# HRD Testing in Advanced Ovarian Cancer: A Patient Guide to the 2025 Intergroup Statement A new intergroup position statement from the German Ovarian Cancer Commission, NOGGO, AGO Austria, and AGO Swiss explains how doctors should use homologous recombination deficiency (HRD) testing in advanced ovarian cancer. HRD is a biomarker — a measurable biological signal — that helps identify which patients are likely to benefit from PARP inhibitors (PARPi), a class of oral maintenance drugs. The statement reviews every major HRD assay category, defines who should and should not be tested, and sets minimum quality standards for tumor tissue samples. The authors stress that test choice, timing, and interpretation near cutoff values all require careful interdisciplinary discussion. # HRD Testing in Advanced Ovarian Cancer: A Patient Guide to the 2025 Intergroup Statement ## Table of Contents - Key Points - Why This Statement Matters - How This Statement Was Developed - What Is HRD? Understanding DNA Repair and Ovarian Cancer - How PARP Inhibitors Exploit HRD - The Landscape of HRD Tests - Clinically Approved Tests Available in Germany - Emerging Tests and Bridging Concordance - Cutoff Values: A Critical Practical Issue - The Official Recommendations of the Intergroup - When HRD Testing Is Appropriate - When HRD Testing Is Not Recommended - Minimum Standards for Tumor Tissue Samples - What This Means for Patients - Limitations and Open Questions - Practical Advice for Patients - Frequently Asked Questions - Source Information ## Key Points - HRD testing helps identify patients with advanced ovarian cancer likely to benefit from PARP inhibitors, but it is not a single uniform test. - A positive germline BRCA1/2 result makes further HRD testing unnecessary; a negative result allows HRD testing as a second step. - HRD testing is relevant for high-grade serous, endometrioid, clear cell carcinoma, and carcinosarcoma, but not low-grade epithelial ovarian carcinoma. - Reliable results need tissue at least 5 mm in diameter with at least 30% tumor cells; lymph node samples may have much lower tumor content. - Results near a test cutoff are uncertain and should be discussed by an interdisciplinary team before a final treatment decision. ## Why This Statement Matters Ovarian cancer treatment has changed dramatically in the past decade. The reason is a class of drugs called PARP inhibitors (PARPi), which work best in tumors that carry a specific weakness in their DNA repair machinery. That weakness is called homologous recombination deficiency, or HRD. Testing for HRD helps doctors decide who should receive maintenance therapy after initial treatment. But there is a problem: many different HRD tests exist, and they do not all measure the same thing or use the same cutoffs. This intergroup statement was written to bring clarity. It is endorsed by four organizations: the German Ovarian Cancer Commission, the North-Eastern German Society of Gynecological Oncology (NOGGO), AGO Austria, and AGO Swiss. Its goal is simple — help clinicians decide when to order HRD testing, which test to choose, and how to interpret the result. For patients, the practical takeaway is this: HRD testing is not a single, uniform test. Where and when it is done, and which laboratory performs it, can affect your treatment options. ## How This Statement Was Developed The statement is not a clinical trial. It is a consensus document, meaning it reflects expert agreement rather than new experimental data. The authors performed an interdisciplinary review of three sources of information: the available published literature, data from major clinical trials, and expert consensus among the participating groups. The resulting recommendations focus on three areas. First, the current landscape of HRD assays, including their different methodologies. Second, the clinical applicability of these tests — meaning where they actually change treatment decisions. Third, practical considerations about the best timing and the right indications for testing. The document also defines exclusion criteria. These are situations where HRD testing is not appropriate, either because the test has not been sufficiently validated or because the result would not change what doctors would do. Finally, it sets out the minimum pathological requirements for tissue samples, so that results are reliable. ## What Is HRD? Understanding DNA Repair and Ovarian Cancer Genomic instability (GIS) — a state in which the genome accumulates errors — is one of the most common causes of tumorigenesis (the formation of cancer). Cells have several DNA repair systems that normally keep the genome stable. One of the most important is the homologous recombination repair (HRR) system. During genomic replication (the process of copying DNA), two dangerous types of damage can occur: double-strand breaks and interstrand cross-links (ICL, abnormal chemical bonds that link the two DNA strands together). The HRR system responds to these problems using its specialized proteins to repair the damage. When the HRR pathway is