Thomas A. Williams
Senior Assistant Professor
Also affiliated: Indiana Department of Transportation (2003); United States Department of Veterans Affairs (1976–1977); State University of New York (2008); NewYork–Presbyterian Hospital (1965); Davidson College (1966); Eastern Virginia Medical School (1978–2005); The University of Texas at San Antonio Health Science Center (1989); University of Pittsburgh (1971); Simon Fraser University (2008); SUNY Downstate Health Sciences University (2008–2012); National Training Service (2013); Purdue University West Lafayette (2003); University of Utah (1975–1977); University of Szeged (2013–2025); Sheppard and Enoch Pratt Hospital (1980); University of Utah Hospital (1975–1977); VA Salt Lake City Healthcare System (1977); Centre Hospitalier Universitaire de Tours (2012); Nautilus (United States) (2011); Hankook Tire (South Korea) (1995); Nautilus Environmental (2011); Centre Hospitalier Régional Universitaire de Brest (2012–2013); Webster Groves Nature Study Society (1981); Hôpital Maison Blanche (2012–2020); University of Virginia (1981); University of Cincinnati (1973–1974); Columbia University (1965–1967); Cardiff University (2010); Virginia Tech (2006)
Faculty Researcher
Research Areas
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Biography and Research Information
OverviewAI-generated summary
Thomas A. Williams is a Senior Assistant Professor at the University of Arkansas for Medical Sciences with a research focus that spans multiple disciplines, including behavioral psychology, medical education, and cellular biology. His work has been recognized with a high-impact researcher designation, evidenced by an h-index of 21 and over 3,100 citations across 144 publications. Williams has collaborated with researchers at his institution, including Brian Koss, Katherine Wallis, Daniel Fil, and Lora J. Rogers, with whom he has co-authored three publications each.
Recent publications from Williams include work on webinar interventions to reduce stigma, theoretical and practical applications of task-based language teaching, and research into the molecular mechanisms of T cell function and immunotherapy. His scholarly output also includes investigations into EZH2 inhibition's effect on CAR-T cell persistence and the role of CD28 costimulation in T cell effector function within challenging metabolic environments. He has also explored methods for manipulating the DNA damage response to enhance immunotherapy outcomes.
Williams maintains an active lab website, suggesting a continued engagement with research and mentorship. His recent activity and consistent publication record indicate an ongoing contribution to his fields of study.
Metrics
- h-index: 21
- Publications: 144
- Citations: 3,113
Selected Publications
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685 EZH2 inhibition impairs CD8+ CAR-T cell persistence (2025)
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762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments (2025)
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236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response (2025)
Collaboration Network
Top Collaborators
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments
- 685 EZH2 inhibition impairs CD8+ CAR-T cell persistence
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments
- 685 EZH2 inhibition impairs CD8+ CAR-T cell persistence
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments
- 685 EZH2 inhibition impairs CD8+ CAR-T cell persistence
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments
- 685 EZH2 inhibition impairs CD8+ CAR-T cell persistence
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments
- 685 EZH2 inhibition impairs CD8+ CAR-T cell persistence
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 236 Manipulating the DNA damage response to combat T cell exhaustion and improve immunotherapy response
- 762 CD28 costimulation induces PCK2 to support T cell effector function in metabolically hostile environments
- 685 EZH2 inhibition impairs CD8+ CAR-T cell persistence
- 685 EZH2 inhibition impairs CD8+ CAR-T cell persistence
- 685 EZH2 inhibition impairs CD8+ CAR-T cell persistence
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