Philip J. Moos
· Associate Professor, Pharmacology and ToxicologyUniversity of Utah · Department of Pharmacology & Toxicology
Active 1990–2026
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About
Philip J. Moos, PhD, is an Associate Professor in the College of Pharmacy, specializing in Pharmacology and Toxicology. His research broadly focuses on understanding cancer susceptibility and the development of resistance, with particular attention to tumor heterogeneity and the role of genotype and phenotype in therapeutic responses during cancer progression. His laboratory employs genomic strategies, including whole genome sequencing and single cell-RNA sequencing, to elucidate subclonal structures within tumors and identify pathways that drive their growth. Additionally, Dr. Moos's work involves testing unique drugs and drug combinations to develop new therapeutic strategies. Beyond cancer research, Dr. Moos investigates the toxicological effects of nanoparticles and airborne pollutants. His team uses transcript profiling and apoptotic studies to evaluate the inflammatory potential and toxicity of metal oxide manufactured nanoparticles, aiming to understand and mitigate their adverse effects. His collaborations with experts such as Dr. Ghandehari and Dr. Reilly focus on the toxicology of biomedical materials and the genomic consequences of environmental pollutants, respectively. Dr. Moos's educational background includes a BS and MS in Aerospace Engineering Sciences from the University of Colorado and a PhD in Biology from Kansas State University.
Research topics
- Genetics
- Biology
- Machine Learning
- Medicine
- Computer Science
- Psychology
- Immunology
- Cancer research
- Computational biology
- Business
Selected publications
Proceedings of the National Academy of Sciences · 2020 · 99 citations
The extent to which immune cell phenotypes in the peripheral blood reflect within-tumor immune activity prior to and early in cancer therapy is unclear. To address this question, we studied the population dynamics of tumor and immune cells, and immune phenotypic changes, using clinical tumor and immune cell measurements and single-cell genomic analyses. These samples were serially obtained from a cohort of advanced gastrointestinal cancer patients enrolled in a trial with chemotherapy and immuno…
Evolution of core archetypal phenotypes in progressive high grade serous ovarian cancer
Nature Communications · 2021 · 55 citations
The evolution of resistance in high-grade serous ovarian cancer (HGSOC) cells following chemotherapy is only partially understood. To understand the selection of factors driving heterogeneity before and through adaptation to treatment, we profile single-cell RNA-sequencing (scRNA-seq) transcriptomes of HGSOC tumors collected longitudinally during therapy. We analyze scRNA-seq data from two independent patient cohorts to reveal that HGSOC is driven by three archetypal phenotypes, defined as oncog…
Cancer Cell International · 2020 · 25 citations
BACKGROUND: CDK4/6 inhibitors such as ribociclib are becoming widely used targeted therapies in hormone-receptor-positive (HR+) human epidermal growth factor receptor 2-negative (HER2-) breast cancer. However, cancers can advance due to drug resistance, a problem in which tumor heterogeneity and evolution are key features. METHODS: Ribociclib-resistant HR+/HER2- CAMA-1 breast cancer cells were generated through long-term ribociclib treatment. Characterization of sensitive and resistant cells wer…
Frontiers in Immunology · 2024-07-19 · 14 citations
articleOpen access1st authorIntroduction Genetic mutations in critical nodes of pulmonary epithelial function are linked to the pathogenesis of pulmonary fibrosis (PF) and other interstitial lung diseases. The slow progression of these pathologies is often intermitted and accelerated by acute exacerbations, complex non-resolving cycles of inflammation and parenchymal damage, resulting in lung function decline and death. Excess monocyte mobilization during the initial phase of an acute exacerbation, and their long-term pers…
Virulence · 2022-02-15 · 13 citations
articleOpen accesssystem to model HIV-1 infection of macrophages, and single-cell RNA sequencing (scRNA-seq) to compare the transcriptomes of uninfected cells, cells harboring pre-integration complexes (PIC), and those containing integrated provirus and making late HIV proteins. scRNA-seq can distinguish between provirus and PIC cells because their background transcriptomes vary dramatically. PIC cell transcriptomes are characterized by NFkB and AP-1 promoted transcription, while transcriptomes of cells transcrib…
Recent grants
NIH · $945k · 2010
NIH · $18.0M · 2017–2023
Frequent coauthors
- 24 shared
Pamela B. Cassidy
Oregon Health & Science University
- 23 shared
F.A. Fitzpatrick
- 21 shared
Andrea H. Bild
City Of Hope National Medical Center
- 20 shared
Elizabeth A. Raetz
NYU Langone Health
- 17 shared
Sancy A. Leachman
Oregon Health & Science University
- 16 shared
Kornelia Edes
University of Utah
- 15 shared
William L. Carroll
St. Jude Children's Research Hospital
- 13 shared
Jasmine A. McQuerry
Children's Mercy Hospital
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