ArticleCell death & disease2026
18F-FDG-PET/CT-negative gastric cancer employs glutamine-based gluconeogenesis and fatty acid oxidation to support tumor growth.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Most tumors exhibit increased glucose uptake and reprogram metabolism to aerobic glycolysis to meet their demands for macromolecule biosynthesis and energy production. Consequently, PET/CT using 18F-2-fluoro-2-deoxy-D-glucose (18F-FDG-PET/CT) has been developed and is clinically utilized in cancer imaging diagnostics. However, numerous cancers demonstrate negative imaging during 18F-FDG-PET/CT detection, suggesting these cancers employ alternative metabolic rewiring. In this study, we discovered that 18F-FDG-PET/CT-negative gastric cancers coordinate glutamine-based gluconeogenesis and fatty acid oxidation to meet DNA and ATP demands, sustaining tumor growth despite low glucose uptake. PCK and CPT1A, the key enzymes which are responsible for remodeling the metabolism, were highly expressed in FDG-PET/CT-negative gastric cancers. Accordingly, PCK/CPT1A negatively correlated with 18F-FDG imaging levels and positively correlated with poorer clinical classifications. Mechanistically, PPARγ is highly expressed in FDG-PET/CT-negative cells and drives the transcription of the PCK and genes. Pharmacological inhibition of the PCK/CPT1A significantly suppressed tumor growth in 18F-FDG-PET/CT-negative gastric cancers, as demonstrated in both cell-derived xenograft (CDX) and patient-derived xenograft (PDX) models. Together, these results highlight the heterogeneity of tumor cells from metabolic perspective, and identify PCK/CPT1A as a target for metabolic reprogramming and precision therapy of 18F-FDG-PET/CT-negative cancers.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.