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Kimberly Stegmaier, MD


Pediatric Hematology/Oncology

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Physician

  • Co-Director of the Hematologic Malignancy Center (Basic and Translational Research)
  • Physician
  • Ted Williams Chair
  • Professor of Pediatrics, Harvard Medical School

Clinical Interests

  • Cancer genomics
  • Chemical screening
  • Ewing sarcoma
  • Hematologic malignancies
  • Neuroblastoma

Contact Information

  • Appointments888-733-4662 (new)
    617-632-3270 (established)
  • Office Phone Number617-632-4438
  • Fax617-632-4850

Bio

Kimberly Stegmaier, M.D., is a Professor of Pediatrics at Harvard Medical School, a Principal Investigator in Pediatric Oncology at the Dana-Farber Cancer Institute (DFCI), and an Attending Physician at the Boston Children’s Hospital Boston (BCH) and DFCI. She is the Co-director of the Pediatric Hematologic Malignancies Program at DFCI and BCH and is also an Associate Member of the Broad Institute of Harvard and MIT. She received her B.S. from Duke University and her M.D. from Harvard Medical School. She completed her residency at BCH and a post-doctoral pediatric hematology-oncology fellowship at DFCI/BCH. In 2006, she launched her own laboratory effort at DFCI.

Dr. Stegmaier’s laboratory integrates chemical biology, genomic, and proteomic approaches to discover new lead compounds and protein targets for cancer therapy. She has focused her efforts on the acute leukemias and two pediatric solid tumors of childhood: Ewing sarcoma and neuroblastoma.

Board Certification:

  • Pediatric Hematology/Oncology, 2002

Fellowship:

  • Boston Children's Hospital/Dana-Farber Cancer Institute, Pediatric Hematology/Oncology

Residency:

  • Boston Combined Residency Program, Boston Children's Hospital/Boston Medical Center, Pediatrics

Medical School:

  • Harvard Medical School

Recent Awards:

  • Joanne Levy, MD, Memorial Award for Outstanding Achievement, American Society of Hematology, 2006
  • Genome Technology "Tomorrow's Principal Investigator" Award, 2007
  • American Society for Clinical Investigation, Elected Member, 2009
  • SU2C Innovative Research Grant Recipient, 2009
  • Society for Pediatric Research (SPR) Young Investigator Award, 2012
  • Stephen E. Sallan Leadership Award, 2012
  • Osler Young Investigator Award, Interurban Clinical Club, 2013
  • Clifford Barger Excellence in Mentoring Award, Harvard Medical School, 2014
  • Helen Mentor, Dana-Farber Cancer Institute's Helen Gurley Brown (HGB) Presidential Initiative, 2020-2022

Research

Principal Investigator

My research program focuses on the integration of “omic” approaches for the identification of new protein targets and small-molecule modulators of malignancy with an eye toward clinical translation. Cancer discovery efforts in my laboratory have focused on the alteration of the malignant state (e.g., AML and neuroblastoma differentiation) and the modulation of pharmacologically challenging oncoproteins (e.g., EWS/FLI in Ewing sarcoma, MYCN in neuroblastoma, and NOTCH1 in T-ALL.) Most recently, we are applying an integrated approach to discover new therapeutic opportunities in these malignancies with deep genomic characterization of primary tumors, kinase activity profiling for immediately druggable targets, functional genomic screening for new tumor dependencies and chemical screening for modulators of relevant oncogenic drivers. Clinical trials for patients with AML and Ewing sarcoma have resulted from our research and a trial testing BET bromodomain inhibitors in patients with MYCN amplified neuroblastoma is in development.

