Thomas J. O'Hare, Ph.D.

Research Interests

  • Design and Synthesis of Targeted Cancer Drugs
  • Leukemia, Myeloid, Philadelphia-Positive
  • Drug Resistance
  • Tyrosine Kinase Activating Mutations

Labs

Lab Website

Languages

  • English

Academic Information

  • Departments: Internal Medicine - Research Associate Professor
  • Divisions: Hematology/BMT
  • Cancer Center Programs: Cell Response & Regulation

Academic Office Information

  • (801) 585-0256
  • Huntsman Cancer Institute
    HCI4264
    2000 Circle of Hope
    Salt Lake City, UT 84112

Academic Bio

Thomas J. O'Hare, Ph.D. is a an Associate Professor of Medicine (career track) in the Division of Hematology and Hematologic Malignancies, Department of Internal Medicine at the University of Utah. His lab is located in the Huntsman Cancer Institute and he is a member of the Cell Response and Regulation Program. He received his B.Sc. in Chemistry from Southern Oregon University in Ashland, followed by his Ph.D. in Chemistry at the University of Washington in Seattle. Dr. O'Hare completed two Postdoctoral Fellowships: one in Chemistry at Oregon State University and one in Molecular Microbiology and Immunology at Oregon Health & Science University in Portland.

Dr. O'Hare's research focuses on Chronic Myeloid Leukemia, a cancer of white blood cells.

Education History

Type School Degree
Postdoctoral Fellowship Oregon Health & Science University
Molecular Microbiology and Immunology
Postdoctoral Fellow
Postdoctoral Fellowship Oregon State University
Chemistry
Postdoctoral Fellow
Doctoral Training University of Washington
Chemistry
Ph.D.
Undergraduate Southern Oregon University
Chemistry
B.Sc.

