About

Vasilis Vasiliou is the Susan Dwight Bliss Professor of Epidemiology (Environmental Health Sciences) and of Ophthalmology and Visual Science at Yale University. His research focuses on environmental health sciences, with particular expertise in the study of PFAS 'forever chemicals', liver toxicity, gut microbiome, neuroplasticity genomics, and the exposome. He has contributed extensively to understanding the mechanisms of toxicity related to environmental chemicals and their impact on human health. Vasiliou has authored numerous publications in the field, advancing knowledge in mass spectrometry imaging, toxicology, and molecular biology related to environmental exposures.

Research topics

• Artificial Intelligence
• Computer Science
• Biology
• Chromatography
• Chemistry
• Medicine
• Pathology
• Psychiatry
• Environmental health
• Bioinformatics
• Database
• Internal medicine
• Genetics
• Virology
• Environmental chemistry
• Operating system

Selected publications

• Glutathione is critical for NK cell-mediated immunity

  Cell Reports · 2026-02-23

  articleOpen access

  Natural killer (NK) cells are essential for immune protection against tumors and viruses. Disease environments impose oxidative stress and impair immune cell functions. Glutathione (GSH) is a major cellular antioxidant and is critical for the immune response, but how it modulates NK cell function remains largely unknown. Using a mouse model with a specific deletion of the catalytic subunit of glutamate-cysteine ligase (Gclc) in NK cells, we demonstrate that GSH supports interleukin-15 (IL-15)-driven activation of NK cells. Gclc deficiency causes an intracellular accumulation of reactive oxygen species (ROS), which impairs the metabolism of NK cells. This is accompanied by defective proliferation and cytokine production concurrent with subverted mTOR and STAT5 activation. During acute lymphocytic choriomeningitis virus (LCMV) infection, Gclc-deficient NK cells are unable to suppress the antiviral T cell response. Remarkably, Gclc deficiency impairs NK cell-mediated protection against tumor lung metastases. Our findings highlight an essential role of GSH in maintaining NK cell functionality.

  PublisherOA PDFDOI

• Catabolism of extracellular glutathione supplies cysteine to support tumours

  Nature · 2026-03-18 · 1 citations

  articleOpen access

  , glutathione (GSH), as a tripeptide of cysteine, glutamate and glycine, can be catabolized to release amino acids. The extent to which GSH-derived amino acids are essential to cancers is unclear. Here we show that depletion of intracellular GSH does not alter tumour growth and extracellular GSH is highly abundant in the tumour microenvironment, highlighting the potential importance of GSH outside tumours. Supplementation with GSH rescues cancer cell survival and growth in cystine-deficient conditions, and this rescue depends on the catabolic activity of γ-glutamyltransferases. Finally, pharmacological targeting of the activity of γ-glutamyltransferases prevents the breakdown of circulating GSH, reduces tumour cysteine levels and slows tumour growth. Our findings indicate a non-canonical role for GSH in supporting tumours by acting as a reservoir of amino acids. Depriving tumours of extracellular GSH or inhibiting its breakdown is potentially a therapeutically tractable approach for patients with cancer. Furthermore, these findings change our view of GSH and how amino acids, including cysteine, are supplied to cells.

  PublisherDOI

• Nor Any Drop to Drink: Creating a Community‐Based Assessment Tool to Address 1,4‐Dioxane Water Contamination

