Biography and Research Information
OverviewAI-generated summary
Caitlin Caperton studies the metabolic and molecular mechanisms underlying cancer development and progression, with a particular focus on thyroid and lung cancers. Her research has explored the development of novel follicular thyroid cancer models that progress to poorly differentiated and anaplastic thyroid cancer. She has also investigated the role of the lung metabolome in response to environmental exposures, such as 1,3-butadiene, and its reflection of human lung cancer phenotypes. Dr. Caperton's work also extends to understanding macrophage-tumor crosstalk in thyroid cancer pathogenesis and identifying associations between macrophage abundance and PD-L1 expression in oncocytic thyroid cancer. Additionally, her research has addressed rare metabolic disorders, including uncovering late-onset urea cycle deficiency following valproate initiation.
Her scholarship metrics include an h-index of 3, with 10 total publications and 42 citations. Dr. Caperton has collaborated with several researchers at the University of Arkansas for Medical Sciences, including Nicole Massoll, Samidha Tripathi, Marjorie L Hershberger, and Gunnar Boysen, with whom she shares multiple publications.
Metrics
- h-index: 3
- Publications: 10
- Citations: 44
Selected Publications
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53. Uncovering Late Onset Urea Cycle Deficiency Following Initiation of Valproate: A Smoldering Disease With Fatal Consequences (2025)
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Macrophage abundance in oncocytic thyroid cancer is associated with PD-L1 expression (2025)
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Lung metabolome of 1,3-butadiene exposed Collaborative Cross mice reflects metabolic phenotype of human lung cancer (2021)
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Macrophage-Tumor Crosstalk in the Pathogenesis of Follicular Thyroid Cancer (2021)
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Development of Novel Follicular Thyroid Cancer Models Which Progress to Poorly Differentiated and Anaplastic Thyroid Cancer (2021)
Collaboration Network
Top Collaborators
- Development of Novel Follicular Thyroid Cancer Models Which Progress to Poorly Differentiated and Anaplastic Thyroid Cancer
- Macrophage-Tumor Crosstalk in the Pathogenesis of Follicular Thyroid Cancer
- Macrophage abundance in oncocytic thyroid cancer is associated with PD-L1 expression
- Development of Novel Follicular Thyroid Cancer Models Which Progress to Poorly Differentiated and Anaplastic Thyroid Cancer
- Macrophage abundance in oncocytic thyroid cancer is associated with PD-L1 expression
- Development of Novel Follicular Thyroid Cancer Models Which Progress to Poorly Differentiated and Anaplastic Thyroid Cancer
- Development of Novel Follicular Thyroid Cancer Models Which Progress to Poorly Differentiated and Anaplastic Thyroid Cancer
- Lung metabolome of 1,3-butadiene exposed Collaborative Cross mice reflects metabolic phenotype of human lung cancer
- Lung metabolome of 1,3-butadiene exposed Collaborative Cross mice reflects metabolic phenotype of human lung cancer
- Lung metabolome of 1,3-butadiene exposed Collaborative Cross mice reflects metabolic phenotype of human lung cancer
- Lung metabolome of 1,3-butadiene exposed Collaborative Cross mice reflects metabolic phenotype of human lung cancer
- Lung metabolome of 1,3-butadiene exposed Collaborative Cross mice reflects metabolic phenotype of human lung cancer
- Lung metabolome of 1,3-butadiene exposed Collaborative Cross mice reflects metabolic phenotype of human lung cancer
- Lung metabolome of 1,3-butadiene exposed Collaborative Cross mice reflects metabolic phenotype of human lung cancer
- Lung metabolome of 1,3-butadiene exposed Collaborative Cross mice reflects metabolic phenotype of human lung cancer
- Macrophage abundance in oncocytic thyroid cancer is associated with PD-L1 expression
- Macrophage abundance in oncocytic thyroid cancer is associated with PD-L1 expression
- 53. Uncovering Late Onset Urea Cycle Deficiency Following Initiation of Valproate: A Smoldering Disease With Fatal Consequences
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