ArticleOncogene2026
Dexamethasone promotes neutrophil ROS-mediated tumor killing through the glucocorticoid receptor.
Article in Oncogene, 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
12 authors.
Funding
Abstract
Glucocorticoids are frequently administered to alleviate therapy-related side effects in cancer patients, yet their role in tumor progression remains controversial and mechanistically unresolved. Here, we demonstrate that the long-acting glucocorticoid dexamethasone (Dex) exerts antitumor effects that are mediated by neutrophils. In murine models of Lewis lung carcinoma (LLC) and B16F10 melanoma, Dex markedly suppressed tumor growth and prolonged survival of tumor-bearing mice. These effects were independent of adaptive immunity, macrophages, and tumor cell-intrinsic glucocorticoid signaling, but required functional glucocorticoid receptor (GR) signaling in neutrophils. Dex-treated neutrophils exhibited longer survival and higher cytotoxicity toward tumor cells via increased production of reactive oxygen species (ROS). Disruption of this GR-ROS axis, either through neutrophil-specific GR deletion or pharmacological inhibition of ROS, abolished the antitumor activity of Dex. Together, these findings uncover a neutrophil-mediated tumoricidal function of Dex and suggest that neutrophil GR-ROS signaling may be harnessed for cancer therapy.
Indexed as
Identifiers
41792468What 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.