Kelly L. Harris
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Staff Fellow
Staff Researcher
Research Areas
Biomedical Subjects
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Biography and Research Information
OverviewAI-generated summary
Kelly L. Harris is a Staff Fellow at the National Center for Toxicological Research. Her research focuses on the molecular mechanisms of carcinogenesis, particularly the effects of environmental agents on DNA and gene expression. Harris has investigated the impact of benzo(a)pyrene on human colon cancer cells, examining cytotoxicity, proliferation, and DNA damage.
Her work also includes the development and application of methods for measuring cancer driver mutations. This includes studies using the CarcSeq approach to assess mutations in rat mammary and mouse lung cancer models, correlating these findings with incidence rates and strain/sex-specific variations. Collaborations within the National Center for Toxicological Research include work with Barbara L. Parsons, Binsheng Gong, Jennifer Faske, and Meagan B. Myers, with whom she has co-authored multiple publications. Harris has an h-index of 11 and has published 45 papers, accumulating 952 citations.
Metrics
- h-index: 11
- Publications: 45
- Citations: 952
Selected Publications
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Abstract C054: Pharmacogenomics evaluation of histone deacetylase inhibitors on the treatment of triple-negative breast cancer subtypes (2025)
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Tissue and Sex‐Specific Performance of a Cancer Driver Based Biomarker in <scp>rasH2</scp> ‐Tg Mice (2025)
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Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations (2024)
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Abstract 2440: Cancer driver mutations as quantitative biomarkers of cancer risk interspecies analyses using CarcSeq (2024)
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Assessment of Clonal Expansion Using CarcSeq Measurement of Lung Cancer Driver Mutations and Correlation With Mouse Strain- and Sex-Related Incidence of Spontaneous Lung Neoplasia (2021)
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Quantification of cancer driver mutations in human breast and lung <scp>DNA</scp> using targeted, error‐corrected <scp>CarcSeq</scp> (2020)
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Rationale and Roadmap for Developing Panels of Hotspot Cancer Driver Gene Mutations as Biomarkers of Cancer Risk (2019)
Collaboration Network
Top Collaborators
- Assessment of Clonal Expansion Using CarcSeq Measurement of Lung Cancer Driver Mutations and Correlation With Mouse Strain- and Sex-Related Incidence of Spontaneous Lung Neoplasia
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Tissue and Sex‐Specific Performance of a Cancer Driver Based Biomarker in <scp>rasH2</scp> ‐Tg Mice
- Abstract 2440: Cancer driver mutations as quantitative biomarkers of cancer risk interspecies analyses using CarcSeq
- Assessment of Clonal Expansion Using CarcSeq Measurement of Lung Cancer Driver Mutations and Correlation With Mouse Strain- and Sex-Related Incidence of Spontaneous Lung Neoplasia
- Tissue and Sex‐Specific Performance of a Cancer Driver Based Biomarker in <scp>rasH2</scp> ‐Tg Mice
- Abstract 2440: Cancer driver mutations as quantitative biomarkers of cancer risk interspecies analyses using CarcSeq
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Tissue and Sex‐Specific Performance of a Cancer Driver Based Biomarker in <scp>rasH2</scp> ‐Tg Mice
- Abstract 2440: Cancer driver mutations as quantitative biomarkers of cancer risk interspecies analyses using CarcSeq
- Assessment of Clonal Expansion Using CarcSeq Measurement of Lung Cancer Driver Mutations and Correlation With Mouse Strain- and Sex-Related Incidence of Spontaneous Lung Neoplasia
- Abstract 2440: Cancer driver mutations as quantitative biomarkers of cancer risk interspecies analyses using CarcSeq
- Assessment of Clonal Expansion Using CarcSeq Measurement of Lung Cancer Driver Mutations and Correlation With Mouse Strain- and Sex-Related Incidence of Spontaneous Lung Neoplasia
- Assessment of Clonal Expansion Using CarcSeq Measurement of Lung Cancer Driver Mutations and Correlation With Mouse Strain- and Sex-Related Incidence of Spontaneous Lung Neoplasia
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
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