defective — because of genetic (inherited or acquired) or epigenetic changes — the result is the phenotype (observable characteristic) known as homologous repair deficiency, or HRD. In plain terms, the cell loses its ability to repair double-strand breaks. Once HRD is present, genomic instability can develop and spread. GIS shows up in three measurable patterns used by HRD tests: - **Genomic loss of heterozygosity (gLOH)** — the loss of one of the two copies of a gene region in the tumor. - **Telomeric imbalance (TAI)** — an imbalance in the lengths of telomeres, the protective caps at the ends of chromosomes, between the two alleles of a gene. - **Large-scale transitions (LST)** — structural changes in chromosomes on a large scale, such as rearrangements, copy number alterations, or changes in chromosome arm status. In high-grade serous ovarian cancer (HGSOC) specifically, the HRR system plays a major role in how the cancer develops. Germline and somatic mutations in the breast-cancer genes BRCA1 and BRCA2 are the main cause of HRR pathway defects. The numbers matter here. Approximately **13 to 15% of patients with HGSOC** carry a germline (inherited) mutation in BRCA1 or BRCA2. Up to **3 to 7%** have somatic mutations — mutations that arise in the tumor itself, not inherited from parents. But BRCA1 and BRCA2 are not the only genes involved. Many other genes can lead to HRD, including BARD1 (BRCA1-associated RING domain 1), BRIP1 (BRCA-interacting protein 1), CHEK1 (checkpoint kinase 1), CHEK2 (checkpoint kinase 2), FAM175A, NBN (nibrin), PALB2 (partner and localizer of BRCA2), RAD51C, RAD51D, "and many more," as the authors note. ## How PARP Inhibitors Exploit HRD The clinical importance of HRR defects became clear with the arrival of poly(ADP-ribose) polymerase inhibitors (PARPi). These drugs block base excision repair — a different DNA repair pathway that fixes single-strand breaks. When base excision repair is blocked, single-strand breaks accumulate during DNA replication. This causes the repair system to collapse and creates double-strand breaks. In cells with HRD, those breaks cannot be repaired properly. The result is a process called synthetic lethality — the cancer cell dies because it has lost two repair mechanisms at once. Several major trials demonstrated that PARPi work as maintenance therapy (treatment given after the main therapy to keep the cancer from returning) in HGSOC. The statement cites: - **SOLO1** — olaparib monotherapy (given alone). - **PAOLA1** — the combination of olaparib plus bevacizumab. - **PRIMA** — niraparib monotherapy. These trials led to approval by the European Medicines Agency (EMA) and the U.S. Food and Drug Administration (FDA). BRCA germline mutations were the first marker understood as predicting effective PARPi use. Then the PAOLA1 trial showed something broader. Patients with pathogenic BRCA1/2 mutations benefited from olaparib maintenance — *and so did patients whose tumors showed genomic instability on the Myriad MyChoice assay*, even without a BRCA mutation. This finding elevated the importance of other HRD-related genes. The authors argue that including these genes in routine testing for ovarian cancer patients is warranted, because it allows clinicians to make well-grounded decisions about PARPi use. ## The Landscape of HRD Tests Different tests are available to determine HRD status. The statement organizes them into three broad categories. **1. Next-generation sequencing (NGS) assays.** These analyze genomic DNA to detect mutations in genes associated with HRD, such as BRCA1 and BRCA2, plus other HRD-related genes. Within this category: - **Genetic testing:** BRCA1 and BRCA2 mutations are well-established indicators of HRD, particularly in breast and ovarian cancers. Genetic testing can identify these mutations, and their presence suggests HRD. Testing methods include targeted sequencing, multiplex ligation dependent probe amplification (MLPA), and next-generation sequencing (NGS). - **Homologous Recombination Deficiency Score (HRD Score):** some commercial tests, such as the Myriad myChoice® HRD test, calculate a score based on multiple genomic markers associated with HRD. This score predicts HRD and guides treatment decisions. It includes measures of genomic instability such as loss of heterozygosity (LOH), telomeric allelic imbalance (TAI), and large-scale state transitions (LSTs). **2. Genomic instability assays.** These measure genomic instability directly through three features: - **Loss of Heterozygosity (LOH) testing:** LOH is a common feature of HRD, marked by the loss of one of the two copies of a gene in a tumor. LOH testing identifies regions of the genome where one copy has been lost, indicating HRD. - **Telomeric allelic imbalance (TAI):** an imbalance in telomere lengths between the two alleles of a gene. TAI is a form of genomic instability that can indicate defects in DNA repair pathways such as HRR, and it is associated with certain cancers, including ovarian cancer. - **Large-scale state transitions (LSTs):** structural genomic alterations occurring on a large scale, involving changes in chromosomal structure or organization. These may include chromosomal rearrangements, copy number alterations, or changes in chromosome arm status. **3. Functional assays.