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Ann Mullally, MD


Medical Oncology

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Physician

  • Physician
  • Associate Professor of Medicine, Harvard Medical School

Clinical Interests

  • Hematopoietic stem cells (HSC)
  • Myeloid malignancies (primarily myeloproliferative neoplasms)
  • Myeloproliferative neoplasms

Contact Information

  • Appointments617-632-6140 (Hematologic Oncology)
    617-732-6089 (Hematology - New patients)
    617-525-8337 (Hematology - Established patients)
  • Office Phone Number617-732-5190 (Hematology Main Line)
  • Fax617-732-5706

Bio

Dr. Ann Mullally is a physician-scientist at Brigham and Women’s Hospital (BWH) / Dana-Farber Cancer Institute (DFCI). Her laboratory studies the genetics, biology and therapy of myeloproliferative neoplasms (MPN) using MPN patient samples, mouse models and multiple different laboratory approaches. Dr. Mullally’s MPN research interests include myelofibrosis, the biology of mutant calreticulin (CALR) in MPN, JAK2V617F MPN stem cells, improving the efficacy of JAK2 inhibitors and familial forms of MPN. The overarching goal of the research in her laboratory is to advance the understanding of the biology of MPN and to translate this into improved treatment options for patients dealing with these diseases.

Board Certification:

  • Hematology, 2009
  • Internal Medicine
  • Medical Oncology, 2010

Fellowship:

  • Dana-Farber/Partners CancerCare, Hematology/Oncology

Residency:

  • Johns Hopkins Hospital, Internal Medicine
  • Mayo Clinic, Internal Medicine

Medical School:

