bims-ovdlit Biomed News
on Ovarian cancer: early diagnosis, liquid biopsy and therapy
Issue of 2025–09–21
three papers selected by
Lara Paracchini, Humanitas Research



  1. Mod Pathol. 2025 Sep 12. pii: S0893-3952(25)00188-7. [Epub ahead of print] 100890
      In patients with high-grade endometrial carcinoma (HG-EC), concurrent isolated serous tubal intraepithelial carcinoma (STIC) or STIC-like lesions (STIC-LLs) in the fallopian tube(s) may be found. We sought to determine whether concurrently diagnosed HG-ECs and STIC-LLs are genetically related. Six HG-ECs, including serous carcinomas (n=4) and carcinosarcomas with serous epithelial component (n=2), with co-occurring STIC-LLs were identified, and subjected to microdissection, DNA extraction and panel sequencing targeting 468 cancer-related genes, or, if DNA quantities were limited, to Sanger sequencing. WT1 and p53 protein expression was assessed by immunohistochemistry (IHC). We found that three HG-ECs and concurrent STIC-LLs shared pathogenic mutations, such as TP53 hotspot, NF2, FBXW7 and PIK3CA mutations. IHC analysis revealed that the HG-EC of case 5 lacked WT1 expression and had p53 aberrant expression, while the matched STIC-LL displayed diffuse WT1 expression. Of the remaining three cases that did not show evidence of genetic relatedness based on the targeted sequencing panel, one STIC-LL harbored a clonal TP53 missense mutation, whereas the matched HG-EC had a distinct clonal TP53 hotspot mutation, a clonal FBXW7 hotspot mutation, and ERBB2 amplification. At the protein level, the p53 expression patterns of the HG-ECs and STIC-LLs were concordant in these three cases. Here we demonstrate that co-occurring HG-ECs and STIC-LLs are genetically related in a subset of cases.
    Keywords:  carcinosarcomas; genetic relatedness; sequencing; serous endometrial carcinoma; serous tubal intraepithelial carcinoma
    DOI:  https://doi.org/10.1016/j.modpat.2025.100890
  2. Aging Dis. 2025 Sep 04.
      Circulating cell-free DNA (cfDNA) comprises DNA fragments released into bodily fluids via apoptosis, necrosis, or phagocytosis. cfDNA encapsulates both fragmentomics (structural) and non-fragmentomics (sequence/epigenetic) information from source cells, thereby representing a promising biomarker. While non-fragmentomics analyses have enabled diverse diagnostic applications, they often falter in diseases with subtle or widespread genomic changes due to low cfDNA abundance and clonal hematopoiesis interference. Emerging evidence reveals that cfDNA fragmentation is shaped by nucleosome occupancy, nuclease activity, and epigenetic factors, yielding distinct patterns in fragment size, end motifs, nucleosome footprints, and topology. These fragmentomics signatures diverge markedly between healthy and diseased states, and across age group, offering opportunities to complement non-fragmentomics and enhance accuracy. This review delineates key cfDNA fragmentomics targets, elucidates fragmentation mechanisms, and explores clinical applications in the context of diseases and aging. We further survey cutting-edge technologies and computational algorithms and discuss implementation challenges alongside future prospects.
    DOI:  https://doi.org/10.14336/AD.2025.1029