** These evaluate how well the HRD repair pathways actually work in cells. They typically use laboratory-based experiments measuring the ability of cells to repair DNA damage — for example, the RAD51 Foci assay. ## Clinically Approved Tests Available in Germany The statement lists the following tests as clinically approved and commonly accessible in Germany. This table preserves the original details on mechanism, what counts as HRD-positive, the patient sample required, and the trial in which each was evaluated. Test name Mechanism HRD-positive Patient's probe Trial evaluated BRACAnalysis CDx test (genetic testing) Germline mutation in BRCA1/2 Mutation detectable Blood — Myriad myChoice CDx test Mutation status of BRCA1/2 AND GIS (gLOH + TAI + LST) BRCA mutation OR GIS > 42 Tumor tissue PRIMA / PAOLA-1 / VELIA / NOVA FoundationOne CDx panel Mutation status of BRCA1/2 AND genomic instability (gLOH) BRCA mutation OR LOH-Score ≥ 16% Tumor tissue ATHENA Mono / ARIEL 2/3 / QUADRA NOGGO GIS assay NGS hybrid-capture biomarker assay detecting BRCA1/2 plus 55 further HRR-relevant genes and structural alterations to establish GIS BRCA mutation or GIS > 83 Tumor tissue PAOLA-1 cohort Geneva test OncoScan plus number of large-scale state transitions (nLST) nLST threshold of 15 Tumor tissue PAOLA-1 cohort Academic Leuven HRD test Targeted sequencing of genome-wide single-nucleotide polymorphisms and coding exons of eight HR genes including BRCA1, BRCA2, and TP53 — Tumor tissue PAOLA-1 cohort SOPHiA DDM™ Dx HRD Solution Detects SNVs (single nucleotide variants) and Indels in 28 genes involved in the HRR pathway, including BRCA1 and BRCA2 — Tumor tissue PAOLA-1 cohort Illumina TSO 500 Low-WGS (shallow whole genome sequencing) for LOH + TAI + LST — Tumor tissue PAOLA-1 cohort BRCA-like classifier Discriminates BRCA-associated from sporadic cancers using the shrunken centroid algorithm; low-WGS BRCA-like > 0.5; non-BRCA-like ≤ 0.5 Tumor tissue PAOLA-1, AGO-TR1 ## Emerging Tests and Bridging Concordance Additional tests exist that have not yet been clinically evaluated for progression-free survival (PFS — how long patients live without the cancer getting worse) and overall survival (OS — how long patients live overall). However, these tests show high concordance (agreement) with the Myriad myChoice test. This agreement is referred to as "bridging." These emerging tests include: - **CytoSNP:** a single nucleotide polymorphism (SNP) array for LOH + TAI + LST. - **Affymetrix OncoScan:** a SNP array for LOH + TAI + LST. - **OncoMine:** shallow whole genome sequencing (low-WGS) for an LOH score. - **AmoyDX:** a low-WGS HRD focus panel for detecting BRCA1/2 mutation and genomic instability — "and many more," the authors add. Real-world data have shown that a genomic loss of heterozygosity greater than 16% (gLOH > 16%) and a genomic instability score greater than 42 (GIS > 42) overlap significantly. Clinically, they are comparable with regard to time to treatment discontinuation (TTD) — how long a patient stays on a treatment before it is stopped. ## Cutoff Values: A Critical Practical Issue Regarding the cutoff values of each test, the authors issue an important caution. The 95% confidence intervals (the statistical range within which the true value likely falls) are generally not reported. This means the precision of each cutoff is uncertain. Because of this, results near the threshold should be discussed in an interdisciplinary setting — among pathologists, gynecologic oncologists, and other specialists — considering multiple factors and the patient's clinical context. A result just above or just below the cutoff is not always a clear answer. ## The Official Recommendations of the Intergroup The statement includes three formal recommendations. 1. Because patients are considered HRD positive — and therefore eligible for maintenance therapy with olaparib — either through a germline or somatic BRCA1/2 mutation **OR** through a positive genomic instability score, **both the GIS and the BRCA1/2 status must be evaluated together** to reach a conclusive result. 1. Because GIS is a continuous marker to which a hard cutoff is applied, ideally all assays used to stratify patients for treatment decisions should have demonstrated effectiveness by providing clinical PFS and ideally OS data. However, in most settings these data are not available, due to limited access to clinical trial specimens. 