 

Targeting serine hydroxymethyltransferases 1 and 2 for T-cell acute lymphoblastic leukemia therapy. Leukemia. 2021 Aug 02.
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TRIM8 modulates the EWS/FLI oncoprotein to promote survival in Ewing sarcoma. Cancer Cell. 2021 Jul 22.
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Synthetic Lethal Interaction between the ESCRT Paralog Enzymes VPS4A and VPS4B in Cancers Harboring Loss of Chromosome 18q or 16q. Cell Rep. 2021 Jul 13; 36(2):109367.
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STAG2 loss rewires oncogenic and developmental programs to promote metastasis in Ewing sarcoma. Cancer Cell. 2021 Jun 14; 39(6):827-844.e10.
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The synergy of BET inhibitors with aurora A kinase inhibitors in MYCN-amplified neuroblastoma is heightened with functional TP53. Neoplasia. 2021 06; 23(6):624-633.
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Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival. Cancer Res. 2021 Aug 01; 81(15):3971-3984.
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Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer. Cancer Discov. 2021 Sep; 11(9):2282-2299.
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Structure-activity relationship study of THZ531 derivatives enables the discovery of BSJ-01-175 as a dual CDK12/13 covalent inhibitor with efficacy in Ewing sarcoma. Eur J Med Chem. 2021 Oct 05; 221:113481.
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Targeting acute myeloid leukemia dependency on VCP-mediated DNA repair through a selective second-generation small-molecule inhibitor. Sci Transl Med. 2021 03 31; 13(587).
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RAD21 is a driver of chromosome 8 gain in Ewing sarcoma to mitigate replication stress. Genes Dev. 2021 04 01; 35(7-8):556-572.
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A first-generation pediatric cancer dependency map. Nat Genet. 2021 04; 53(4):529-538.
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Bromodomain and extra-terminal inhibitors-A consensus prioritisation after the Paediatric Strategy Forum for medicinal product development of epigenetic modifiers in children-ACCELERATE. Eur J Cancer. 2021 Mar; 146:115-124.
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Matched Targeted Therapy for Pediatric Patients with Relapsed, Refractory, or High-Risk Leukemias: A Report from the LEAP Consortium. Cancer Discov. 2021 Jun; 11(6):1424-1439.
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Network-based systems pharmacology reveals heterogeneity in LCK and BCL2 signaling and therapeutic sensitivity of T-cell acute lymphoblastic leukemia. Nat Cancer. 2021 Mar; 2(3):284-299.
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Synthetic Lethal Interaction between the ESCRT Paralog Enzymes VPS4A and VPS4B in Cancers Harboring Loss of Chromosome 18q or 16q. Cell Rep. 2020 12 15; 33(11):108493.
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Paediatric Strategy Forum for medicinal product development of epigenetic modifiers for children: ACCELERATE in collaboration with the European Medicines Agency with participation of the Food and Drug Administration. Eur J Cancer. 2020 11; 139:135-148.
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Rapid and direct control of target protein levels with VHL-recruiting dTAG molecules. Nat Commun. 2020 09 18; 11(1):4687.
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The Folate Cycle Enzyme MTHFR Is a Critical Regulator of Cell Response to MYC-Targeting Therapies. Cancer Discov. 2020 12; 10(12):1894-1911.
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Blockade of Oncogenic NOTCH1 with the SERCA Inhibitor CAD204520 in T Cell Acute Lymphoblastic Leukemia. Cell Chem Biol. 2020 06 18; 27(6):678-697.e13.
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Targeting EZH2 for the treatment of hepatosplenic T-cell lymphoma. Blood Adv. 2020 04 14; 4(7):1265-1269.
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Selective USP7 inhibition elicits cancer cell killing through a p53-dependent mechanism. Sci Rep. 2020 03 24; 10(1):5324.
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Targeting DUBs to degrade oncogenic proteins. Br J Cancer. 2020 04; 122(8):1121-1123.
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Preclinical efficacy for a novel tyrosine kinase inhibitor, ArQule 531 against acute myeloid leukemia. J Hematol Oncol. 2020 01 28; 13(1):8.
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STRIPAK directs PP2A activity toward MAP4K4 to promote oncogenic transformation of human cells. Elife. 2020 Jan 08; 9.
