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Anthony D. Pomicter
Researcher at Huntsman Cancer Institute
Publications - 49
Citations - 1432
Anthony D. Pomicter is an academic researcher from Huntsman Cancer Institute. The author has contributed to research in topics: Imatinib & Myeloid leukemia. The author has an hindex of 17, co-authored 45 publications receiving 1098 citations. Previous affiliations of Anthony D. Pomicter include Virginia Commonwealth University & University of Utah.
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Journal ArticleDOI
BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.
Matthew S. Zabriskie,Christopher A. Eide,Christopher A. Eide,Srinivas K. Tantravahi,Nadeem A. Vellore,Johanna Estrada,Franck E. Nicolini,Hanna Jean Khoury,Richard A. Larson,Marina Konopleva,Jorge E. Cortes,Hagop M. Kantarjian,Elias J. Jabbour,Steven M. Kornblau,Jeffrey H. Lipton,Delphine Rea,Leif Stenke,Gisela Barbany,Thoralf Lange,Juan Carlos Hernández-Boluda,Gert J. Ossenkoppele,Richard D. Press,Charles Chuah,Stuart L. Goldberg,Meir Wetzler,François Xavier Mahon,Gabriel Etienne,Michele Baccarani,Simona Soverini,Gianantonio Rosti,Philippe Rousselot,Ran Friedman,Marie Deininger,Kimberly R. Reynolds,William L. Heaton,Anna M. Eiring,Anthony D. Pomicter,Jamshid S. Khorashad,Todd W. Kelley,Riccardo Baron,Brian J. Druker,Brian J. Druker,Michael W. Deininger,Thomas O'Hare +43 more
TL;DR: These findings demonstrate that BCR-ABL1 compound mutants confer different levels of TKI resistance, necessitating rational treatment selection to optimize clinical outcome, and in vitro resistance profiling was predictive of treatment outcomes in Ph(+) leukemia patients.
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
Combining the Allosteric Inhibitor Asciminib with Ponatinib Suppresses Emergence of and Restores Efficacy against Highly Resistant BCR-ABL1 Mutants
Christopher A. Eide,Christopher A. Eide,Matthew S. Zabriskie,Samantha L. Savage Stevens,Orlando Antelope,Nadeem A. Vellore,Hein Than,Anna Reister Schultz,Phillip M. Clair,Amber D. Bowler,Anthony D. Pomicter,Dongqing Yan,Anna V. Senina,Wang Qiang,Wang Qiang,Todd W. Kelley,Philippe Szankasi,Michael Heinrich,Jeffrey W. Tyner,Delphine Rea,Jean Michel Cayuela,Dong-Wook Kim,Cristina E. Tognon,Cristina E. Tognon,Thomas O'Hare,Thomas O'Hare,Brian J. Druker,Brian J. Druker,Michael W. Deininger,Michael W. Deininger +29 more
TL;DR: It is demonstrated that combining asciminib with ATP site TKIs enhances target inhibition and suppression of resistant outgrowth in Ph+ clinical isolates and cell lines and restores ponatinib's effectiveness against currently untreatable compound mutants at clinically achievable concentrations.
Journal ArticleDOI
Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia
Anna M. Eiring,Brent D. G. Page,Ira L. Kraft,Clinton C. Mason,Nadeem A. Vellore,Diana Resetca,Matthew S. Zabriskie,Tian Y. Zhang,Jamshid S. Khorashad,A J Engar,Kimberly R. Reynolds,David J. Anderson,Anna V. Senina,Anthony D. Pomicter,Carolynn C. Arpin,S Ahmad,William L. Heaton,Srinivas K. Tantravahi,A Todic,Robert Colaguori,Richard Moriggl,Derek J. Wilson,Riccardo Baron,Thomas O'Hare,Patrick T. Gunning,Michael W. Deininger +25 more
TL;DR: The findings implicate STAT3 as a critical signaling node in BCR-ABL1 kinase-independent TKI resistance, and suggest that BP-5-087 has clinical utility for treating malignancies characterized by STAT3 activation.
Journal ArticleDOI
Age-related mutations and chronic myelomonocytic leukemia.
Clinton C. Mason,Jamshid S. Khorashad,Srinivas K. Tantravahi,Todd W. Kelley,Matthew S. Zabriskie,Dongqing Yan,Anthony D. Pomicter,Kimberly R. Reynolds,Anna M. Eiring,Zev N. Kronenberg,Recinda L. Sherman,Jeffrey W. Tyner,Brian Dalley,Kim Hien T. Dao,Mark Yandell,B. J. Druker,Jason Gotlib,Thomas O'Hare,Thomas O'Hare,Michael W. Deininger,Michael W. Deininger +20 more
TL;DR: Age-adjusted population incidence and reported ARCH mutation rates are consistent with a model in which clinical CMML ensues when a sufficient number of stochastically acquired age-related mutations has accumulated, suggesting that CMML represents the leukemic conversion of the myelomonocytic-lineage-biased aged hematopoietic system.