Piotrowska Massachusetts General Hospital, Boston, MA Matthew J. Niederst Massachusetts General Hospital, Boston, MA Chris A. Karlovich Clovis Oncology, San Francisco, CA Heather A. Wakelee Stanford Cancer Institute, Stanford University, Stanford, CA Joel W. Neal Stanford Cancer Institute, Stanford University, Stanford, CA Mari Mino-Kenudson(More)
Purpose: A secondary EGFR mutation, T790M, is the most common resistance mechanism in EGFR-mutant adenocarcinomas that have progressed on erlotinib. Third-generation EGFR inhibitors capable of inhibiting mutant EGFR with T790M produce responses innearly two thirds of patients.However, acquired resistance mechanisms in patients treated with these drugs are(More)
Extracellular vesicles (EVs) are secreted from many cells, carrying cargoes including proteins and nucleic acids. Research has shown that EVs play a role in a variety of biological processes including immunity, bone formation and recently they have been implicated in promotion of a metastatic phenotype. EVs were isolated from HCT116 colon cancer cells, 1459(More)
PURPOSE Epithelial-to-mesenchymal transition (EMT) confers resistance to a number of targeted therapies and chemotherapies. However, it has been unclear why EMT promotes resistance, thereby impairing progress to overcome it. EXPERIMENTAL DESIGN We have developed several models of EMT-mediated resistance to EGFR inhibitors (EGFRi) in EGFR mutant lung(More)
Conflicts of Interest J.A.E. is a consultant for Novartis, Sanofi, Genentech, Clovis and Astra Zeneca; owns equity in Gatekeeper Pharmaceuticals, which has interest in T790M inhibitors; has research agreements with Novartis and Astra Zeneca. Z.P. has provided consulting services for Clovis Oncology. L.V.S. has provided uncompensated consulting services to(More)
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