Rebecca Wynne Data-verified
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Biography and Research Information
OverviewAI-generated summary
Rebecca Wynne's research investigates the genotoxicity of various chemical aerosols using human in vitro airway tissue models. Her work includes assessing DNA damage with the CometChip assay and evaluating mutagenesis using Duplex Sequencing. Recent publications focus on the toxicity of glutaraldehyde and ortho-phthalaldehyde aerosols in these models, comparing in vitro results with standard genotoxicity assays. Wynne also studies the accumulation of somatic cell mutations in airway cultures treated with ethyl methanesulfonate and has explored the role of alcohol consumption in promoting diethylnitrosamine-induced hepatocarcinogenesis in male mice through the Wnt/β-catenin signaling pathway.
Wynne collaborates with researchers including Thomas M. Badger and Kelly E. Mercer from the National Center for Toxicological Research. Her scholarship metrics include an h-index of 19, with 31 total publications and 1,442 total citations.
Metrics
- h-index: 19
- Publications: 33
- Citations: 1,459
Selected Publications
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Comparative genotoxicity assessment of ortho-phthalaldehyde using human in vitro organotypic airway epithelial cultures and standard in vitro genotoxicity assays (2026)
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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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Subacute Pulmonary Toxicity of Glutaraldehyde Aerosols in a Human In Vitro Airway Tissue Model (2022)
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Genetic toxicity testing using human in vitro organotypic airway cultures: Assessing <scp>DNA</scp> damage with the <scp>CometChip</scp> and mutagenesis by Duplex Sequencing (2021)
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Toxicity of Ortho-phthalaldehyde Aerosols in a Human <i>In Vitro</i> Airway Tissue Model (2021)
Collaboration Network
Top Collaborators
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Data from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
Showing 5 of 6 shared publications
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Data from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
Showing 5 of 6 shared publications
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Data from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
Showing 5 of 6 shared publications
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Data from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
Showing 5 of 6 shared publications
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Data from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
Showing 5 of 6 shared publications
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Data from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
Showing 5 of 6 shared publications
- Genetic toxicity testing using human in vitro organotypic airway cultures: Assessing <scp>DNA</scp> damage with the <scp>CometChip</scp> and mutagenesis by Duplex Sequencing
- Toxicity of Ortho-phthalaldehyde Aerosols in a Human <i>In Vitro</i> Airway Tissue Model
- Subacute Pulmonary Toxicity of Glutaraldehyde Aerosols in a Human In Vitro Airway Tissue Model
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Genetic toxicity testing using human in vitro organotypic airway cultures: Assessing <scp>DNA</scp> damage with the <scp>CometChip</scp> and mutagenesis by Duplex Sequencing
- Toxicity of Ortho-phthalaldehyde Aerosols in a Human <i>In Vitro</i> Airway Tissue Model
- Subacute Pulmonary Toxicity of Glutaraldehyde Aerosols in a Human In Vitro Airway Tissue Model
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Genetic toxicity testing using human in vitro organotypic airway cultures: Assessing <scp>DNA</scp> damage with the <scp>CometChip</scp> and mutagenesis by Duplex Sequencing
- Toxicity of Ortho-phthalaldehyde Aerosols in a Human <i>In Vitro</i> Airway Tissue Model
- Subacute Pulmonary Toxicity of Glutaraldehyde Aerosols in a Human In Vitro Airway Tissue Model
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Supplementary Table 2 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Supplementary Table 1 from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Data from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Data from Alcohol Consumption Promotes Diethylnitrosamine-Induced Hepatocarcinogenesis in Male Mice through Activation of the Wnt/β-Catenin Signaling Pathway
- Toxicity of Ortho-phthalaldehyde Aerosols in a Human <i>In Vitro</i> Airway Tissue Model
- Subacute Pulmonary Toxicity of Glutaraldehyde Aerosols in a Human In Vitro Airway Tissue Model
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Genetic toxicity testing using human in vitro organotypic airway cultures: Assessing <scp>DNA</scp> damage with the <scp>CometChip</scp> and mutagenesis by Duplex Sequencing
- Repeat treatment of organotypic airway cultures with ethyl methanesulfonate causes accumulation of somatic cell mutations without expansion of bronchial-carcinoma-specific cancer driver mutations
- Comparative genotoxicity assessment of ortho-phthalaldehyde using human in vitro organotypic airway epithelial cultures and standard in vitro genotoxicity assays
- Toxicity of Ortho-phthalaldehyde Aerosols in a Human <i>In Vitro</i> Airway Tissue Model
- Subacute Pulmonary Toxicity of Glutaraldehyde Aerosols in a Human In Vitro Airway Tissue Model
- Toxicity of Ortho-phthalaldehyde Aerosols in a Human <i>In Vitro</i> Airway Tissue Model
- Subacute Pulmonary Toxicity of Glutaraldehyde Aerosols in a Human In Vitro Airway Tissue Model
- Genetic toxicity testing using human in vitro organotypic airway cultures: Assessing <scp>DNA</scp> damage with the <scp>CometChip</scp> and mutagenesis by Duplex Sequencing
- 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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