Disease Site Focus:
Cutaneous/Melanoma, Thoracic/ Lung, No Specific Disease Site
Research Focus Area:
Systems biology, Computational modeling, Signal transduction pathways, Cell-cell interactions
Type of Research:
Research Interest Statement:
My expertise is in computational modeling of intracellular signaling pathways and cell-cell interactions in tumors. Before joining the Department of Biomedical Engineering at UA-Fayetteville, I worked as a postdoctoral researcher in the Center for Cancer Systems Biology at Vanderbilt University School of Medicine. I maintain an active role in the Center and work closely with experimentalists to build computational models that can provide insight and aid in the interpretation of experimental data at both the single-cell and cell population levels in a variety of cancer types. Examples include live-cell fluorescence imaging, bulk and single-cell RNA sequencing, and whole-exome sequencing in small cell lung cancer, EGFR-mutant non-small cell lung cancer, and BRAF-mutant melanoma cell lines. Our goal is to understand the roles of genetic heterogeneity and phenotypic plasticity in anticancer drug response and treatment evasion. I also continue to work closely with collaborators in the Vanderbilt Center for Bone Biology to build biochemical and cell-cell interaction models of tumor-induced bone disease. My research goals here at UA-Fayetteville include building detailed mechanistic models of whole cancer cells and whole tumors that can be used as in silico platforms for identifying new therapeutic targets and developing personalized treatments for patients. This work is highly interdisciplinary and I hope to forge new collaborations with researchers at UAMS to address important questions relevant to the residents of Arkansas.
Wandishin CM, Robbins CJ, Tyson DR, [et al., including Harris LA]. Real-time luminescence enables continuous drug-response analysis in adherent and suspension cell lines. Cancer biology & therapy. 2022 23(1):358-368. PMID: 35443861. PMCID: PMC9037430.
Hayford CE, Tyson DR, Robbins CJ 3rd, [et al., including Harris LA]. An in vitro model of tumor heterogeneity resolves genetic, epigenetic, and stochastic sources of cell state variability. PLoS biology. 2021 19(6):e3000797. PMID: 34061819.
Prugger M, Einkemmer L, Beik SP, [et al., including Harris LA]. Unsupervised logic-based mechanism inference for network-driven biological processes. PLoS computational biology. 2021 17(6):e1009035. PMID: 34077417.
Keating SM, Harris L, Waltemath D, [et al.]. SBML Level 3: an extensible format for the exchange and reuse of biological models. Molecular systems biology. 2020 16(8):e9110. PMID: 32845085.
Zhang F, Smith LP, Blinov ML, [et al., including Harris LA]. Systems biology markup language (SBML) level 3 package: multistate, multicomponent and multicompartment species, version 1, release 2. Journal of integrative bioinformatics. 2020 17(2-3). PMID: 32628633. PMCID: PMC7756619.
Harris LA, Beik S, Ozawa PMM, [et al.]. Modeling heterogeneous tumor growth dynamics and cell-cell interactions at single-cell and cell-population resolution. Current opinion in systems biology. 2019 17:24-34. PMID: 32642602. PMCID: PMC7343346.
Meyer CT, Wooten DJ, Paudel BB, [et al., including Harris LA]. Quantifying Drug Combination Synergy along Potency and Efficacy Axes. Cell systems. 2019 8(2):97-108.e16. PMID: 30797775. PMCID: PMC6675406.
Paudel BB, Harris LA, Hardeman KN, [et al.]. A Nonquiescent "Idling" Population State in Drug-Treated, BRAF-Mutated Melanoma. Biophysical journal. 2018 114(6):1499-1511. PMID: 29590606. PMCID: PMC5883941.
Jones ZW, Leander R, Quaranta V, [et al., including Harris LA]. A drift-diffusion checkpoint model predicts a highly variable and growth-factor-sensitive portion of the cell cycle G1 phase. PloS one. 2018 13(2):e0192087. PMID: 29432467. PMCID: PMC5809023.