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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, PhD7/2/2020
Daniel T. Starczynowski, PhD4/30/2020
Daniel T. Starczynowski, PhD4/20/2020
Daniel T. Starczynowski, PhD9/4/2019
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.
TNFAIP3 Plays a Role in Aging of the Hematopoietic System.
Smith, MA; Culver-Cochran, AE; Adelman, ER; Rhyasen, GW; Ma, A; Figueroa, ME; Starczynowski, DT.
Frontiers in Immunology.
FBXO11 is a candidate tumor suppressor in the leukemic transformation of myelodysplastic syndrome.
Schieber, M; Marinaccio, C; Bolanos, LC; Haffey, WD; Greis, KD; Starczynowski, DT; Crispino, JD.
Blood Cancer Journal.
TIFA and TIFAB: FHA-domain proteins involved in inflammation, hematopoiesis, and disease.
Niederkorn, M; Agarwal, P; Starczynowski, DT.
HHEX expression drives AML development.
Adaptive response to inflammation contributes to sustained myelopoiesis and confers a competitive advantage in myelodysplastic syndrome HSCs.
Muto, T; Walker, CS; Choi, K; Hueneman, K; Smith, MA; Gul, Z; Garcia-Manero, G; Ma, A; Zheng, Y; Starczynowski, DT.
Targeting AML-associated FLT3 mutations with a type I kinase inhibitor.
Jones, LM; Melgar, K; Bolanos, L; Hueneman, K; Walker, MM; Jiang, J; Wilson, KM; Zhang, X; Shen, J; Jiang, F; et al.
Journal of Clinical Investigation.
TIFAB Regulates USP15-Mediated p53 Signaling during Stressed and Malignant Hematopoiesis.
Niederkorn, M; Hueneman, K; Choi, K; Varney, ME; Romano, L; Pujato, MA; Greis, KD; Inoue, J; Meetei, R; Starczynowski, DT.
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.
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