1. A number of assays with their specific cutoffs have been evaluated and validated using tissue samples from the PAOLA-1 clinical trial, made available by the ENGOT/ARCA GY group. For some of these assays, PFS and OS data are available, and the survival curves show highly comparable results with comparable hazard ratios (a measure of how much a treatment reduces risk). The authors therefore recommend using assays for which a significant clinical benefit — and comparable PFS and OS advantages — has been shown on samples from the PAOLA-1 trial or other clinical trials looking at outcomes in HRD and HRP (homologous recombination proficient) populations. ## When HRD Testing Is Appropriate All patients diagnosed with ovarian cancer should undergo genetic counseling and testing for BRCA1 and BRCA2 and other BRCA-related genes, as recommended by guidelines. This testing is typically included in a broad standardized panel covering the most common mutations associated with hereditary cancer syndromes. The statement then sets out criteria that should be considered for further HRD testing: - **Contextual relevance:** the HRD test must fit within the overall clinical context of the patient's condition and treatment plan. The ability to take oral medications is mandatory, since all PARP inhibitors are taken by mouth. - **Negative germline mutations:** if germline testing for BRCA1/2 alone (performed by human genetics) is negative, HRD can be pursued as a second test in a two-step procedure. This can be done immediately after a negative germline result. Ideally, HRD testing should be performed simultaneously with germline testing. - **Primary setting:** HRD testing should ideally be conducted after the initial diagnosis, using tumor tissue. If tumor tissue cannot be obtained during cytoreductive surgery (surgery to remove as much tumor as possible), multiple minimally invasive biopsies should be taken to gather sufficient material. The choice of biopsy sites should prioritize obtaining a high tumor sample size to optimize results. Tissue can be collected via laparoscopy (keyhole surgery) or interventional radiology. - **Histological subtypes:** HRD testing is particularly relevant for certain histological subtypes — that is, the types of cells the tumor is made of. These include high-grade serous, endometrioid, and clear cell epithelial ovarian carcinoma, as well as ovarian carcinosarcoma, following the WHO classification of 2014 (p53-mutated). ## When HRD Testing Is Not Recommended The statement defines several situations where further HRD testing is not eligible or not appropriate. - **Positive germline mutation for BRCA:** the use of additional HRD testing is obsolete (unnecessary). The germline result already answers the question. - **Recurrent disease or previously treated ovarian cancer:** there is a lack of clinical and preclinical trials on this topic. HRD testing may not be reliable in the setting of recurrent disease or pretreated cancer, because alterations in tumor cells and the tumor microenvironment could affect the significance of results. Patients who have already received PARP inhibition or other immunogenic therapy during ovarian cancer treatment should be excluded from testing outside of clinical trials. However, therapies for other, pre-existing cancer sites are not part of this exclusion. If an HRD test was already done in a recurrent disease setting, there is no need to reevaluate HRD again. If no HRD test was done before, and if the result would support the treatment decision-making process, testing can be considered in a recurrence situation on an individual basis. - **Tumor tissue obtained after neoadjuvant chemotherapy within the primary diagnosis:** the significance of an HRD test in tissue obtained after neoadjuvant chemotherapy (chemotherapy given before surgery) at the time of primary diagnosis remains unclear. Tumor necrosis (tumor cell death) at the time of interval surgery can negatively influence the test results. - **Histological subtype:** all forms of low-grade epithelial ovarian carcinoma, following the WHO classification of 2014, are not eligible for further HRD testing. ## Minimum Standards for Tumor Tissue Samples Reliable HRD results depend on good-quality tissue. The statement sets minimum requirements for the molecular pathological report, which should include the following information. **1. Patient identification and short clinical background:** - The date of initial diagnosis. - The date the test was performed. - A statement of any previous administration of systemic treatment. **2. Details on the assay used:** - The name of the assay. - The assay's performance parameters (specification of the mechanism used within the test). - The minimum and maximum tumor cell content. - A listing of all genes covered by the test. - Confirmation of sufficiency of sequencing depth (in the case of NGS assays). - The cutoff and threshold for a test result. - A clear statement on the clinical test approval, its eligibility for HRD testing, and the name of the reference. **3. Details of the specimen taken for testing:** - The histological diagnosis (confirmation that high-grade epithelial ovarian cancer is present). - The anatomic site where the specimen was taken. - The tumor cell content. - A statement on the adequacy of sample measurements: **an adequate sample should be at least 5 mm in diameter with at least 30% tumor cell count**. CAVE (caution): in lymph node metastasis, the tumor cell count can be low due to a high