Daniel Starczynowski

Daniel T. Starczynowski, PhD

  • Institute Associate Director, Cancer and Blood Diseases Institute
  • Member, Division of Experimental Hematology and Cancer Biology
  • Co-Leader, Hematologic Malignancies Program
  • Co-Chief Scientific Officer, Innovations Ventures
  • Associate Director for Basic Sciences, UC Cancer Center
  • Katherine Stewart Waters Endowed Chair of Hematologic Malignancies
  • Professor, UC Department of Pediatrics
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About

Biography

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.

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.

Research Areas

Experimental Hematology and Cancer Biology, Cancer and Blood Diseases, Inflammation and Tolerance

Publications

Discordant pathologic diagnoses of myelodysplastic neoplasms and their implications for registries and therapies. Gorak, EJ; Otterstatter, M; Al Baghdadi, T; Gillis, N; Foran, JM; Liu, JJ; Bejar, R; Gore, SD; Kroft, SH; Harrington, A; et al. Blood Advances. 2023; 7:6120-6129.

Inactivation of p53 provides a competitive advantage to del(5q) myelodysplastic syndrome hematopoietic stem cells during inflammation. Muto, T; Walker, CS; Agarwal, P; Vick, E; Sampson, A; Choi, K; Niederkorn, M; Ishikawa, C; Hueneman, K; Varney, M; et al. Haematologica: the hematology journal. 2023; 108:2715-2729.

Paralog-specific signaling by IRAK1/4 maintains MyD88-independent functions in MDS/AML. Bennett, J; Ishikawa, C; Agarwal, P; Yeung, J; Sampson, A; Uible, E; Vick, E; Bolanos, LC; Hueneman, K; Wunderlich, M; et al. Blood. 2023; 142:989-1007.

Innate immune mediator, Interleukin-1 receptor accessory protein (IL1RAP), is expressed and pro-tumorigenic in pancreatic cancer. Zhang, Y; Chen, X; Wang, H; Gordon-Mitchell, S; Sahu, S; Bhagat, TD; Choudhary, G; Aluri, S; Pradhan, K; Sahu, P; et al. Journal of Hematology and Oncology. 2022; 15:70.

The Impact of Inflammation-Induced Tumor Plasticity during Myeloid Transformation. Yeaton, A; Cayanan, G; Loghavi, S; Dolgalev, I; Leddin, EM; Loo, CE; Torabifard, H; Nicolet, D; Wang, J; Corrigan, K; et al. Cancer Discovery. 2022; 12:2392-2413.

IKAROS and MENIN in synergy in AML. Jones, LQ M; Starczynowski, DT. 2022; 3:528-529.

Blocking UBE2N abrogates oncogenic immune signaling in acute myeloid leukemia. Barreyro, L; Sampson, AM; Ishikawa, C; Hueneman, KM; Choi, K; Pujato, MA; Chutipongtanate, S; Wyder, M; Haffey, WD; O'Brien, E; et al. Science Translational Medicine. 2022; 14:eabb7695.

Momelotinib is a highly potent inhibitor of FLT3-mutant AML. Azhar, M; Kincaid, Z; Kesarwani, M; Ahmed, A; Wunderlich, M; Latif, T; Starczynowski, D; Azam, M. Blood Advances. 2022; 6:1186-1192.

TRAF6 functions as a tumor suppressor in myeloid malignancies by directly targeting MYC oncogenic activity. Muto, T; Guillamot, M; Yeung, J; Fang, J; Bennett, J; Nadorp, B; Lasry, A; Redondo, LZ; Choi, K; Gong, Y; et al. Cell Stem Cell. 2022; 29:298-314.e9.

The deubiquitinase USP15 modulates cellular redox and is a therapeutic target in acute myeloid leukemia. Niederkorn, M; Ishikawa, C; M. Hueneman, K; Bartram, J; Stepanchick, E; R. Bennett, J; E. Culver-Cochran, A; Bolanos, LC; Uible, E; Choi, K; et al. Leukemia. 2022; 36:438-451.

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