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Salt-inducible kinase inhibition suppresses acute myeloid leukemia progression in vivo. Blood. 2020 01 02; 135(1):56-70.
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Resistance Mechanisms to SYK Inhibition in Acute Myeloid Leukemia. Cancer Discov. 2020 02; 10(2):214-231.
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EWS-FLI1 modulated alternative splicing of ARID1A reveals novel oncogenic function through the BAF complex. Nucleic Acids Res. 2019 10 10; 47(18):9619-9636.
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Small-Molecule and CRISPR Screening Converge to Reveal Receptor Tyrosine Kinase Dependencies in Pediatric Rhabdoid Tumors. Cell Rep. 2019 08 27; 28(9):2331-2344.e8.
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Single-cell cloning of human T-cell lines reveals clonal variation in cell death responses to chemotherapeutics. Cancer Genet. 2019 09; 237:69-77.
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Neuronal differentiation and cell-cycle programs mediate response to BET-bromodomain inhibition in MYC-driven medulloblastoma. Nat Commun. 2019 06 03; 10(1):2400.
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Targeting chromatin complexes in fusion protein-driven malignancies. Nat Rev Cancer. 2019 05; 19(5):255-269.
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Therapeutic discovery for marrow failure with MDS predisposition using pluripotent stem cells. JCI Insight. 2019 04 30; 5.
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Synthetic Lethality of Wnt Pathway Activation and Asparaginase in Drug-Resistant Acute Leukemias. Cancer Cell. 2019 04 15; 35(4):664-676.e7.
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High-throughput Chemical Screening Identifies Focal Adhesion Kinase and Aurora Kinase B Inhibition as a Synergistic Treatment Combination in Ewing Sarcoma. Clin Cancer Res. 2019 07 15; 25(14):4552-4566.
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Correction: Detection of circulating tumour DNA is associated with inferior outcomes in Ewing sarcoma and osteosarcoma: a report from the Children's Oncology Group. Br J Cancer. 2019 Apr; 120(8):869.
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Ushering in the next generation of precision trials for pediatric cancer. Science. 2019 Mar 15; 363(6432):1175-1181.
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Virtual Screening Identifies Irreversible FMS-like Tyrosine Kinase 3 Inhibitors with Activity toward Resistance-Conferring Mutations. J Med Chem. 2019 03 14; 62(5):2428-2446.
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MDM2 and MDM4 Are Therapeutic Vulnerabilities in Malignant Rhabdoid Tumors. Cancer Res. 2019 05 01; 79(9):2404-2414.
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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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Resistance to Epigenetic-Targeted Therapy Engenders Tumor Cell Vulnerabilities Associated with Enhancer Remodeling. Cancer Cell. 2018 12 10; 34(6):922-938.e7.
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A Combination CDK4/6 and IGF1R Inhibitor Strategy for Ewing Sarcoma. Clin Cancer Res. 2019 02 15; 25(4):1343-1357.
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Creatine kinase pathway inhibition alters GSK3 and WNT signaling in EVI1-positive AML. Leukemia. 2019 03; 33(3):800-804.
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TRPS1 Is a Lineage-Specific Transcriptional Dependency in Breast Cancer. Cell Rep. 2018 10 30; 25(5):1255-1267.e5.
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Precision Targeting of BFL-1/A1 and an ATM Co-dependency in Human Cancer. Cell Rep. 2018 09 25; 24(13):3393-3403.e5.
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Comparative proteomics reveals a diagnostic signature for pulmonary head-and-neck cancer metastasis. EMBO Mol Med. 2018 09; 10(9).
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Detection of circulating tumour DNA is associated with inferior outcomes in Ewing sarcoma and osteosarcoma: a report from the Children's Oncology Group. Br J Cancer. 2018 08; 119(5):615-621.
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Selective gene dependencies in MYCN-amplified neuroblastoma include the core transcriptional regulatory circuitry. Nat Genet. 2018 09; 50(9):1240-1246.
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Targeted therapy for fusion-driven high-risk acute leukemia. Blood. 2018 09 20; 132(12):1241-1247.
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Genome-scale CRISPR-Cas9 screen identifies druggable dependencies in TP53 wild-type Ewing sarcoma. J Exp Med. 2018 08 06; 215(8):2137-2155.