  • University College, Dublin

Research

Genomic Profiling of a Randomized Trial of Interferon-a versus Hydroxyurea in MPN Reveals Mutation-Specific Responses. Blood Adv. 2021 Sep 10.
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Hydroxycarbamide effects on DNA methylation and gene expression in myeloproliferative neoplasms. Genome Res. 2021 Aug; 31(8):1381-1394.
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Zinc-dependent multimerization of mutant calreticulin is required for MPL binding and MPN pathogenesis. Blood Adv. 2021 04 13; 5(7):1922-1932.
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Reconstructing the Lineage Histories and Differentiation Trajectories of Individual Cancer Cells in Myeloproliferative Neoplasms. Cell Stem Cell. 2021 03 04; 28(3):514-523.e9.
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Splicing factor YBX1 mediates persistence of JAK2-mutated neoplasms. Nature. 2020 12; 588(7836):157-163.
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COVID-19 and myeloproliferative neoplasms: some considerations. Leukemia. 2021 01; 35(1):279-281.
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Augmenting emergency granulopoiesis with CpG conditioned mesenchymal stromal cells in murine neutropenic sepsis. Blood Adv. 2020 10 13; 4(19):4965-4979.
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Pregnancy outcomes, risk factors, and cell count trends in pregnant women with essential thrombocythemia. Leuk Res. 2020 11; 98:106459.
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Remodeling the Bone Marrow Microenvironment - A Proposal for Targeting Pro-inflammatory Contributors in MPN. Front Immunol. 2020; 11:2093.
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Murine Models of Myelofibrosis. Cancers (Basel). 2020 Aug 23; 12(9).
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Busy signal: platelet-derived growth factor activation in myelofibrosis. Haematologica. 2020 08; 105(8):1988-1990.
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Working in the shadows, under the spotlight - Reflections on lessons learnt in the Republic of Ireland after the first 18?months of more liberal Abortion Care. Contraception. 2020 11; 102(5):305-307.
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Fedratinib in myelofibrosis. Blood Adv. 2020 04 28; 4(8):1792-1800.
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The Molecular Genetics of Myeloproliferative Neoplasms. Cold Spring Harb Perspect Med. 2020 02 03; 10(2).
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Both sides now: losses and gains of mutant CALR. Blood. 2020 01 09; 135(2):82-83.
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Mutant calreticulin in myeloproliferative neoplasms. Blood. 2019 12 19; 134(25):2242-2248.
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Distinct effects of ruxolitinib and interferon-alpha on murine JAK2V617F myeloproliferative neoplasm hematopoietic stem cell populations. Leukemia. 2020 04; 34(4):1075-1089.
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The kinases IKBKE and TBK1 regulate MYC-dependent survival pathways through YB-1 in AML and are targets for therapy. Blood Adv. 2018 12 11; 2(23):3428-3442.
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JAK2 (and other genes) be nimble with MPN diagnosis, prognosis, and therapy. Hematology Am Soc Hematol Educ Program. 2018 11 30; 2018(1):110-117.
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Gli1+ Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target. Cell Stem Cell. 2018 Aug 02; 23(2):308-309.
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Increased neutrophil extracellular trap formation promotes thrombosis in myeloproliferative neoplasms. Sci Transl Med. 2018 04 11; 10(436).
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Using CRISPR/Cas9 Gene Editing to Investigate the Oncogenic Activity of Mutant Calreticulin in Cytokine Dependent Hematopoietic Cells. J Vis Exp. 2018 01 05; (131).
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Defining the requirements for the pathogenic interaction between mutant calreticulin and MPL in MPN. Blood. 2018 02 15; 131(7):782-786.
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JAK2, CALR, MPL and ASXL1 mutational status correlates with distinct histological features in Philadelphia chromosome-negative myeloproliferative neoplasms. Haematologica. 2018 02; 103(2):e63-e68.
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Kinase Inhibitors in the Treatment of Myeloid Malignancies. Hematol Oncol Clin North Am. 2017 08; 31(4):ix-x.
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The Development and Use of Janus Kinase 2 Inhibitors for the Treatment of Myeloproliferative Neoplasms. Hematol Oncol Clin North Am. 2017 08; 31(4):613-626.
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Gli1+ Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target. Cell Stem Cell. 2017 06 01; 20(6):785-800.e8.
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Myeloproliferative neoplasm stem cells. Blood. 2017 03 23; 129(12):1607-1616.
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Gain of function in Jak2V617F-positive T-cells. Leukemia. 2017 04; 31(4):1000-1003.
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Underlying mechanisms of the JAK2V617F mutation in the pathogenesis of myeloproliferative neoplasms. Pathologe. 2016 Nov; 37(Suppl 2):175-179.
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Physiologic Expression of Sf3b1(K700E) Causes Impaired Erythropoiesis, Aberrant Splicing, and Sensitivity to Therapeutic Spliceosome Modulation. Cancer Cell. 2016 09 12; 30(3):404-417.
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Mutant Calreticulin Requires Both Its Mutant C-terminus and the Thrombopoietin Receptor for Oncogenic Transformation. Cancer Discov. 2016 Apr; 6(4):368-81.
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RECQL5 Suppresses Oncogenic JAK2-Induced Replication Stress and Genomic Instability. Cell Rep. 2015 Dec 22; 13(11):2345-2352.
