L
Lauren T. Adrian
Researcher at Oregon Health & Science University
Publications - 11
Citations - 1503
Lauren T. Adrian is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Nilotinib & Dasatinib. The author has an hindex of 7, co-authored 11 publications receiving 1332 citations. Previous affiliations of Lauren T. Adrian include Howard Hughes Medical Institute.
Papers
More filters
Journal ArticleDOI
AP24534, a Pan-BCR-ABL Inhibitor for Chronic Myeloid Leukemia, Potently Inhibits the T315I Mutant and Overcomes Mutation-Based Resistance
Thomas O'Hare,Thomas O'Hare,William C. Shakespeare,Xiaotian Zhu,Christopher A. Eide,Christopher A. Eide,Victor M. Rivera,Frank Wang,Lauren T. Adrian,Lauren T. Adrian,Tianjun Zhou,Huang Wei Sheng,Qihong Xu,Chester A. Metcalf,Jeffrey W. Tyner,Marc M. Loriaux,Amie S. Corbin,Amie S. Corbin,Scott Wardwell,Yaoyu Ning,Jeffrey A. Keats,Yihan Wang,Raji Sundaramoorthi,Mathew Thomas,Dong Zhou,Joseph Snodgrass,Lois Commodore,Tomi K. Sawyer,David C. Dalgarno,Michael W. Deininger,Brian J. Druker,Brian J. Druker,Tim Clackson +32 more
TL;DR: Design and preclinical evaluation of AP24534, a potent, orally available multitargeted kinase inhibitor active against T315I and other BCR-ABL mutants, and clinical evaluation ofAP24534 as a pan-BCR-ABl inhibitor for treatment of CML are reported.
Journal ArticleDOI
BCR-ABL1 compound mutations in tyrosine kinase inhibitor–resistant CML: frequency and clonal relationships
Jamshid S. Khorashad,Todd W. Kelley,Philippe Szankasi,Clinton C. Mason,Simona Soverini,Lauren T. Adrian,Christopher A. Eide,Christopher A. Eide,Matthew S. Zabriskie,Thoralf Lange,Johanna Estrada,Anthony D. Pomicter,Anna M. Eiring,Ira L. Kraft,David J. Anderson,Zhimin Gu,Mary Alikian,Alistair Reid,Letizia Foroni,David Marin,Brian J. Druker,Brian J. Druker,Thomas O'Hare,Michael W. Deininger +23 more
TL;DR: It is concluded that compound mutations are common in patients with sequencing evidence for 2 BCR-ABL1 mutations and frequently reflect a highly complex clonal network, the evolution of which may be limited by the negative impact of missense mutations on kinase function.
Journal ArticleDOI
The ABL Switch Control Inhibitor DCC-2036 Is Active against the Chronic Myeloid Leukemia Mutant BCR-ABLT315I and Exhibits a Narrow Resistance Profile
Christopher A. Eide,Lauren T. Adrian,Lauren T. Adrian,Jeffrey W. Tyner,Mary Mac Partlin,David J. Anderson,Scott C. Wise,Bryan D. Smith,Peter A. Petillo,Daniel L. Flynn,Michael W. Deininger,Thomas O'Hare,Thomas O'Hare,Brian J. Druker +13 more
TL;DR: Evaluated the efficacy of DCC-2036 against BCR-ABL(T315I) and other mutants in cellular and biochemical assays and conducted cell-based mutagenesis screens, which support continued evaluation of D CC-20 36 as an important new agent for treatment-refractory CML.
Journal ArticleDOI
Acute dasatinib exposure commits Bcr-Abl-dependent cells to apoptosis.
Jennifer Snead,Thomas O'Hare,Thomas O'Hare,Lauren T. Adrian,Lauren T. Adrian,Christopher A. Eide,Christopher A. Eide,Thoralf Lange,Brian J. Druker,Brian J. Druker,Michael W. Deininger,Michael W. Deininger +11 more
TL;DR: It is demonstrated that in vitro assays designed to model in vivo pharmacokinetics can predict clinical efficacy and challenge the widely held notion that continuous target inhibition is required for optimal efficacy of kinase inhibitors.
Journal ArticleDOI
The BCR-ABL35INS insertion/truncation mutant is kinase-inactive and does not contribute to tyrosine kinase inhibitor resistance in chronic myeloid leukemia
Thomas O'Hare,Thomas O'Hare,Thomas O'Hare,Matthew S. Zabriskie,Matthew S. Zabriskie,Christopher A. Eide,Christopher A. Eide,Anupriya Agarwal,Lauren T. Adrian,Lauren T. Adrian,Huihong You,Amie S. Corbin,Fei Yang,Richard D. Press,Victor M. Rivera,Julie Toplin,Stephane Wong,Michael W. Deininger,Brian J. Druker,Brian J. Druker +19 more
TL;DR: It is found that detection of BCR-ABL(35INS) does not consistently track with or explain resistance in clinical samples from chronic myeloid leukemia patients, and this mutant is kinase-inactive and does not contribute to TKI resistance.