James C. Fuscoe
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Researcher
Also affiliated: University of Vermont (1993); Lawrence Livermore National Laboratory (1985–2008); Oak Ridge National Laboratory (1978–1982); Arkansas Children's Hospital (2009); Environmental Protection Agency (1993–2003); Research Triangle Park Foundation (1992–2003); St. Jude Children's Research Hospital (1998); United States Food and Drug Administration (2003–2026); Center for Drug Evaluation and Research (2020); Howard Hughes Medical Institute (1983–1984); University of Connecticut (1991); Illumina (United States) (2014); Baylor College of Medicine (1982–1984); American Association of Colleges of Pharmacy (1998); Center for Environmental Health (1991); Centre National pour la Recherche Scientifique et Technique (CNRST) (1995); National Institute of Environmental Health Sciences (1992–1994); Cell Biotech (South Korea) (1983); Biolog (United States) (1983); Food and Drug Administration (2004); Genomics (United Kingdom) (2004); University of Tennessee at Knoxville (1978–1998); Louisiana State University Health Sciences Center New Orleans (2008); Institut Curie (1995); Jefferson College (2009)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
James C. Fuscoe's research centers on understanding and identifying biomarkers for drug-induced toxicities, particularly cardiotoxicity. His work has investigated the mechanisms behind doxorubicin-induced cardiotoxicity, exploring its delayed-onset and subclinical manifestations in preclinical models.
His recent publications highlight the potential of microRNA-34a-5p as an early circulating biomarker for chronic cardiotoxicity. Fuscoe has also examined the role of the apelin-APJ pathway in sex-related differential cardiotoxicity caused by doxorubicin. Furthermore, his research includes studies on predictive risk factors for myocardial injury in pediatric patients treated with anthracyclines.
Fuscoe holds a high-impact researcher designation, evidenced by his h-index of 47 and over 13,000 citations across 168 publications. He collaborates with researchers at the National Center for Toxicological Research and the University of Arkansas for Medical Sciences, maintaining an active laboratory website.
Metrics
- h-index: 47
- Publications: 168
- Citations: 13,517
Selected Publications
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Correction: Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study (2026)
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Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study (2025)
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Potential role of the apelin‐APJ pathway in sex‐related differential cardiotoxicity induced by doxorubicin in mice (2022)
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MicroRNA‐34a‐5p as a promising early circulating preclinical biomarker of doxorubicin‐induced chronic cardiotoxicity (2022)
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Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice (2021)
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Simultaneous Quantification of t(14;18) and HPRT Exon 2/3 Deletions in Human Lymphocytes (2020)
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A comprehensive rat transcriptome built from large scale RNA-seq-based annotation (2020)
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Hepatic Transcript Profiles of Cytochrome P450 Genes Predict Sex Differences in Drug Metabolism (2020)
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Rebuttal to the comments by Dr. Yan Xu on the article “Transcript profiling in the testes and prostates of postnatal day 30 Sprague-Dawley rats exposed prenatally and lactationally to 2-hydroxy-4-methoxybenzophenone” (2019)
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Candidate early predictive plasma protein markers of doxorubicin-induced chronic cardiotoxicity in B6C3F1 mice (2018)
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Transcript profiling in the testes and prostates of postnatal day 30 Sprague-Dawley rats exposed prenatally and lactationally to 2-hydroxy-4-methoxybenzophenone (2018)
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Transcriptomics analysis of early embryonic stem cell differentiation under osteoblast culture conditions: Applications for detection of developmental toxicity (2017)
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Sex and age differences in the expression of liver microRNAs during the life span of F344 rats (2017)
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Stably Expressed Genes Involved in Basic Cellular Functions (2017)
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Sex-related differential susceptibility to doxorubicin-induced cardiotoxicity in B6C3F1 mice (2016)
Collaboration Network
Top Collaborators
- Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice
- MicroRNA‐34a‐5p as a promising early circulating preclinical biomarker of doxorubicin‐induced chronic cardiotoxicity
- Potential role of the apelin‐APJ pathway in sex‐related differential cardiotoxicity induced by doxorubicin in mice
- Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Correction: Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice
- MicroRNA‐34a‐5p as a promising early circulating preclinical biomarker of doxorubicin‐induced chronic cardiotoxicity
- Potential role of the apelin‐APJ pathway in sex‐related differential cardiotoxicity induced by doxorubicin in mice
- Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Correction: Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice
- MicroRNA‐34a‐5p as a promising early circulating preclinical biomarker of doxorubicin‐induced chronic cardiotoxicity
- Potential role of the apelin‐APJ pathway in sex‐related differential cardiotoxicity induced by doxorubicin in mice
- Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice
- MicroRNA‐34a‐5p as a promising early circulating preclinical biomarker of doxorubicin‐induced chronic cardiotoxicity
- Potential role of the apelin‐APJ pathway in sex‐related differential cardiotoxicity induced by doxorubicin in mice
- Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice
- MicroRNA‐34a‐5p as a promising early circulating preclinical biomarker of doxorubicin‐induced chronic cardiotoxicity
- Potential role of the apelin‐APJ pathway in sex‐related differential cardiotoxicity induced by doxorubicin in mice
- Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice
- MicroRNA‐34a‐5p as a promising early circulating preclinical biomarker of doxorubicin‐induced chronic cardiotoxicity
- Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice
- MicroRNA‐34a‐5p as a promising early circulating preclinical biomarker of doxorubicin‐induced chronic cardiotoxicity
- Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Correction: Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Correction: Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study
- Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice
- Doxorubicin‐induced delayed‐onset subclinical cardiotoxicity in mice
- MicroRNA‐34a‐5p as a promising early circulating preclinical biomarker of doxorubicin‐induced chronic cardiotoxicity
- Potential role of the apelin‐APJ pathway in sex‐related differential cardiotoxicity induced by doxorubicin in mice
- Potential role of the apelin‐APJ pathway in sex‐related differential cardiotoxicity induced by doxorubicin in mice
- Potential role of the apelin‐APJ pathway in sex‐related differential cardiotoxicity induced by doxorubicin in mice
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