Evidence map›Paper›PMID 41747586›Full record

ArticleESMO open2026

Multimodal tumor-agnostic ctDNA analysis for minimal residual disease detection and risk stratification in ovarian cancer: results from the MITO16a/MaNGO-OV2 trial.

L Paracchini, A Velle, P Di Gennaro, L Mannarino, L Ancona, D Lorusso, S C Cecere, N Colombo, L Beltrame, A Fagotti and 13 more

Abstract read
In one paragraph

Article in ESMO open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors.

L ParacchiniDepartment of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy; Laboratory of Cancer Pharmacology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.
A VelleDepartment of Biology, University of Padova, Padua, Italy.
P Di GennaroMedical Statistics Unit, University of Campania 'Luigi Vanvitelli', Naples, Italy.
L MannarinoDepartment of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy; Laboratory of Cancer Pharmacology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.
L AnconaLaboratory of Cancer Pharmacology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.
D LorussoDepartment of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy; Unit of Gynecologic Oncology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.
S C CecereUro-Gynecological Medical Oncology, Istituto Nazionale Tumori, IRCCS-Fondazione G. Pascale, Naples, Italy.
N ColomboDivision of Gynecologic Oncology, European Institute of Oncology, IRCCS, Milan, Italy; Department of Medicine and Surgery, University of Milan-Bicocca, Milan, Italy.
L BeltrameLaboratory of Cancer Pharmacology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.
A FagottiFondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy.
G TascaVeneto Institute of Oncology IOV-IRCCS, Padua, Italy.
M PiemonteseDepartment of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy; Laboratory of Cancer Pharmacology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.
L ArenareMedical Statistics Unit, University of Campania 'Luigi Vanvitelli', Naples, Italy.
D CalifanoMicroenvironment Molecular Targets Unit, Istituto Nazionale Tumori, IRCCS-Fondazione G. Pascale, Naples, Italy.
F GaldieroMicroenvironment Molecular Targets Unit, Istituto Nazionale Tumori, IRCCS-Fondazione G. Pascale, Naples, Italy.
R ZadroDepartment of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy; Laboratory of Cancer Pharmacology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.
P ChiodiniMedical Statistics Unit, University of Campania 'Luigi Vanvitelli', Naples, Italy.
F PerroneClinical Trial Unit, Istituto Nazionale Tumori, IRCCS-Fondazione G. Pascale, Naples, Italy.
E BiagioliOncology Department, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.
M D'IncalciDepartment of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy; Laboratory of Cancer Pharmacology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy. Electronic address: maurizio.dincalci@hunimed.eu.
C RomualdiDepartment of Biology, University of Padova, Padua, Italy. Electronic address: chiara.romualdi@unipd.it.
S PignataUro-Gynecological Medical Oncology, Istituto Nazionale Tumori, IRCCS-Fondazione G. Pascale, Naples, Italy.
S MarchiniLaboratory of Cancer Pharmacology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdvanced-stage epithelial ovarian cancer (EOC) remains a therapeutic challenge due to high relapse rates and limited survival, while standard post-surgical parameters such as residual tumor (RT) incompletely capture minimal residual disease (MRD) and offer limited insight into tumor evolution. To address this gap, we investigated whether a multimodal, tumor-agnostic analysis of circulating tumor DNA (ctDNA)-integrating tumor fraction (TF) and genome-wide fragmentomic profiles (PF)-could refine early risk stratification after cytoreductive surgery and enable longitudinal monitoring during therapy. MATERIALS AND

methodsA total of 393 plasma samples from 173 patients in the phase IV MITO16a/MaNGO-OV2a trial were analyzed by shallow whole-genome sequencing at three time points: post-surgery/pre-chemotherapy (B1), post-chemotherapy (B2), and at the end of maintenance therapy or upon disease progression during maintenance (B3). Associations with progression-free survival (PFS) and overall survival (OS) were assessed using multivariable Cox models adjusted for clinical covariates.

resultsTF was detectable in 97% of patients at B1, including those classified as optimally debulked, and outperformed established clinical covariates in predicting survival [PFS: hazard ratio (HR) 1.02, P = 0.008; OS: HR 1.04, P = 0.005]. PF provided independent prognostic values (PFS: HR 1.06, P = 0.010; OS: HR 1.10, P = 0.005), and combined TF/PF modeling identified subgroups with distinct survival trajectories beyond clinical predictors (PFS: HR 1.76, P = 0.015; OS: HR 2.06, P = 0.029). Longitudinal copy number profiling revealed dynamic remodeling under treatment pressure, with recurrent 19q13.42 amplification emerging at B2 and B3.

conclusionsTogether, these findings establish multimodal ctDNA profiling as a sensitive, non-invasive strategy for MRD detection and longitudinal surveillance in advanced EOC, refining prognostic assessment beyond clinical and surgical factors while paving the way for precision-guided therapeutic management.

Indexed as

Biomarkers, TumorCarcinoma, Ovarian EpithelialCirculating Tumor DNANeoplasm, ResidualOvarian NeoplasmsAgedFemaleHumansMiddle AgedPrognosisRisk AssessmentBiomarkers, TumorCirculating Tumor DNAagnostic ctDNA analysisctDNAEOC prognosisgenome-wide fragmentomic analysismultimodal analysistumor fraction

Identifiers

PMID41747586
PMCPMC12955674

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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.