ResearcherNational Institutes of HealthActive in the last 2 years
James H. Doroshow
Matched on ORCID iD 0000-0002-4463-1790; OpenAlex author ID A5041200743; NIH RePORTER profile ID 9692531. Sources: OpenAlex.
Their work
- Papers
- 7 (first author 0, last author 6)
- Trials
- 0
- Grants
- 1
- Labs led
- 1
- Collaborators
- 6
2011: 1 paper · 2012: none · 2013: 2 papers · 2014: none · 2015: none · 2016: 1 paper · 2017: none · 2018: none · 2019: 1 paper · 2020: none · 2021: none · 2022: 1 paper · 2023: 1 paper · 2024: none · 2025: 1 grant
Papers 7
- Exogenous DNA enhances DUOX2 expression and function in human pancreatic cancer cells by activating the cGAS-STING signaling pathway. Last author DOI 10.1016/j.freeradbiomed.2023.06.012↗
- Dexamethasone Inhibits Cytokine-Induced, DUOX2-Related VEGF-A Expression and DNA damage in Human Pancreatic Cancer Cells and Growth of Pancreatic Cancer Xenogr… Last author DOI 10.1101/2022.02.13.480277↗
- IL-4 and IL-17A Cooperatively Promote Hydrogen Peroxide Production, Oxidative DNA Damage, and Upregulation of Dual Oxidase 2 in Human Colon and Pancreatic Canc… Last author DOI 10.4049/jimmunol.1800469↗
- Dual oxidase 2 and pancreatic adenocarcinoma: IFN-γ-mediated dual oxidase 2 overexpression results in H2O2-induced, ERK-associated up-regulation of HIF-1α and … Last author DOI 10.18632/oncotarget.12032↗
- Functional activity and tumor-specific expression of dual oxidase 2 in pancreatic cancer cells and human malignancies characterized with a novel monoclonal ant… Co-author DOI 10.3892/ijo.2013.1821↗
- Activation of TLR4 is required for the synergistic induction of dual oxidase 2 and dual oxidase A2 by IFN-γ and lipopolysaccharide in human pancreatic cancer c… Last author DOI 10.4049/jimmunol.1201725↗
- Up-regulation and sustained activation of Stat1 are essential for interferon-gamma (IFN-gamma)-induced dual oxidase 2 (Duox2) and dual oxidase A2 (DuoxA2) expr… Last author DOI 10.1074/jbc.m110.191031↗
Grants 1
Closest collaborators
The 6 strongest of 6 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Krishnendu Roy · 7 shared papers, 2011–2023 · strength 0.53
- Paper Exogenous DNA enhances DUOX2 expression and function in human pancreatic cancer cells by activating the cGAS-STING sign… DOI 10.1016/j.freeradbiomed.2023.06.012↗
- Paper Dexamethasone Inhibits Cytokine-Induced, DUOX2-Related VEGF-A Expression and DNA damage in Human Pancreatic Cancer Cell… DOI 10.1101/2022.02.13.480277↗
- Paper IL-4 and IL-17A Cooperatively Promote Hydrogen Peroxide Production, Oxidative DNA Damage, and Upregulation of Dual Oxid… DOI 10.4049/jimmunol.1800469↗
- Yongzhong Wu · 6 shared papers, 2011–2023 · strength 0.49
- Paper Exogenous DNA enhances DUOX2 expression and function in human pancreatic cancer cells by activating the cGAS-STING sign… DOI 10.1016/j.freeradbiomed.2023.06.012↗
- Paper Dexamethasone Inhibits Cytokine-Induced, DUOX2-Related VEGF-A Expression and DNA damage in Human Pancreatic Cancer Cell… DOI 10.1101/2022.02.13.480277↗
- Paper IL-4 and IL-17A Cooperatively Promote Hydrogen Peroxide Production, Oxidative DNA Damage, and Upregulation of Dual Oxid… DOI 10.4049/jimmunol.1800469↗
- Mariam M. Konaté · 3 shared papers, 2019–2023 · strength 0.38
- Paper Exogenous DNA enhances DUOX2 expression and function in human pancreatic cancer cells by activating the cGAS-STING sign… DOI 10.1016/j.freeradbiomed.2023.06.012↗
- Paper Dexamethasone Inhibits Cytokine-Induced, DUOX2-Related VEGF-A Expression and DNA damage in Human Pancreatic Cancer Cell… DOI 10.1101/2022.02.13.480277↗
- Paper IL-4 and IL-17A Cooperatively Promote Hydrogen Peroxide Production, Oxidative DNA Damage, and Upregulation of Dual Oxid… DOI 10.4049/jimmunol.1800469↗
- Stephen L. Wang · 1 shared paper, 2023 · strength 0.16
- Yonghzong Wu · 1 shared paper, 2013 · strength 0.03
- Stephen M. Hewitt · 1 shared paper, 2013 · strength 0.03
How to reach this person
A chain of introductions through people who have published, run trials or held grants together (warm_path@1: fewest links first, then the strongest). Built from public records only; no contact details are kept.