Dan A. Dixon
Professor
Also affiliated: Northwestern University (1991–1993); University of Geneva (2020); Novartis (Switzerland) (2011); The University of Texas MD Anderson Cancer Center (2020); Johns Hopkins University (1999); University of Kansas (2015–2024); University of South Carolina (2005–2023); Vanderbilt University (2003–2004); University of Utah (1998–2005); Johns Hopkins Medicine (1999); Huntsman Cancer Institute (1998–2003); The Ohio State University Wexner Medical Center (2020); The University of Kansas Cancer Center (2015–2025); Cancer Research Center (2009–2012); University of Kansas Medical Center (2012–2023); Department of Biological Sciences (2023); Novartis Institutes for BioMedical Research (2011); University of California, Davis (1993–1995); Vanderbilt University Medical Center (2003–2004)
COM | Biochemistry & Molecular Biology
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Dan A. Dixon's research focuses on understanding the molecular mechanisms that drive cancer development and progression, with a particular emphasis on the role of RNA-binding proteins and extracellular vesicles. His work investigates how these components influence gene expression and cellular behavior in various cancer types, including colorectal and pancreatic cancer.
Dixon has published research on the tumor-initiating stem cell's ability to shape its microenvironment into an immunosuppressive and pro-tumorigenic niche. He also studies the targeting of the RNA-binding protein HuR in cancer, exploring how HuR posttranscriptionally regulates key pro-tumorigenic factors like YAP1 in pancreatic cancer. Furthermore, his group investigates the involvement of IMP1/IGF2BP1 in colorectal cancer extracellular vesicles and how exosomes containing HuR can promote lung cell proliferation by stabilizing c-Myc mRNA. His work also includes examining the effects of compounds like pyrvinium pamoate on pancreatic cancer cells under nutrient-depleted conditions by targeting mitochondria, and the pro-tumorigenic activities promoted by extracellular vesicles from APCMin/+ mice via the NF-κB signaling pathway.
With a career marked by extensive publication and high citation counts (h-index: 46, total citations: 8,542), Dixon leads an active research group at the University of Arkansas for Medical Sciences, where he holds the position of Professor in the Department of Biochemistry & Molecular Biology.
Metrics
- h-index: 46
- Publications: 197
- Citations: 8,586
Positions
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Associate Director of Community Outreach and Engagement 2024–presentUniversity of Arkansas for Medical Sciences Winthrop P. Rockefeller Cancer Institute ORCID
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Professor publications 2025–2026University of Arkansas for Medical Sciences COM | Biochemistry & Molecular Biology Institutional directory
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Co-Leader 2019–2024The University of Kansas Cancer Center Drug Discovery, Delivery & Experimental Therapeutics (D3ET) Program ORCID
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Professor 2018–2024University of Kansas Department of Molecular Biosciences ORCID
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Co-Leader 2013–2019The University of Kansas Comprehensive Cancer Center Cancer Prevention & Survivorship Program ORCID
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Associate Professor 2012–2018University of Kansas Medical Center Cancer Biology ORCID
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Associate Professor 2004–2012University of South Carolina Department of Biological Science ORCID
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Research Assistant Professor 2001–2004Vanderbilt University Medical Center Department of Surgical Sciences ORCID
Selected Publications
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Mapping risk: Spatial analysis of 2,4-D herbicide emissions and colorectal cancer (2025)
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Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies (2025)
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Abstract 2358: XPO1 inhibition serves as an effective chemoprevention strategy in colorectal cancer mouse models (2025)
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Suppression of stress granule formation is a vulnerability imposed by mutant p53 (2025)
Grants & Funding
As listed on this researcher's institutional profile.
- Nano-Engineered Lab-on-a-Chip for Assessing HuR-Regulated Exosomes for Cancer Monitoring and Targeted Therapy NIH/Nat. Cancer Institute via University of Kansas Principal Investigator
Collaboration Network
Top Collaborators
- Suppression of stress granule formation is a vulnerability imposed by mutant p53
- Suppression of stress granule formation is a vulnerability imposed by mutant p53
- Suppression of stress granule formation is a vulnerability imposed by mutant p53
- Suppression of stress granule formation is a vulnerability imposed by mutant p53
- Suppression of stress granule formation is a vulnerability imposed by mutant p53
- Suppression of stress granule formation is a vulnerability imposed by mutant p53
- Abstract 2358: XPO1 inhibition serves as an effective chemoprevention strategy in colorectal cancer mouse models
- Abstract 2358: XPO1 inhibition serves as an effective chemoprevention strategy in colorectal cancer mouse models
- Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies
- Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies
- Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies
- Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies
- Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies
- Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies
- Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies
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