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Ann M. Mullally, MD
Associate Physician, Brigham and Women's Hospital
Associate Professor of Medicine, Harvard Medical School

Brigham and Women's Hospital
Department of Medicine
Hematology
75 Francis Street
Boston, MA 02115

Research Location: Harvard Institute of Medicine

Research Email: amullally@partners.org

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Research Narrative:

Dr. Ann Mullally is a physician-scientist at Brigham and Women’s Hospital (BWH). She holds a weekly clinic for patients with myeloproliferative neoplasms (MPN) at Dana-Farber Cancer Institute (DFCI) and runs a research laboratory focused on myeloid malignancies, primarily MPN. Her clinical interests include early intervention strategies to target disease-propagating MPN stem cells and the development of immunological approaches to target mutant calreticulin (CALR) in MPN. Her laboratory studies the genetics, biology and therapy of MPN using primary patient samples, mouse models and multiple in vitro model systems. Dr. Mullally’s laboratory research interests include the biology of mutant CALR and JAK2V617F in MPN, the biology of myelofibrosis, MPN stem cells and the development of novel therapeutic strategies to preferentially target them. The overarching goal of her research is to advance the understanding of the biology of MPN and to translate this into improved treatment options for patients dealing with these diseases.


Education:
University College Dublin Medical School, 1999, MBBCh

Additional News:



Publications (Pulled from Harvard Catalyst Profiles):

1. Liu S, Marneth AE, Alexe G, Walker SR, Gandler HI, Ye DQ, Labella K, Mathur R, Toniolo PA, Tillgren M, Gokhale PC, Barbie D, Mullally A, Stegmaier K, Frank DA. 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.

2. Ciboddo M, Mullally A. 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.

3. Schneider RK, Mullally A, Dugourd A, Peisker F, Hoogenboezem R, Van Strien PMH, Bindels EM, Heckl D, Büsche G, Fleck D, Müller-Newen G, Wongboonsin J, Ventura Ferreira M, Puelles VG, Saez-Rodriguez J, Ebert BL, Humphreys BD, Kramann R. Gli1+ Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target. Cell Stem Cell. 2018 08 02; 23(2):308-309.

4. Wolach O, Sellar RS, Martinod K, Cherpokova D, McConkey M, Chappell RJ, Silver AJ, Adams D, Castellano CA, Schneider RK, Padera RF, DeAngelo DJ, Wadleigh M, Steensma DP, Galinsky I, Stone RM, Genovese G, McCarroll SA, Iliadou B, Hultman C, Neuberg D, Mullally A, Wagner DD, Ebert BL. Increased neutrophil extracellular trap formation promotes thrombosis in myeloproliferative neoplasms. Sci Transl Med. 2018 04 11; 10(436).

5. Abdelfattah NS, Mullally A. 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).

6. Elf S, Abdelfattah NS, Baral AJ, Beeson D, Rivera JF, Ko A, Florescu N, Birrane G, Chen E, Mullally A. Defining the requirements for the pathogenic interaction between mutant calreticulin and MPL in MPN. Blood. 2018 02 15; 131(7):782-786.

7. Wong WJ, Hasserjian RP, Pinkus GS, Breyfogle LJ, Mullally A, Pozdnyakova O. 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.

8. Mullally A. Kinase Inhibitors in the Treatment of Myeloid Malignancies. Hematol Oncol Clin North Am. 2017 08; 31(4):ix-x.

9. Hobbs GS, Rozelle S, Mullally A. 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.

10. Schneider RK, Mullally A, Dugourd A, Peisker F, Hoogenboezem R, Van Strien PMH, Bindels EM, Heckl D, Büsche G, Fleck D, Müller-Newen G, Wongboonsin J, Ventura Ferreira M, Puelles VG, Saez-Rodriguez J, Ebert BL, Humphreys BD, Kramann R. 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.