  Public Health Nursing · 2026-03-10

  article

  OBJECTIVE: 1,4-Dioxane (DX), a synthetic organic chemical solvent prevalent in water systems, has been monitored by the U.S. Environmental Protection Agency (EPA) as a possible carcinogen since 2013. Delegation of risk tolerance levels to states has resulted in varying exposure standards across the U.S., concerning DX-impacted communities. This study employed a community-based participatory research (CBPR) to design a survey that identifies DX-impacted communities' concerns and preferred risk management strategies. METHODS: CBPR survey design drew on descriptions of two DX-impacted communities in Michigan and North Carolina to target key issues and outcomes. An addendum to the survey was designed to gather expert reviewer feedback and face-validate the draft survey using mixed methods. Snowball sampling increased the expert-reviewer sample size (N = 29). Targeted reliability statistics were applied to eight Likert-scale evaluation questions. RESULTS: Thematic scoring of responses highlighted requests for tools that may prompt timelier and more effective control of related health risks. Cronbach's alpha coefficient (0.93) showed high internal consistency regarding the respondents' expression of the validity of the survey. DISCUSSION: Experts supported advancing the survey's criterion testing in one DX-impacted community. This design approach may be used by public health nursing teams to amplify community voices, integrate contextual evidence with epidemiology, strengthen advocacy, and guide multisector collaboration regarding DX-related health risks.

  PublisherDOI

• Integrated Multi-Omics Reveals Synergistic Hepatotoxicity of Ethanol and PFOS Co-Exposure

  Chemico-Biological Interactions · 2026-04-24

  articleSenior author
  PublisherDOI

• Glutathione-deficiency promotes basal hyperinsulinemia in the insulin secreting cell line INS-1 (832/13)

  Chemico-Biological Interactions · 2026-04-09

  articleSenior author
  PublisherDOI

• Integrating the exposome framework in CBRNe risk assessment: a holistic approach to chemical, biological, radiological, nuclear, and explosive threats

  The European Physical Journal Plus · 2025-11-15 · 4 citations

  articleOpen accessSenior author

  Abstract This paper introduces the exposome framework as a transformative approach to improving Chemical, Biological, Radiological, Nuclear, and Explosive (CBRNe) risk assessments. Historically, CBRNe evaluations have concentrated on acute exposures and immediate health effects, often overlooking long-term and cumulative risks. By incorporating the exposome—defined as the totality of exposures experienced throughout an individual’s life—this paper advocates for a more holistic understanding of health consequences posed by CBRNe agents. The exposome framework enhances the ability to account for low-dose, chronic exposures, residual contamination, and their synergistic interactions with other environmental and physiological factors. It is vital for assessing the health risks faced by vulnerable populations, such as first responders and communities living near CBRNe events. This paper explores emerging technological advances in biological and personal monitoring, omics technologies (genomics, proteomics, and metabolomics), and artificial intelligence (AI)-based modeling, which facilitate precise health outcome predictions. The policy implications of integrating the exposome perspective into CBRNe preparedness are also discussed, emphasizing the importance of proactive strategies that address immediate and long-term health effects of CBRNe agents.

  PublisherDOI

• Aldehyde Dehydrogenases

  Elsevier eBooks · 2025-01-01

  book-chapter1st authorCorresponding
  PublisherDOI

• Update of the sideroflexin (SLC56) gene family

  Human Genomics · 2025-06-20 · 4 citations

  reviewOpen accessSenior author

  The human sideroflexin (SFXN) gene family, also classified as solute carrier family 56 (SLC56), encodes a group of five mitochondrial transmembrane proteins (SFXN1-SFXN5) involved in key aspects of mitochondrial metabolism, cellular homeostasis, and development. SFXNs are highly conserved across eukaryotic species, with evolutionary the origin traced back to the earliest metazoans. Functionally, each of the five family members exhibits distinct functional specialization. Particularly, SFXN1 and SFXN3 facilitate mitochondrial serine transport, supporting one-carbon metabolism. SFXN2 and SFXN4 are implicated in mitochondrial iron regulation, heme biosynthesis, and iron-sulfur cluster assembly. SFXN5, predominantly expressed in the brain, is proposed to regulate citrate metabolism and immune cell functions. Mutations or dysregulation of SFXN genes have been linked to certain human diseases, including congenital sideroblastic anemia, oxidative phosphorylation disorders, neurodegenerative conditions, and cancers. Structurally, SFXNs share conserved transmembrane domains and key motifs critical for substrate transport, mitochondrial iron homeostasis, and overall mitochondrial function. The evolutionary trajectory of the SFXN family-from amino acid transport to functionally specialized roles in higher organisms-highlights their biological and clinical significance. Comparative studies across model organisms reveal both conserved and divergent functions, emphasizing their importance in health and disease. A comprehensive understanding of the SFXN family not only advances fundamental mitochondrial research but also opens avenues for novel therapeutic interventions.

