ArticleEnvironmental toxicology and pharmacology2025
The role of lipid metabolism and peroxisome proliferator activation in mediating pro-cancer phenotypes of poly- and perfluoroalkyl substances in testicular cancer.
Article in Environmental toxicology and pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Impact of PFAS exposure on lipid metabolic pathways: mechanisms and implicatins in carcinogenesis.Frontiers in toxicology · 2026Review
- From environment to organs: individual and combined effects of MPs and PFAS on urinary system health.Frontiers in physiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Poly- and perfluoroalkyl substances (PFAS) are of human health concern as epidemiological studies show significant associations with testicular germ cell tumors (TGCTs). Here, the effects of perfluorooctanesulfonic acid (PFOS), lithium bis(trifluoromethylsulfonyl)imide (HQ-115), and hexafluoropropylene oxide dimer acid (GenX) on TGCT cells were investigated. Concentrations (10 nM to 1 µM) modelled PFAS doses in relevant human exposure ranges and acute and short-term timepoints (18 h and 4 days) captured proximal mechanisms of action. Metabolomic studies revealed that HQ-115 altered metabolites associated with steroid biosynthesis and lipid metabolism. Peroxisome-proliferator activation receptor (PPAR) target gene expression was altered upon HQ-115 and GenX exposure. Lastly, PFAS exposure altered the activity of PPARs, in TGCT cells, with the most prominent effects being antagonist activity toward PPARγ. These data support that PFAS may act as fatty acid mimics to modulate fatty acid metabolic and steroidogenic endocrine outcome leading to pro-cancer phenotypes in TGCTs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.