ArticleMagma (New York, N.Y.)2026
Assessing the treatment of pancreatic ductal adenocarcinoma by deuterium metabolic imaging: a preclinical study.
Article in Magma (New York, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Special issue on "deuterium metabolic imaging".Magma (New York, N.Y.) · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
purposeTo evaluate the utility of Deuterium Metabolic Imaging (DMI) as a tool for monitoring disease progression and assessing the therapeutic efficacy of cyclophosphamide in pancreatic ductal adenocarcinoma (PDAC).
methodsThe study utilized C57BL mice implanted with a PDAC model, and separated into two experimental groups: One cohort served as an untreated control, while the second was treated with the chemotherapeutic agent cyclophosphamide (CP). Metabolic mapping for the two cohorts was performed over the course of weeks using 2H MRSI at 15.2T, tracking the metabolic pathway of deuterated glucose as it converts by the PDAC into lactate.
resultsCP administration led to a significant reduction in tumor growth and improved survival rates compared to the control group. Tumor growth rates for the untreated, control group, showed a strong inverse correlation for glucose's uptake and a strong direct correlation with the glucose-to-lactate conversion rates as seen by DMI. CP treatment disrupted both these correlations: Post-treatment, tumor growth rates became statistically uncorrelated with either glucose consumption or lactate production which, when normalized for tumor size, remained relatively constant during the treatment period.
conclusionThe study demonstrates that CP treatment fundamentally alters the metabolic kinetics of glucose in PDAC tumors, inducing disruptions in metabolic correlations that may serve for distinguishing therapeutic success from failure.
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