Selected Publications

Journal Article

  1. Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia.Eiring AM, Page BD, Kraft IL, Mason CC, Vellore NA, Resetca D, Zabriskie MS, Zhang TY, Khorashad JS, Engar AJ, Reynolds KR, Anderson DJ, Senina A, Pomicter AD, Arpin CC, Ahmad S, Heaton WL, Tantravahi SK, Todic A, Colaguori R, Moriggl R, Wilson DJ, Baron R, OHare T, Gunning PT, Deininger MW (2015). Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemia. Leukemia, 29(3), 586-97.
  2. BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.Zabriskie MS, Eide CA, Tantravahi SK, Vellore NA, Estrada J, Nicolini FE, Khoury HJ, Larson RA, Konopleva M, Cortes JE, Kantarjian H, Jabbour EJ, Kornblau SM, Lipton JH, Rea D, Stenke L, Barbany G, Lange T, Hernandez-Boluda JC, Ossenkoppele GJ, Press RD, Chuah C, Goldberg SL, Wetzler M, Mahon FX, Etienne G, Baccarani M, Soverini S, Rosti G, Rousselot P, Friedman R, Deininger M, Reynolds KR, Heaton WL, Eiring AM, Pomicter AD, Khorashad JS, Kelley TW, Baron R, Druker BJ, Deininger MW, OHare T (2014). BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia. Cancer Cell, 26(3), 428-42.
  3. BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein.Agarwal A, Mackenzie RJ, Besson A, Jeng S, Carey A, LaTocha DH, Fleischman AG, Duquesnes N, Eide CA, Vasudevan KB, Loriaux MM, Firpo E, Cortes JE, McWeeney S, OHare T, Roberts JM, Druker BJ, Deininger MW (2014). BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein. Blood, 124(22), 3260-73.
  4. Kinase inhibitor therapy in CML: it's what's inside that counts.Eide CA, Druker BJ, OHare T (2013). Kinase inhibitor therapy in CML: it's what's inside that counts. Oncotarget, 4(9), 1332-3.
  5. Integrating in vitro sensitivity and dose-response slope is predictive of clinical response to ABL kinase inhibitors in chronic myeloid leukemia.Vainstein V, Eide CA, OHare T, Shukron O, Druker BJ (2013). Integrating in vitro sensitivity and dose-response slope is predictive of clinical response to ABL kinase inhibitors in chronic myeloid leukemia. Blood, 122(19), 3331-4.
  6. KIT signaling governs differential sensitivity of mature and primitive CML progenitors to tyrosine kinase inhibitors.Corbin AS, OHare T, Gu Z, Kraft IL, Eiring AM, Khorashad JS, Pomicter AD, Zhang TY, Eide CA, Manley PW, Cortes JE, Druker BJ, Deininger MW (2013). KIT signaling governs differential sensitivity of mature and primitive CML progenitors to tyrosine kinase inhibitors. Cancer Res, 73(18), 5775-86.
  7. Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid leukemia cells determine their commitment to apoptosis.OHare T, Eide CA, Agarwal A, Adrian LT, Zabriskie MS, Mackenzie RJ, Latocha DH, Johnson KJ, You H, Luo J, Riddle SM, Marks BD, Vogel KW, Koop DR, Apgar J, Tyner JW, Deininger MW, Druker BJ (2013). Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid leukemia cells determine their commitment to apoptosis. Cancer Res, 73(11), 3356-70.
  8. Kinase pathway dependence in primary human leukemias determined by rapid inhibitor screening.Tyner JW, Yang WF, Bankhead A 3rd, Fan G, Fletcher LB, Bryant J, Glover JM, Chang BH, Spurgeon SE, Fleming WH, Kovacsovics T, Gotlib JR, Oh ST, Deininger MW, Zwaan CM, Den Boer ML, van den Heuvel-Eibrink MM, OHare T, Druker BJ, Loriaux MM (2013). Kinase pathway dependence in primary human leukemias determined by rapid inhibitor screening. Cancer Res, 73(1), 285-96.
  9. BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships.Khorashad JS, Kelley TW, Szankasi P, Mason CC, Soverini S, Adrian LT, Eide CA, Zabriskie MS, Lange T, Estrada JC, Pomicter AD, Eiring AM, Kraft IL, Anderson DJ, Gu Z, Alikian M, Reid AG, Foroni L, Marin D, Druker BJ, OHare T, Deininger MW (2013). BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships. Blood, 121(3), 489-98.
  10. Blockade of JAK2-mediated extrinsic survival signals restores sensitivity of CML cells to ABL inhibitors.Traer E, MacKenzie R, Snead J, Agarwal A, Eiring AM, OHare T, Druker BJ, Deininger MW (2012). Blockade of JAK2-mediated extrinsic survival signals restores sensitivity of CML cells to ABL inhibitors. Leukemia, 26(5), 1140-3.
  11. Ponatinib in refractory Philadelphia chromosome-positive leukemias.Cortes JE, Kantarjian H, Shah NP, Bixby D, Mauro MJ, Flinn I, OHare T, Hu S, Narasimhan NI, Rivera VM, Clackson T, Turner CD, Haluska FG, Druker BJ, Deininger MW, Talpaz M (2012). Ponatinib in refractory Philadelphia chromosome-positive leukemias. N Engl J Med, 367(22), 2075-88.
  12. Wnt/Ca2+/NFAT signaling maintains survival of Ph+ leukemia cells upon inhibition of Bcr-Abl.Gregory MA, Phang TL, Neviani P, Alvarez-Calderon F, Eide CA, OHare T, Zaberezhnyy V, Williams RT, Druker BJ, Perrotti D, Degregori J (2010). Wnt/Ca2+/NFAT signaling maintains survival of Ph+ leukemia cells upon inhibition of Bcr-Abl. Cancer Cell, 18(1), 74-87.
  13. AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance.OHare T, Shakespeare WC, Zhu X, Eide CA, Rivera VM, Wang F, Adrian LT, Zhou T, Huang WS, Xu Q, Metcalf CA 3rd, Tyner JW, Loriaux MM, Corbin AS, Wardwell S, Ning Y, Keats JA, Wang Y, Sundaramoorthi R, Thomas M, Zhou D, Snodgrass J, Commodore L, Sawyer TK, Dalgarno DC, Deininger MW, Druker BJ, Clackson T (2009). AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance. Cancer Cell, 16(5), 401-12.

Review

  1. Pushing the limits of targeted therapy in chronic myeloid leukaemia.OHare T, Zabriskie MS, Eiring AM, Deininger MW (2012). Pushing the limits of targeted therapy in chronic myeloid leukaemia. [Review]. Nat Rev Cancer, 12(8), 513-26.

Book Chapter

  1. Agarwal A, OHare T, Deininger M (2012). CXCR4 antagonists for the treatment of CML. In Fruehauf S, Zeller WJ, Calandra, G (Eds.), Novel developments in stem cell mobilization: Focus on CXCR4 (XIV, pp. 351-367). Springer.

Editorial

  1. New concepts for CML clonality.Khorashad JS, Deininger MW, OHare T (2013). New concepts for CML clonality. Oncotarget, 4(1), 7-8.

Video