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KLF5 controls glutathione metabolism to suppress p190-BCR-ABL+ B-cell lymphoblastic leukemia. Oncotarget. 2018 Jul 03; 9(51):29665-29679.
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Author Correction: EWS-FLI1 increases transcription to cause R-loops and block BRCA1 repair in Ewing sarcoma. Nature. 2018 07; 559(7715):E11.
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Phase I trial of the mTOR inhibitor everolimus in combination with multi-agent chemotherapy in relapsed childhood acute lymphoblastic leukemia. Pediatr Blood Cancer. 2018 07; 65(7):e27062.
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Bepridil exhibits anti-leukemic activity associated with NOTCH1 pathway inhibition in chronic lymphocytic leukemia. Int J Cancer. 2018 08 15; 143(4):958-970.
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EWS-FLI1 increases transcription to cause R-loops and block BRCA1 repair in Ewing sarcoma. Nature. 2018 03 15; 555(7696):387-391.
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Exploiting an Asp-Glu "switch" in glycogen synthase kinase 3 to design paralog-selective inhibitors for use in acute myeloid leukemia. Sci Transl Med. 2018 03 07; 10(431).
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EWS/FLI Confers Tumor Cell Synthetic Lethality to CDK12 Inhibition in Ewing Sarcoma. Cancer Cell. 2018 02 12; 33(2):202-216.e6.
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CRISPR-Cas9 screen reveals a MYCN-amplified neuroblastoma dependency on EZH2. J Clin Invest. 2018 01 02; 128(1):446-462.
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Leukemia-specific delivery of mutant NOTCH1 targeted therapy. J Exp Med. 2018 01 02; 215(1):197-216.
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Computational correction of copy number effect improves specificity of CRISPR-Cas9 essentiality screens in cancer cells. Nat Genet. 2017 Dec; 49(12):1779-1784.
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Identification of an allosteric benzothiazolopyrimidone inhibitor of the oncogenic protein tyrosine phosphatase SHP2. Bioorg Med Chem. 2017 12 15; 25(24):6479-6485.
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TOX Regulates Growth, DNA Repair, and Genomic Instability in T-cell Acute Lymphoblastic Leukemia. Cancer Discov. 2017 11; 7(11):1336-1353.
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Scratching the Surface of Immunotherapeutic Targets in Neuroblastoma. Cancer Cell. 2017 09 11; 32(3):271-273.
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Characterization of midostaurin as a dual inhibitor of FLT3 and SYK and potentiation of FLT3 inhibition against FLT3-ITD-driven leukemia harboring activated SYK kinase. Oncotarget. 2017 Aug 08; 8(32):52026-52044.
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Characterization of midostaurin as a dual inhibitor of FLT3 and SYK and potentiation of FLT3 inhibition against FLT3-ITD-driven leukemia harboring activated SYK kinase. Oncotarget. 2017 Jul 06.
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Hoxa9 and Meis1 Cooperatively Induce Addiction to Syk Signaling by Suppressing miR-146a in Acute Myeloid Leukemia. Cancer Cell. 2017 04 10; 31(4):549-562.e11.
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The creatine kinase pathway is a metabolic vulnerability in EVI1-positive acute myeloid leukemia. Nat Med. 2017 Mar; 23(3):301-313.
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Synergistic Drug Combinations with a CDK4/6 Inhibitor in T-cell Acute Lymphoblastic Leukemia. Clin Cancer Res. 2017 Feb 15; 23(4):1012-1024.
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The Public Repository of Xenografts Enables Discovery and Randomized Phase II-like Trials in Mice. Cancer Cell. 2016 07 11; 30(1):183.
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Integrated genetic and pharmacologic interrogation of rare cancers. Nat Commun. 2016 06 22; 7:11987.
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Targeting MTHFD2 in acute myeloid leukemia. J Exp Med. 2016 06 27; 213(7):1285-306.
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Genomic Copy Number Dictates a Gene-Independent Cell Response to CRISPR/Cas9 Targeting. Cancer Discov. 2016 08; 6(8):914-29.
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Inhibitors of Glycogen Synthase Kinase 3 with Exquisite Kinome-Wide Selectivity and Their Functional Effects. ACS Chem Biol. 2016 07 15; 11(7):1952-63.
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Multicenter Feasibility Study of Tumor Molecular Profiling to Inform Therapeutic Decisions in Advanced Pediatric Solid Tumors: The Individualized Cancer Therapy (iCat) Study. JAMA Oncol. 2016 May 01; 2(5):608-615.
