Kelly L. Harris
This is a likely match — the affiliation was inferred from OpenAlex, ORCID, and web sources but has not been fully confirmed. Treat with appropriate caution.
Staff Fellow
Also affiliated: Meharry Medical College (2011–2026); United States Food and Drug Administration (2019–2026)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Kelly L. Harris's research focuses on the molecular mechanisms underlying cancer development and the role of environmental toxicants in this process. Harris has investigated the bioaccessibility and toxicity of polycyclic aromatic hydrocarbons (PAHs), including benzo(a)pyrene, and their relevance to digestive tract cancers. Studies have examined the effects of benzo(a)pyrene on human colon cancer cells, investigating cytotoxicity, DNA damage, and gene expression alterations. Furthermore, Harris's work includes studying the metabolism of benzo(a)pyrene in animal models and human tissues, as well as quantifying cancer driver mutations in human breast and lung DNA using targeted sequencing methods. Harris's research has been supported by collaborations with other researchers at the National Center for Toxicological Research, including Barbara L. Parsons and Binsheng Gong.
Metrics
- h-index: 10
- Publications: 29
- Citations: 637
Positions
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Staff Fellow publications 2019–2026National Center for Toxicological Research Genetic and Molecular Toxicology ORCID
Selected Publications
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Development of an error-corrected next-generation sequencing method for the quantification of hotspot cancer driver mutations (2026)
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Zileuton nanocrystals alter intestinal phase I/II metabolic enzymes and epithelial permeability in a sex-dependent manner (2025)
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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 rasH2 ‐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 DNA using targeted, error‐corrected CarcSeq (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
- Quantification of cancer driver mutations in human breast and lung DNA using targeted, error‐corrected CarcSeq
- Rationale and Roadmap for Developing Panels of Hotspot Cancer Driver Gene Mutations as Biomarkers of Cancer Risk
- 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 rasH2 ‐Tg Mice
Showing 5 of 6 shared publications
- Quantification of cancer driver mutations in human breast and lung DNA using targeted, error‐corrected 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 rasH2 ‐Tg Mice
- Abstract 2440: Cancer driver mutations as quantitative biomarkers of cancer risk interspecies analyses using CarcSeq
- Quantification of cancer driver mutations in human breast and lung DNA using targeted, error‐corrected CarcSeq
- Rationale and Roadmap for Developing Panels of Hotspot Cancer Driver Gene Mutations as Biomarkers of Cancer Risk
- 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
- Quantification of cancer driver mutations in human breast and lung DNA using targeted, error‐corrected CarcSeq
- Rationale and Roadmap for Developing Panels of Hotspot Cancer Driver Gene Mutations as Biomarkers of Cancer Risk
- 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
- Quantification of cancer driver mutations in human breast and lung DNA using targeted, error‐corrected 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
- 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 rasH2 ‐Tg Mice
- Abstract 2440: Cancer driver mutations as quantitative biomarkers of cancer risk interspecies analyses using CarcSeq
- Rationale and Roadmap for Developing Panels of Hotspot Cancer Driver Gene Mutations as Biomarkers of Cancer Risk
- Quantification of cancer driver mutations in human breast and lung DNA using targeted, error‐corrected 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
- 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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