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Targeting megakaryocytic-induced fibrosis in myeloproliferative neoplasms by AURKA inhibition. Nat Med. 2015 Dec; 21(12):1473-80.
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Haemophagocytic lymphohistiocytosis in adults: a multicentre case series over 7 years. Br J Haematol. 2016 Feb; 172(3):412-9.
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Marked hyperferritinemia does not predict for HLH in the adult population. Blood. 2015 Mar 05; 125(10):1548-52.
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Role of the clathrin adaptor PICALM in normal hematopoiesis and polycythemia vera pathophysiology. Haematologica. 2015 Apr; 100(4):439-51.
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Dynamin 2-dependent endocytosis is required for normal megakaryocyte development in mice. Blood. 2015 Feb 05; 125(6):1014-24.
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How does JAK2V617F contribute to the pathogenesis of myeloproliferative neoplasms? Hematology Am Soc Hematol Educ Program. 2014 Dec 05; 2014(1):268-76.
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Hit the spleen, JAK! Blood. 2014 Nov 06; 124(19):2898-900.
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JAK2V617F promotes replication fork stalling with disease-restricted impairment of the intra-S checkpoint response. Proc Natl Acad Sci U S A. 2014 Oct 21; 111(42):15190-5.
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Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms. Blood. 2015 Jan 08; 125(2):327-35.
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Role of casein kinase 1A1 in the biology and targeted therapy of del(5q) MDS. Cancer Cell. 2014 Oct 13; 26(4):509-20.
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Loss of function of TET2 cooperates with constitutively active KIT in murine and human models of mastocytosis. PLoS One. 2014; 9(5):e96209.
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Csnk1a1 inhibition has p53-dependent therapeutic efficacy in acute myeloid leukemia. J Exp Med. 2014 Apr 07; 211(4):605-12.
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Sinister symbiosis: pathological hematopoietic-stromal interactions in CML. Cell Stem Cell. 2013 Sep 05; 13(3):257-8.
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Depletion of Jak2V617F myeloproliferative neoplasm-propagating stem cells by interferon-a in a murine model of polycythemia vera. Blood. 2013 May 02; 121(18):3692-702.
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Janus reveals another face: the biologic rationale for targeting Janus kinase 2 in lymphoma. J Clin Oncol. 2012 Nov 20; 30(33):4168-70.
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Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy. Nature. 2012 Sep 06; 489(7414):155-9.
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Myeloproliferative neoplasm animal models. Hematol Oncol Clin North Am. 2012 Oct; 26(5):1065-81.
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miR-433 is aberrantly expressed in myeloproliferative neoplasms and suppresses hematopoietic cell growth and differentiation. Leukemia. 2013 Feb; 27(2):344-52.
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Distinct roles for long-term hematopoietic stem cells and erythroid precursor cells in a murine model of Jak2V617F-mediated polycythemia vera. Blood. 2012 Jul 05; 120(1):166-72.
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EXEL-8232, a small-molecule JAK2 inhibitor, effectively treats thrombocytosis and extramedullary hematopoiesis in a murine model of myeloproliferative neoplasm induced by MPLW515L. Leukemia. 2012 Apr; 26(4):720-7.
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Coordinate loss of a microRNA and protein-coding gene cooperate in the pathogenesis of 5q- syndrome. Blood. 2011 Oct 27; 118(17):4666-73.
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Mutations with epigenetic effects in myeloproliferative neoplasms and recent progress in treatment: Proceedings from the 5th International Post-ASH Symposium. Blood Cancer J. 2011 Mar 04; 1:e7.
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STATistical power of clonal analysis: differential STAT1 pathway activation downstream of the JAK2V617F mutation. Cancer Cell. 2010 Nov 16; 18(5):405-6.
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Haploinsufficiency for ribosomal protein genes causes selective activation of p53 in human erythroid progenitor cells. Blood. 2011 Mar 03; 117(9):2567-76.
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NF1 inactivation revs up Ras in adult acute myelogenous leukemia. Clin Cancer Res. 2010 Aug 15; 16(16):4074-6.
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Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells. Cancer Cell. 2010 Jun 15; 17(6):584-96.
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CNS relapse in acute promyeloctyic leukemia. J Clin Oncol. 2010 Aug 20; 28(24):e409-11.
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Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies. Blood. 2009 Jul 02; 114(1):144-7.
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A germline JAK2 SNP is associated with predisposition to the development of JAK2(V617F)-positive myeloproliferative neoplasms. Nat Genet. 2009 Apr; 41(4):455-9.
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Frequent TET2 mutations in systemic mastocytosis: clinical, KITD816V and FIP1L1-PDGFRA correlates. Leukemia. 2009 May; 23(5):900-4.
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TET2 mutations and their clinical correlates in polycythemia vera, essential thrombocythemia and myelofibrosis. Leukemia. 2009 May; 23(5):905-11.
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Beyond HLA: the significance of genomic variation for allogeneic hematopoietic stem cell transplantation. Blood. 2007 Feb 15; 109(4):1355-62.
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Wasted sheep and premature infants: the role of trace metals in hematopoiesis. Blood Rev. 2004 Dec; 18(4):227-34.
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