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The Public Repository of Xenografts Enables Discovery and Randomized Phase II-like Trials in Mice. Cancer Cell. 2016 04 11; 29(4):574-586.
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Aberrant activation of the PI3K/mTOR pathway promotes resistance to sorafenib in AML. Oncogene. 2016 09 29; 35(39):5119-31.
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The second European interdisciplinary Ewing sarcoma research summit--A joint effort to deconstructing the multiple layers of a complex disease. Oncotarget. 2016 Feb 23; 7(8):8613-24.
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Corrigendum: The genomic landscape of juvenile myelomonocytic leukemia. Nat Genet. 2016 Jan; 48(1):101.
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Evaluation of Improved Glycogen Synthase Kinase-3a Inhibitors in Models of Acute Myeloid Leukemia. J Med Chem. 2015 Nov 25; 58(22):8907-19.
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The genomic landscape of juvenile myelomonocytic leukemia. Nat Genet. 2015 Nov; 47(11):1326-1333.
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Functional, chemical genomic, and super-enhancer screening identify sensitivity to cyclin D1/CDK4 pathway inhibition in Ewing sarcoma. Oncotarget. 2015 Oct 06; 6(30):30178-93.
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Increased SYK activity is associated with unfavorable outcome among patients with acute myeloid leukemia. Oncotarget. 2015 Sep 22; 6(28):25575-87.
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Long noncoding RNA EWSAT1-mediated gene repression facilitates Ewing sarcoma oncogenesis. J Clin Invest. 2014 Dec; 124(12):5275-90.
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Erratum: Parallel genome-scale loss of function screens in 216 cancer cell lines for the identification of context-specific genetic dependencies. Sci Data. 2014; 1:140044.
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Parallel genome-scale loss of function screens in 216 cancer cell lines for the identification of context-specific genetic dependencies. Sci Data. 2014; 1:140035.
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Molecular rationale for the use of PI3K/AKT/mTOR pathway inhibitors in combination with crizotinib in ALK-mutated neuroblastoma. Oncotarget. 2014 Sep 30; 5(18):8737-49.
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The genomic landscape of pediatric Ewing sarcoma. Cancer Discov. 2014 Nov; 4(11):1326-41.
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New Approaches to Target T-ALL. Front Oncol. 2014; 4:170.
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Triplication of a 21q22 region contributes to B cell transformation through HMGN1 overexpression and loss of histone H3 Lys27 trimethylation. Nat Genet. 2014 Jun; 46(6):618-23.
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Targeting Csnk1a1 in leukemia. J Exp Med. 2014 Apr 07; 211(4):594.
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An epigenetic mechanism of resistance to targeted therapy in T cell acute lymphoblastic leukemia. Nat Genet. 2014 Apr; 46(4):364-70.
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SYK is a critical regulator of FLT3 in acute myeloid leukemia. Cancer Cell. 2014 Feb 10; 25(2):226-42.
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MUC1-C oncoprotein promotes FLT3 receptor activation in acute myeloid leukemia cells. Blood. 2014 Jan 30; 123(5):734-42.
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A phase II study of the EGFR inhibitor gefitinib in patients with acute myeloid leukemia. Leuk Res. 2014 Apr; 38(4):430-4.
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Mutational heterogeneity in cancer and the search for new cancer-associated genes. Nature. 2013 Jul 11; 499(7457):214-218.
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In Vivo RNAi screening identifies a leukemia-specific dependence on integrin beta 3 signaling. Cancer Cell. 2013 Jul 08; 24(1):45-58.
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Selective HDAC1/HDAC2 inhibitors induce neuroblastoma differentiation. Chem Biol. 2013 May 23; 20(5):713-25.
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SYK regulates mTOR signaling in AML. Leukemia. 2013 Nov; 27(11):2118-28.
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High-throughput tyrosine kinase activity profiling identifies FAK as a candidate therapeutic target in Ewing sarcoma. Cancer Res. 2013 May 01; 73(9):2873-83.
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Complementary genomic screens identify SERCA as a therapeutic target in NOTCH1 mutated cancer. Cancer Cell. 2013 Mar 18; 23(3):390-405.
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Targeting MYCN in neuroblastoma by BET bromodomain inhibition. Cancer Discov. 2013 Mar; 3(3):308-23.
