ArticleGynecologic oncology2025
Whole-genome sequencing-based characterization of endometrial serous carcinoma.
Article in Gynecologic 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.
- A Phase II Trial of Olaparib plus Pembrolizumab in Patients with Recurrent Copy Number-High/p53-Abnormal Endometrial Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Trial
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
objectiveTo define the structural variants, mutational signatures, and DNA repair defects in serous endometrial carcinoma (EC) using whole-genome sequencing (WGS).
methodsTen primary untreated classic serous ECs diagnosed between 2012 and 2018 were selected. Tumor and matched normal DNAs were subjected to WGS, and sequencing data were analyzed using state-of-the-art bioinformatics methods.
resultsAll serous ECs harbored TP53 somatic mutations (100 %), as well as recurrent PIK3CA (60 %), FBXW7 (40 %), PPP2R1A (30 %) mutations, CCNE1 (50 %) and AKT2 amplification (30 %). All serous ECs were homologous recombination DNA repair (HR)-proficient by HRDetect, and all but one case had dominant aging/clock- or ABOPEC-related mutational signatures. The levels of genomic instability varied, with a median fraction of genome altered (FGA) of 45 % (range 17-68 %). Seven serous ECs had high levels of copy number alterations (CNAs) (distinct CNA size ≥1Mbp, median 59; range 26-86) and three had low levels of CNAs (median 12 distinct CNA size ≥1Mbp; range 6-23). While there was no difference in age or stage of disease between patients with high versus low CNA levels, all three serous EC patients with lower CNA levels are still alive to date (68-99 months follow-up), as opposed to only one of seven serous EC patients with higher CNA levels (range 16-69 months follow-up) after 58 months of follow-up.
conclusionsAlthough serous ECs are characterized by TP53 mutations and generally high levels of CNAs, genomic features of HR-deficiency are not prominent. Larger prospective studies of the impact of chromosomal instability on outcome in serous EC patients are warranted.
Indexed as
Identifiers
What Socratic 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 Socratic graph.