ArticleFrontiers in oncology2025
The genetic landscape of primary malignant melanoma of the cervix using integrated bioinformatics analysis and whole-exome sequencing.
Article in Frontiers in oncology, 2025. 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.
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Primary malignant melanoma in the cervix (PMMC) currently has no standardized therapy. Its pathogenesis remains unclear, and the prognosis is poor. Given the high mortality of PMMC, its causes and pathogenic mechanisms need to be unraveled, and novel biomarkers must be identified. Methods: To further understand the genomic characteristics of PMMC, whole-exome sequencing was performed on the cancerous and adjacent tissues from three patients with PMMC, and PMMC-related tumor-susceptibility genes, mutation spectrum, mutation characteristics, driver genes, and high-frequency tumor mutations were analyzed. Concurrently, SNP and copy number variation (CNV) data from melanoma patients in the COSMIC and TCGA datasets were analyzed.Key protein interactions were further validated in vitro using co-immunoprecipitation assays. Results: The results showed that C>T/G>A is predominant in PMMC, with mutation characteristics more closely resembling those of SBS5 and SBS40, though not completely matching those of melanoma. Comparison with the COSMIC and TCGA databases revealed overlapping genes between PMMC and melanoma, such as TP53, AHNAK2, and PMMC, as well as previously unreported mutated genes such as AKT3, SMYD4, ATAD3A, SIRPB1, XKR6, etc. In vitro experiments and co-immunoprecipitation validation revealed that P53 interacts with AKT3, SMYD4, and ATAD3A, forming a network potentially involved in the pathogenesis of PMMC. Finally, integration of significantly mutated genes and CNV analysis revealed that copy number gains may regulate the expression of SIRPB1, AHNAK2, and XKR6, thereby activating the nuclear factor kappa B (NFkB) and protein kinase (AKT) signaling pathways, which could further promote the occurrence and development of PMMC. Conclusion: This study shows that while PMMC has similarities with other melanomas, it also harbors unique mutant genes. These findings provide a basis for exploring PMMC-related molecular markers and developing personalized diagnosis and treatment plans for patients with PMMC.
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.