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The intersection of genetic and chemical genomic screens identifies GSK-3a as a target in human acute myeloid leukemia. J Clin Invest. 2012 Mar; 122(3):935-47.
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Genetic and proteomic approaches to identify cancer drug targets. Br J Cancer. 2012 Jan 17; 106(2):254-61.
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Targeting NOTCH1 in hematopoietic malignancy. Crit Rev Oncog. 2011; 16(1-2):103-15.
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Chemical genomics and combo therapy. Blood. 2010 Dec 23; 116(26):5786-8.
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Characterization of Notch1 antibodies that inhibit signaling of both normal and mutated Notch1 receptors. PLoS One. 2010 Feb 08; 5(2):e9094.
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Proteomic and genetic approaches identify Syk as an AML target. Cancer Cell. 2009 Oct 06; 16(4):281-94.
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Identification of AML1-ETO modulators by chemical genomics. Blood. 2009 Jun 11; 113(24):6193-205.
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Genomic approaches to small molecule discovery. Leukemia. 2009 Jul; 23(7):1226-35.
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Phase II study of intermediate-dose cytarabine in patients with relapsed or refractory Ewing sarcoma: a report from the Children's Oncology Group. Pediatr Blood Cancer. 2009 Mar; 52(3):324-7.
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High-throughput gene expression profiling of memory differentiation in primary human T cells. BMC Immunol. 2008 Aug 01; 9:44.
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Expression-based screening identifies the combination of histone deacetylase inhibitors and retinoids for neuroblastoma differentiation. Proc Natl Acad Sci U S A. 2008 Jul 15; 105(28):9751-6.
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Literature Lab: a method of automated literature interrogation to infer biology from microarray analysis. BMC Genomics. 2007 Dec 18; 8:461.
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Signature-based small molecule screening identifies cytosine arabinoside as an EWS/FLI modulator in Ewing sarcoma. PLoS Med. 2007 Apr; 4(4):e122.
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Gene expression signature-based chemical genomic prediction identifies a novel class of HSP90 pathway modulators. Cancer Cell. 2006 Oct; 10(4):321-30.
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A method for high-throughput gene expression signature analysis. Genome Biol. 2006; 7(7):R61.
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Genomic approaches in acute leukemia. Best Pract Res Clin Haematol. 2006; 19(2):263-8.
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Benzodithiophenes potentiate differentiation of acute promyelocytic leukemia cells by lowering the threshold for ligand-mediated corepressor/coactivator exchange with retinoic acid receptor alpha and enhancing changes in all-trans-retinoic acid-regulated gene expression. Cancer Res. 2005 Sep 01; 65(17):7856-65.
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Gefitinib induces myeloid differentiation of acute myeloid leukemia. Blood. 2005 Oct 15; 106(8):2841-8.
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Gene expression-based high-throughput screening(GE-HTS) and application to leukemia differentiation. Nat Genet. 2004 Mar; 36(3):257-63.
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The TEL gene contributes to the pathogenesis of myeloid and lymphoid leukemias by diverse molecular genetic mechanisms. Curr Top Microbiol Immunol. 1997; 220:67-79.
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TEL/AML-1 dimerizes and is associated with a favorable outcome in childhood acute lymphoblastic leukemia. Blood. 1996 Dec 01; 88(11):4252-8.
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The TEL gene and human leukemia. Biochim Biophys Acta. 1996 Aug 08; 1288(1):M7-10.
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Mutational analysis of the candidate tumor suppressor genes TEL and KIP1 in childhood acute lymphoblastic leukemia. Cancer Res. 1996 Mar 15; 56(6):1413-7.
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Involvement of the TEL gene in hematologic malignancy by diverse molecular genetic mechanisms. Curr Top Microbiol Immunol. 1996; 211:279-88.
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Frequent loss of heterozygosity at the TEL gene locus in acute lymphoblastic leukemia of childhood. Blood. 1995 Jul 01; 86(1):38-44.
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