Katherine R. Calvo, MD, PhD

BA, Reed College
MD PhD, University of California San Diego

Dr. Katherine Calvo earned her BA from Reed College in International Studies and MD PhD from the University of California San Diego in 2003. Her PhD research, in Molecular Pathology, focused on the role of homeobox genes in the development of acute leukemia. While at UCSD she authored multiple papers on the molecular mechanisms of leukemia involving HoxA9, E2A-PBX1 and Nup98-HoxA9. She was also a founder of both the UCSD Student-Run Free Clinic and the medical school literary journal, The Human Condition.

Dr. Calvo came to the National Cancer Institute at NIH in 2003 as a resident in Anatomic Pathology. During residency she did research in post-translational modification of cell signaling proteins in tumors using protein microarrays in the Laboratory of Pathology. Dr. Calvo then entered the NCI Hematopathology fellowship in 2006, and studied the role of cytokines in the lymph node microenvironment of follicular lymphoma. During fellowship, Dr. Calvo was Co-Chair of the NIH Fellows Committee (FelCom).

In 2008 Dr. Calvo completed her fellowship and joined the Department of Laboratory Medicine in the NIH Clinical Center as an attending Hematopathologist in the Hematology Section. She is board certified in Hematology and Anatomic Pathology by the American Board of Pathology. Dr. Calvo is an attending on the bone marrow service, teaches fellows, and directs the Automated Hematology and Peripheral Blood Morphology section in Hematology. Her area of expertise and current research encompasses acquired and germline predisposition to bone marrow failure, GATA2 deficiency, myelodysplasia, and hematolymphoid malignancies. In collaboration with colleagues, Dr. Calvo has published over 70 research and clinical manuscripts and authored multiple book chapters. Dr. Calvo is Co-Chair of the NIH Assembly of Scientists, and has served on the Staff Clinician Council.

• High Quality Service SuperSTAR Award, Office of Patient Safety and Clinical Quality, NIH Clinical Center, July 2019
• NIH Office of the Director Honor Award, 2018 for outstanding leadership to enhance contributions of Staff Clinicians to clinical research and patient care in the NIH Intramural Research Program
• National Institutes of Health Director's Award, 2015
• National Heart Lung and Blood Institute, Intramural Orloff Science Award, 2015 for clinical/translational research team, Eltrombopag and treatment of refractory aplastic anemia
• National Institute of Allergy and Infectious Diseases Director's Award, 2014 for outstanding clinical and basic research leading to the discovery and characterization of GATA2 deficiency
• NIH Clinical Center Director's Award for Patient Care, 2013
• NCI Director's Award for Innovation, 2006, National Cancer Institute
• Arlene and Dr. Bernard Goodhead Service Award in Oncology, 2003, UCSD School of Medicine
• Free-Clinic Student Founder and Leadership Awards, 2001 and 2002, UCSD School of Medicine
• Health Hero 2000 Award, Combined Health Agencies, San Diego, CA
• Overall Outstanding Medical Student Award, 1997, UCSD School of Medicine
• Outstanding Research Award, 1996, Western Medical Student Research Section, American Federation for Clinical Research
• Dean's List, 1994, University of California, Berkeley
• Commendation for Academic Excellence, 1985, Reed College

Weinberg OK, Kuo F, Calvo KR. Germline Predisposition to Hematolymphoid Neoplasia. American Journal of Clinical Pathology. 2019 Aug 1;152(3):258-276.

McReynolds LJ, Yang Y, Yuen Wong H, Tang J, Zhang Y, Mulé MP, Daub J, Palmer C, Foruraghi L, Liu Q, Zhu J, Wang W, West RR, Yohe ME, Hsu AP, Hickstein DD, Townsley DM, Holland SM, Calvo KR*, Hourigan CS*.  MDS-associated mutations in germline GATA2 mutated patients with hematologic manifestations. Leukemia Research. 2019 Jan;76:70-75. * contributed equally

Kallen ME, Dulau-Florea A, Wang W, Calvo KR. Acquired and germline predisposition to bone marrow failure: Diagnostic features and clinical implications. Seminars in Hematology. 2019 Jan;56(1):69-82.

Galera P, Hsu AP, Wang W, Droll S, Chen R, Schwartz JR, Klco JM, Arai S, Maese L, Zerbe C, Parta MJ, Young NS, Holland SM, Hickstein DD, Calvo KR.  Donor-derived MDS/AML in families with germline GATA2 mutation. Blood. 2018 Nov 1;132(18):1994-1998.

Townsley DM, Scheinberg P, Winkler T, Desmond R, Dumitriu B, Rios O, Weinstein B, Valdez J, Lotter J, Feng X, Desierto M, Leuva H, Bevans M, Wu C, Larochelle A, Calvo KR, Dunbar CE, Young NS. Eltrombopag Added to Standard Immunosuppression for Aplastic Anemia. New England Journal of Medicine. 2017 Apr 20;376(16):1540-1550.