  PublisherOA PDFDOI

• 2579P Development of a patient-reported outcome measure for individuals at risk for hereditary cancer: Phase I - IIIa of the EORTC QLQ-HCR30

  Annals of Oncology · 2025-09-01

  articleOpen access
  PublisherOA PDFDOI

• Integrating gut microbiome and neuroplasticity genomics in alcohol use disorder therapy

  Human Genomics · 2025-07-11 · 3 citations

  articleOpen access

  BACKGROUND: Alcohol Use Disorder (AUD) is a chronic neuropsychiatric condition with substantial public health impact. The interplay between gut microbiota and neuroplasticity-related genes presents a novel approach to understand AUD pathophysiology and treatment response. While microbial dysbiosis has been implicated in AUD, its correlation with gene expression changes in neuroplasticity pathways remains unexplored. This study investigates microbiome composition, microbial metabolic pathways, and their correlation with neuroplasticity-related genes in AUD patients undergoing treatment. METHODS: We conducted a prospective observational study integrating gut microbiome 16S rRNA sequencing and host neuroplasticity-related gene expression profiling in AUD patients undergoing treatment which combines psychotherapeutic intervention along with oral diazepam administration followed by Pythagorean Self Awareness Intervention. Patients were classified as responders or non-responders, and microbial composition, functional pathways, and host-microbiota interactions were analyzed using multi-omic correlation frameworks. RESULTS: Responders exhibited a microbiome enriched in short-chain fatty acid (SCFA)-producing bacteria (e.g., Lachnospiraceae), linked to gut barrier integrity and neurotransmitter synthesis. In contrast, non-responders demonstrated enrichment of inflammation-associated taxa (Succinivibrionaceae) and oxidative stress-related metabolic pathways. Correlation analysis revealed microbiome-mediated modulation of neuroplasticity-related genes measured from peripheral blood, including BDNF, GRIA1, CAMK2G, and EGR family genes, suggesting a gut-brain-genomic axis in AUD treatment response. CONCLUSIONS: This study highlights the role of gut microbiota as a modulator of neuroplasticity-related gene expression in AUD patients. Integrating microbiome and host genomic signatures could improve biomarker-based prediction of treatment response and inform precision medicine approaches for AUD. Future studies should expand these findings by incorporating multi-omic approaches, including epigenomics and exposomics, to refine microbiome-targeted interventions for addiction therapy.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01EY011490

  NIH · $4.0M · 2016

• NIH Grant R29EY011490

  NIH · $512k · 2004

• Identification of Biomarkers and Novel Pathways of Alcoholic Liver Disease by Leveraging Metabolomics, Tissue Imaging Mass Spectrometry, and Integrative Machine Learning

  NIH · $680k · 2020–2023

• Novel Role of Corneal Crystallins as Modulators of Cell Growth and Transparency

  NIH · $3.7M · 2007–2022

• The role of ALDH1B1 in ethanol metabolism and colon cancer

  NIH · $397k · 2014–2021

Frequent coauthors

• Daniel W. Nebert

  Cincinnati Children's Hospital Medical Center

  115 shared

• David C. Thompson

  Yale University

  112 shared

• Ying Chen

  Zhejiang Chinese Medical University

  81 shared

• Dennis R. Petersen

  University of Colorado Anschutz Medical Campus

  49 shared

• Satori A. Marchitti

  49 shared

• David C. Thompson

  46 shared

• Vindhya Koppaka

  University of Montana

  46 shared

• Richard A. Deitrich

  University of Colorado Anschutz Medical Campus

  44 shared

Education

• Postdoctoral Training Molecular Toxicology & Pharmacogenetics

  University of Cincinnati

  1995

• Postdoctoral Training Pharmacology

  University of Ioannina

  1990

• PhD Biochemistry, Medical School

  University of Ioannina

  1988

• BS Chemistry, School of Natural Sciences

  University of Ioannina

  1983