ArticleIET systems biology
Pan-Cancer Integrative Analyses Reveal the Crosstalk Between the Intratumoral Microbiome, TP53 Mutation and Tumour Microenvironment.
Article in IET systems biology. 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
3 authors.
Funding
Abstract
Accumulating evidence suggests that the TP53 mutation, intratumoral microbiome, and tumour microenvironment (TME) are closely linked to tumourigenesis, yet the biological mechanisms underlying these connections remain unclear. To explore this, we collected multi-omics data-including genome, transcriptome, and tumour microbiome data-from a wide range of cancer types in The Cancer Genome Atlas (TCGA). Through a pan-cancer analysis, we identified significant correlations between intratumoral microbiota diversity and TP53 mutation status, particularly in hepatocellular carcinoma (HCC) and endometrial cancer (EC). Despite notable differences in microbiota composition between these two cancer types, we consistently observed that TP53 mutations were associated with reduced alpha-diversity. Additionally, we found that TP53 mutation status significantly influenced stromal components within the TME, such as a strong correlation between decreased endothelial cell abundance and TP53 mutation. Our integrated approach reveals the complex interplay between TP53 and factors regulating the host TME, offering new insights into cancer progression and potential therapeutic targets for future research.
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.