ArticleInternational journal of medical sciences2026
Decoding Short- and Long-Term Cellular Adaptations to Cr(VI) Exposure Through High-Throughput Transcriptomics.
Article in International journal of medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hexavalent chromium (Cr(VI)) is a well-established environmental and occupational carcinogen, but its time-dependent molecular effects remain poorly characterized. This study aims to elucidate the transcriptional responses triggered by acute versus chronic Cr(VI) exposure through an integrated analysis of two publicly available transcriptomic datasets: GSE16349 (short-term exposure, 16 hours) and GSE24025 (long-term exposure, 4 weeks). We identified 250 differentially expressed genes across both exposure models. MetaCore pathway enrichment analysis revealed shared activation of apoptosis, survival signaling, DNA damage response and repair, and cell cycle progression. Notably, short-term exposure primarily activated acute stress responses, whereas long-term exposure induced reprograms transcription toward fibrosis, EMT, and oncogenic signaling. Protein-protein interaction (PPI) network analysis identified potential key hub genes, with potential as biomarkers for Cr(VI) exposure monitoring. Our findings highlight distinct molecular trajectories in response to Cr(VI) over time, providing valuable insights into the progression from early toxic stress to chronic carcinogenic transformation. These results advance our understanding of Cr(VI)-induced carcinogenesis and suggest these potential targets for preventive and therapeutic interventions in exposed populations.
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.