Dulau Florea AE, Braylan RC, Schafernak KT, Williams KW, Daub J, Goyal RK, Puck JM, Rao VK, Pittaluga S, Holland SM, Uzel G, Calvo KR. Abnormal B-Cell Maturation in the Bone Marrow of Patients with Germline Mutations in PIK3CD. Journal of Allergy & Clinical Immunology. 2017 Mar;139(3):1032-1035

Saleh LM, Wang W, Herman SEM, Saba NS, BarberE, Corrigan-Cummins M, Anastas V, Zhao Z, Farooqui M, Sun C, Sarasua SM, Abusamra NK, El-Agroudy OE, El-Ghaffar HA, Wiestner A, and Calvo KR. Ibrutinib downregulates a subset of miRNA leading to upregulation of tumor suppressors and inhibition of cell proliferation in Chronic Lymphocytic Leukemia. Leukemia. 2017 Feb;31(2):340-349.

Calvo KR, Price S, Braylan RC, Oliveira JB, Lenardo M, Fleisher TM, and RaoVK. RAS-associated autoimmune leukoproliferative disorder (RALD) and juvenile /chronic myelomonocytic leukemia (JMML/CMML): Common genetic etiology but clinically distinct entities. Blood. 2015 Apr 30;125(18):2753-8

Ganapathi KA, Townsley DM, Hsu AP, ArthurDC, Zerbe CS, Cuellar-Rodriguez J, Hickstein DD, Rosenzweig SD, Braylan RC, Young NS, HollandSM, and Calvo KR. GATA2 deficiency-associated bone marrow disorder differs from idiopathic aplastic anemia. Blood. 2015 Jan 1;125(1):56-70. Epub 2014 Oct 30.

Wang W, Corrigan-Cummins M, Maric I, Simakova O, Neelapu SS, Kwak LW, Janik JE, Gause B, Jaffe ES, and Calvo KR. MicroRNA profiling of follicular lymphoma identifies microRNAs related to cell proliferation and tumor response. Haematologica 2012 Apr;97(4):586-94.

Hsu AP, Sampaio EP, Khan J, Calvo KR, Lemieux JE, Patel SY, Frucht DM, Vinh DC, Auth RD, Freeman AF, Olivier KN, Uzel G, Zerbe CS, Spalding C, Pittaluga S, Raffeld M, Kuhns DB, Ding L, Paulson ML, Marciano BE, Gea-Banacloche JC, Orange JS, Cuellar-Rodriguez J, Hickstein DD, Holland SM. Mutations in GATA2 are associated with the autosomal dominant and sporadic monocytopenia and mycobacterial infection (MonoMAC) syndrome. Blood. 2011 Sep 8;118(10):2653-5.

Calvo KR, Vinh DC, Maric I, Wang W, Noel P, Stetler-Stevenson M, Arthur DC, Raffeld M, Dutra A, Pak E, Myung K, Hsu AP, Hickstein DD, Pittaluga S, Holland SM. Myelodysplasia in autosomal dominant and sporadic monocytopenia immunodeficiency syndrome: diagnostic features and clinical implications. Haematologica. 2011 Aug;96(8):1221-5.

Calvo KR, Dabir B, Kovach L, Devor C, Bond A, Bandle R, Shih J and Jaffe ES. IL-4 protein expression and basal activation of Erk in vivo in follicular lymphoma. Blood. 2008 Nov 1;112(9):3818-26.

Calvo KR, Sykes DB, Pasillas MP, Kamps MP. Nup98-HoxA9 immortalizes myeloid progenitors, enforces expression of Hoxa9, Hoxa7 and Meis1, and alters cytokine-specific responses in a manner similar to that induced by retroviral co-expression of Hoxa9 and Meis1. Oncogene. 2002 Jun 20;21(27):4247-56

Calvo KR, Knoepfler PS, Sykes DB, Pasillas MP, Kamps MP. Meis1a suppresses differentiation by G-CSF and promotes proliferation by SCF: potential mechanisms of cooperativity with HoxA9 in myeloid leukemia. Proceedings of the National Academy of Sciences U S A. 2001 Nov 6;98(23):13120-5

Calvo KR, Sykes DB, Pasillas M, Kamps MP. Hoxa9 immortalizes a granulocyte-macrophage colony-stimulating factor-dependent promyelocyte capable of biphenotypic differentiation to neutrophils or macrophages, independent of enforced Meis expression. Molecular and Cellular Biology. 2000 May;20(9):3274-85

Calvo KR, Knoepfler P, McGrath S, Kamps MP. An inhibitory switch derepressed by Pbx, Hox, and Meis/Prep1 partners regulates DNA-binding by Pbx1 and E2a-Pbx1 and is dispensable for myeloid immortalization by E2a-Pbx1. Oncogene. 1999 Dec 23;18(56):8033-43