Leonard A. Harris
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Assistant Professor
Also affiliated: Lawrence Livermore National Laboratory (2004); National Institute on Drug Abuse (1990); Jet Propulsion Laboratory (2005); Federal Aviation Administration (1958–1961); University of Pittsburgh (2008–2016); Vanderbilt University (2014–2021); University of Washington (2020); PPG Industries (United States) (1951); Cornell University (2004–2009); National Aeronautics and Space Administration (1989–1993); Winthrop Rockefeller Foundation (2021–2026); Vanderbilt Health (2018); Rockwell Automation (United States) (1968–1970); The University of Texas at Austin (2022)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Leonard A. Harris's research program focuses on developing and applying computational and theoretical models to understand complex biological systems, particularly in the context of human pathologies. He has secured federal funding from the NIH/National Cancer Institute for a project investigating the molecular networks underlying non-genetic heterogeneity in cancer cell populations, totaling $187,596.
His work encompasses the creation of biological and chemical models, often utilizing computer simulation and software development. Recent publications explore topics such as immune digital twins for complex human pathologies, in vitro models of tumor heterogeneity, the role of epithelial-mesenchymal transition genes in small cell lung cancer, biochemical models of cell death, and unified tumor growth mechanisms. He also investigates DNA damage response from a multi-omics perspective and develops multi-level dynamical models for understanding disease mechanisms, including squamous cell carcinoma development.
Harris has published 98 papers with over 2,123 citations and an h-index of 19. He collaborates with researchers at the University of Arkansas at Fayetteville, including Saja Alshafeay, Alexandra Gutierrez Vega, Karthik Nayani, and Homa Ghaiedi, with whom he shares multiple publications. He maintains an active laboratory website.
Metrics
- h-index: 19
- Publications: 99
- Citations: 2,148
Selected Publications
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Melanoma RNA-seq and dose-response data from GDSC for ML+mechanistic modeling (2026)
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Capturing Multiscale Dynamics of Aortic Valve Calcification with a Coupled Fluid−Structure and Systems Biology Model (2026)
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A Computational Model of Tumor Interactions with Bone-Resident Cells Predicts Tumor-Type-Specific Responses to Perturbations (2026)
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Melanoma RNA-seq and dose-response data from GDSC for ML+mechanistic modeling (2026)
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Melanoma RNA-seq and dose-response data from GDSC for ML+mechanistic modeling (2026)
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Capturing Multi-Scale Dynamics of Aortic Valve Calcification With a Coupled Fluid–Structure and Systems Biology Model (2025)
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Immune digital twins for complex human pathologies: applications, limitations, and challenges (2024)
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Liquid crystalline collagen assemblies as substrates for directed alignment of human Schwann cells (2024)
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#52. Computational modeling of signaling pathways and cell-cell interactions driving tumor-induced bone disease (2024)
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Concepts of multi-level dynamical modelling: understanding mechanisms of squamous cell carcinoma development in Fanconi anemia (2023)
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Concepts of multi-level dynamical modelling: Understanding mechanisms of squamous cell carcinoma development in Fanconi anemia (2023)
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Unified tumor growth mechanisms from multimodel inference and dataset integration (2023)
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Involvement of Epithelial–Mesenchymal Transition Genes in Small Cell Lung Cancer Phenotypic Plasticity (2023)
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A biochemical necroptosis model explains cell-type-specific responses to cell death cues (2023)
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Processes in DNA damage response from a whole-cell multi-omics perspective (2022)
Federal Grants 1 $187,596 total
Uncovering the molecular networks underlying non-genetic heterogeneity in cancer cell populations
Collaboration Network
Top Collaborators
- An in vitro model of tumor heterogeneity resolves genetic, epigenetic, and stochastic sources of cell state variability
- Involvement of Epithelial–Mesenchymal Transition Genes in Small Cell Lung Cancer Phenotypic Plasticity
- Thunor: visualization and analysis of high-throughput dose–response datasets
- Unified tumor growth mechanisms from multimodel inference and dataset integration
- A heterogeneous drug tolerant persister state in BRAF-mutant melanoma is characterized by ion channel dysregulation and susceptibility to ferroptosis
Showing 5 of 9 shared publications
- An in vitro model of tumor heterogeneity resolves genetic, epigenetic, and stochastic sources of cell state variability
- Involvement of Epithelial–Mesenchymal Transition Genes in Small Cell Lung Cancer Phenotypic Plasticity
- Thunor: visualization and analysis of high-throughput dose–response datasets
- A heterogeneous drug tolerant persister state in BRAF-mutant melanoma is characterized by ion channel dysregulation and susceptibility to ferroptosis
- Real-time luminescence enables continuous drug–response analysis in adherent and suspension cell lines
Showing 5 of 7 shared publications
- A biochemical necroptosis model explains cell-type-specific responses to cell death cues
- Thunor: visualization and analysis of high-throughput dose–response datasets
- Unified tumor growth mechanisms from multimodel inference and dataset integration
- Processes in DNA damage response from a whole-cell multi-omics perspective
- Unsupervised logic-based mechanism inference for network-driven biological processes
Showing 5 of 7 shared publications
- An in vitro model of tumor heterogeneity resolves genetic, epigenetic, and stochastic sources of cell state variability
- Real-time luminescence enables continuous drug–response analysis in adherent and suspension cell lines
- Real-time luminescence enables continuous drug-response analysis in adherent and suspension cell lines
- Unified tumor growth mechanisms from multimodel inference and dataset integration
- Unsupervised logic-based mechanism inference for network-driven biological processes
- Unified Tumor Growth Mechanisms from Multimodel Inference and Dataset Integration
- Liquid crystalline collagen assemblies as substrates for directed alignment of human Schwann cells
- #52. Computational modeling of signaling pathways and cell-cell interactions driving tumor-induced bone disease
- A Computational Model of Tumor Interactions with Bone-Resident Cells Predicts Tumor-Type-Specific Responses to Perturbations
- Thunor: visualization and analysis of high-throughput dose–response datasets
- Processes in DNA damage response from a whole-cell multi-omics perspective
- An in vitro model of tumor heterogeneity resolves genetic, epigenetic, and stochastic sources of cell state variability
- A heterogeneous drug tolerant persister state in BRAF-mutant melanoma is characterized by ion channel dysregulation and susceptibility to ferroptosis
- Real-time luminescence enables continuous drug–response analysis in adherent and suspension cell lines
- Real-time luminescence enables continuous drug-response analysis in adherent and suspension cell lines
- A biochemical necroptosis model explains cell-type-specific responses to cell death cues
- Distinct execution modes of a biochemical necroptosis model explain cell type-specific responses and variability to cell-death cues
- A biochemical necroptosis model explains cell-type-specific responses to cell death cues
- Distinct execution modes of a biochemical necroptosis model explain cell type-specific responses and variability to cell-death cues
- Unified tumor growth mechanisms from multimodel inference and dataset integration
- Unified Tumor Growth Mechanisms from Multimodel Inference and Dataset Integration
- Unified tumor growth mechanisms from multimodel inference and dataset integration
- Unified Tumor Growth Mechanisms from Multimodel Inference and Dataset Integration
- Involvement of Epithelial–Mesenchymal Transition Genes in Small Cell Lung Cancer Phenotypic Plasticity
- Involvement of epithelial-mesenchymal transition genes in small cell lung cancer phenotypic plasticity
- Involvement of Epithelial–Mesenchymal Transition Genes in Small Cell Lung Cancer Phenotypic Plasticity
- Involvement of epithelial-mesenchymal transition genes in small cell lung cancer phenotypic plasticity
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