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Member, Division of Experimental Hematology & Cancer Biology
Co-Leader, Hematologic Malignancies Program, Cancer and Blood Diseases Institute
Katherine Stewart Waters Endowed Chair of Hematologic Malignancies
Professor, UC Department of Pediatrics
Daniel T. Starczynowski, PhD, received his PhD in molecular biology from Boston University. He studied the NF-kB family of transcription factors and their role in B-cell lymphomas. During his postdoctoral fellowship at the BC Cancer Research Center, Dr. Starczynowski identified and characterized novel candidate genes in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).
Following his postdoctoral training, Dr. Starczynowski joined the faculty at Cincinnati Children’s Hospital Medical Center and at the University of Cincinnati as an Assistant Professor. Dr. Starczynowski’s laboratory investigates the molecular and cellular basis of hematologic malignancies with the goal to advance novel therapeutic strategies.
Experimental Hematology and Cancer Biology, Cancer and Blood Diseases, Inflammation and Tolerance
Daniel T. Starczynowski, PhD7/3/2019
Daniel T. Starczynowski, PhD6/29/2019
BS: Fairleigh Dickinson University, Teaneck, NJ, 2000.
PhD: Boston University, Boston, MA, 2006.
Postdoctoral Fellow: University of British Columbia/BC Cancer Research Centre, Vancouver, Canada, 2010.
The National MDS Natural History Study: design of an integrated data and sample biorepository to promote research studies in myelodysplastic syndromes.
Sekeres, MA; Gore, SD; Stablein, DM; DiFronzo, N; Abel, GA; DeZern, AE; Troy, JD; Rollison, DE; Thomas, JW; Waclawiw, MA; et al.
Leukemia and Lymphoma.
Overcoming adaptive therapy resistance in AML by targeting immune response pathways.
Melgar, K; Walker, MM; Jones, LM; Bolanos, LC; Hueneman, K; Wunderlich, M; Jiang, J; Wilson, KM; Zhang, X; Sutter, P; et al.
Science Translational Medicine.
Nuclear deubiquitination in the spotlight: the multifaceted nature of USP7 biology in disease.
Rawat, R; Starczynowski, DT; Ntziachristos, P.
Current Opinion in Cell Biology.
U2AF1 mutations induce oncogenic IRAK4 isoforms and activate innate immune pathways in myeloid malignancies.
Smith, MA; Choudhary, GS; Pellagatti, A; Choi, K; Bolanos, LC; Bhagat, TD; Gordon-Mitchell, S; Von Ahrens, D; Pradhan, K; Steeples, V; et al.
Nature Cell Biology.
Chronic immune response dysregulation in MDS pathogenesis.
Barreyro, L; Chlon, TM; Starczynowski, DT.
KDM6B overexpression activates innate immune signaling and impairs hematopoiesis in mice.
Wei, Y; Zheng, H; Bao, N; Jiang, S; Bueso-Ramos, CE; Khoury, J; Class, C; Lu, Y; Lin, K; Yang, H; et al.
Chronic innate immune signaling results in ubiquitination of splicing machinery.
Culver-Cochran, AE; Starczynowski, DT.
TRAF6 Mediates Basal Activation of NF-kappa B Necessary for Hematopoietic Stem Cell Homeostasis.
Fang, J; Muto, T; Kleppe, M; Bolanos, LC; Hueneman, KM; Walker, CS; Sampson, L; Wellendorf, AM; Chetal, K; Choi, K; et al.
Inhibition of IRAK1 Ubiquitination Determines Glucocorticoid Sensitivity for TLR9-Induced Inflammation in Macrophages.
Kong, F; Liu, Z; Jain, VG; Shima, K; Suzuki, T; Muglia, LJ; Starczynowski, DT; Pasare, C; Bhattacharyya, S.
Journal of immunology (Baltimore, Md. : 1950).
GMP-ing to Spatial Conclusions about Emergency and Leukemic Myelopoiesis.
Niederkorn, M; Starczynowski, DT.
Cell Stem Cell.
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