Pilot Projects

2025 Environment and Cancer RFA

The USC Center of Translational Exposomics (CTER) and USC Norris Comprehensive Cancer Center (NCCC) is pleased to announce a funding opportunity for one-year research projects focused on investigating the environmental influences on cancer. The goal of the program is to provide investigators with an opportunity to collect preliminary data and/or validate the utility of specific methods or techniques to establish the feasibility of larger-scale research projects and ultimately seek external (especially NIH) funding. To be funded through this mechanism, it is essential that the pilot project have an explicit focus on cancer as an outcome. Special consideration will be given to early-stage investigators.

Environment and Cancer RFA Information

Application Submission Portal

Application Instructions

RFA Announcement

The USC Center of Translational Exposomics (CTER) and USC Norris Comprehensive Cancer Center (NCCC) is pleased to announce a funding opportunity for one-year research projects focused on investigating the environmental influences on cancer. The goal of the program is to provide investigators with an opportunity to collect preliminary data and/or validate the utility of specific methods or techniques to establish the feasibility of larger-scale research projects and ultimately seek external (especially NIH) funding. To be funded through this mechanism, it is essential that the pilot project have an explicit focus on cancer as an outcome. Special consideration will be given to early-stage investigators. Individuals with a full-time faculty appointment in any school at USC are eligible to apply. Applicants are encouraged to pursue multi-disciplinary collaborations. Request for Applications - Oct. 27, 2025 Application Deadline - Dec. 15, 2025 Notification of Award - Jan. 31, 2026 Expected Start Date - Feb. 1, 2026

2023 Projects

The Center of Translational Exposomics Research and The Southern California Environmental Health Sciences Center (SCEHSC) award grants to support one-year research projects. These grants allow investigators to collect preliminary data or validate research methods with hopes of establishing feasibility of larger scale research projects that will advance understanding of environmental exposures and human disease.

MPI: Ruth Wood, PhD; Max Aung, PhD, MPH

Elucidating mechanisms of PFAS-induced neurocognitive and behavioral changes in a novel rat model

Childhood neurodevelopmental disorders such as attention deficit hyperreactivity disorder and impaired cognition are increasing in the U.S., leading to high economic costs and long-term health risks. Environmental factors, such as persistent pollutants classified as per- and poly-fluoroalkyl substances (PFAS), play a significant role in these disorders. Past studies have shown that one such PFAS known as perfluorooctanesulfonic acid (PFOS) can negatively impact cognitive and behavioral development in children.

To better understand these effects, this research proposal plans to use a novel in vivo experimental rat model to assess new phenotypes of cognitive function and executive behavior that have not been previously investigated with PFOS, complimented with postmortem in situ assessment of gene expression at three critically important brain regions (hippocampus, medial prefrontal cortex, and nucleus accumbens).

This project will lay the groundwork for future R01 proposals. In addition, a major goal is to build up a biobank of multiple tissue types, serving as a critical resource to investigate multi-organ system omics signatures. This will complement other proposed multi-omics data integration initiatives to better understand PFOS’s impact. Upcoming studies will investigate effects during critical windows of PFOS exposure (e.g. prenatal vs. postnatal exposures) and explore dietary intake interventions as a potential methods to mitigate the harmful effects of PFOS.

MPI: Jesse Goodrich, PhD; Ana C. Maretti Garcia, PhD

Global kidney specific gene changes induced by PFAS and risk of kidney cancer

Renal cell carcinoma (RCC) is the most common type of kidney cancer, representing about 90% of all kidney cancer cases in adults, with approximately 80,000 new cases and 14,000 deaths in the U.S. annually and rising.The disease is often deadly, particularly when diagnosed at an advanced stage, with a five-year survival rate of less than 12%. Recent research has suggested that environmental pollutants, particularly per- and polyfluoroalkyl substances (PFAS), may contribute to RCC risk.

This research proposal aims to investigate the role of PFAS in RCC through a novel translational pilot study. The study will first utilize in-vitro methods, including kidney spheroids, single-cell RNA sequencing, and metabolomics, to identify how PFAS exposure alters molecular pathways related to RCC. Findings from these in-vitro experiments will then be applied to analyze PFAS and metabolic data from the Multiethnic Cohort (MEC), a large and varied study with pre-existing data on PFAS exposure and RCC. The overarching hypothesis is that PFAS exposure triggers oxidative stress and alters glucose, lipid, and xenobiotic metabolism in kidneys, thereby increasing risk of RCC.

By combining PFAS exposure data, single-cell RNA-transcriptomic profiling, metabolomics, and human RCC studies, this project will create a robust model for examining the impact of PFAS chemicals synergy on human kidneys, providing a platform for screening the effect of other harmful agents and potential treatments on human kidneys. The insights from this study will form the foundation for a future R01 application where the investigators will aim to broaden the in-vitro study testing other PFASs found in drinking water to obtain a more comprehensive spectrum of PFAS contribution to kidney dysfunction and RCC. Another significant aspect is the capitalization of the new multi-center collaboration and the intellectual assets of the participating institutions which affect future directions of major ongoing research projects at USC.

PI Jaana Hartiala, PhD

Gene Environment Interactions for Cardiovascular Disease

Cardiovascular Disease (CVD), often taking the form of coronary artery disease (CAD), myocardial infraction, and stroke, is a leading cause of death in western societies. It is generally accepted that CVD is characterized by both genetic and environmental risk factors. Exposure to traffic-related air pollutants (TRAP) has been associated with atherosclerosis in both humans and animal models; in our own studies, we have observed similar associations with CAD, and we identified a gene-environment (GxE) interaction where expression for the potentially atheroprotective TRIP4 protein is significantly downregulated in human coronary artery endothelial cells incubated with plasma from humans exposed to TRAP.

This research proposal aims to further examine the GxE interactions between TRAP and CVD by investigating the in vivo effect of TRAP on cell-specific TRIP4 expression in a mouse exposure system. This has been complemented by their translational approach, where the GxE interaction will be independently replicated in subjects from the Multi-ethnic Cohort (MEC), which tracks over 200,000 participants from diverse backgrounds, to examine the effects on a much larger scale than previously done in literature.

This project will serve as the foundation for future proposals that will further examine other GxE interactions that increase risk of CVD by expanding the analysis to the whole genome. This could include collaborative projects with International Mouse Knockout Project to elucidate the mechanism by which TRAP affects atherosclerosis in TRIP4 deficient mice and with USC colleagues to carry out genome-wide interaction studies for CVD, on a scale and scope never previously done.

MPI: Wendy Setiawan, PhD; Lucy Golden, PhD

Global liver specific gene expression changes induced by PFAS and risk of liver cancer

The incidence and mortality rates of hepatocellular carcinoma (HCC) have increased in recent decades, largely due to the rise of nonalcoholic fatty liver disease (NAFLD), which can progress to more severe liver conditions including HCC. Poly- and perfluoroalkyl substances (PFAS) constitute a class of prevalent endocrine disruptors that partition preferentially to the liver and have been linked to liver damage and potentially to HCC in experimental models.

This proposal will use experimental methods with human liver spheroids to investigate PFAS-induced gene expression changes and use metabolomic measurements in the Multi-ethnic Cohort (MEC) to identify key pathways and genetic interactions influencing HCC risk. Future research will build on this pilot by expanding the use of advanced technologies like single-cell RNA sequencing and high-resolution mass spectrometry to further elucidate PFAS effects on liver disease.