amount of immunocompetent cells — in such cases it can rapidly fall below 10%. - Cutoff definition: if the HRD score lies a few points beneath the medical approval of a certain drug, a new biopsy to score a higher tumor cell count can be considered. Moreover, off-label use of the drug can be discussed. **4. BRCA1/2 status:** - Somatic mutation status of BRCA1/2, including large deletions and information on LOH of BRCA1/2. - Classification of the BRCA mutation according to the consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology. **5. Genomic instability score** reported as either positive or negative, according to the test-specific cutoff or threshold. **6. Final HRD status** based on BRCA1/2 mutation status, GIS, and other HRR-relevant genes tested (HRD positive vs. HRD negative). **7. If applicable,** a recommendation of a specific drug and the name of the reference. ## What This Means for Patients The practical message is that HRD testing is a valuable tool for personalizing ovarian cancer treatment. It helps identify which patients may benefit from PARP inhibitor therapy. However, the statement is equally clear that assay selection, timing, and result interpretation all require careful consideration. Not every test is validated the same way, and not every patient should be tested. Several points deserve emphasis for patients: - If your germline BRCA test is positive, you do not need additional HRD testing. - If your germline test is negative, HRD testing can still identify whether your tumor has a genomic instability signature that predicts PARPi benefit. - Both the BRCA status and the genomic instability score must be read together. One alone is not enough for a conclusive result. - The type of ovarian cancer matters. HRD testing is relevant for high-grade serous, endometrioid, and clear cell carcinomas, and ovarian carcinosarcoma. It is not recommended for low-grade epithelial ovarian carcinoma. - You must be able to take oral medication, because all PARP inhibitors are given by mouth. - Tissue quality matters. A sample of at least 5 mm in diameter with at least 30% tumor cells is needed for a reliable result. The authors conclude that this structured approach is intended to optimize HRD testing, improve clinical decision-making, and ultimately improve patient outcomes. ## Limitations and Open Questions The statement openly acknowledges several gaps in current knowledge. - **Missing confidence intervals:** the 95% confidence intervals for test cutoffs are generally not reported, so precision around the thresholds is uncertain. - **Limited clinical outcome data:** many assays lack their own PFS and ideally OS data, because access to clinical trial specimens is limited. Some tests rely on "bridging" — agreement with an already-validated test — rather than their own outcome data. - **Unclear value in recurrent disease:** there is a lack of clinical and preclinical trials on HRD testing in recurrent or pretreated ovarian cancer. Alterations in tumor cells and the tumor microenvironment could affect how meaningful the results are. - **Unclear value after neoadjuvant chemotherapy:** the significance of HRD testing on tissue obtained after neoadjuvant chemotherapy at the time of primary diagnosis remains unclear, and tumor necrosis at interval surgery can negatively influence results. - **Hard cutoffs on a continuous marker:** GIS is a continuous measurement, but a fixed cutoff is applied to it. Values near the threshold require interdisciplinary discussion. These are the reasons the statement emphasizes interdisciplinary review rather than a single automatic number. ## Practical Advice for Patients 1. Ask for genetic counseling and germline BRCA1/BRCA2 testing if you have been diagnosed with ovarian cancer. Guidelines recommend this for all patients. 1. If your germline test is negative, ask whether HRD testing is appropriate for you. Ideally this should be done at the same time as germline testing. 1. Confirm that your tumor type qualifies for HRD testing — high-grade serous, endometrioid, clear cell, or carcinosarcoma. Low-grade tumors are excluded. 1. Make sure your tissue sample is adequate: at least 5 mm in diameter with at least 30% tumor cells. If a lymph node was used, tumor content may be much lower (below 10%) and the result less reliable. 1. Ask which specific assay is being used, and whether it has been validated in a clinical trial such as PAOLA-1 with PFS and ideally OS data. 1. If your result falls close to the cutoff, ask for it to be discussed in an interdisciplinary tumor board before a final treatment decision is made. 1. If your disease has recurred after prior PARP inhibitor or immunogenic therapy, discuss with your team whether testing outside a clinical trial is appropriate for you. ## Frequently Asked Questions ### What is HRD testing and why does it matter for ovarian cancer? HRD is a measurable biological signal showing a weakness in a tumor's DNA repair. Testing for it helps doctors identify which patients with advanced ovarian cancer are likely to benefit from PARP inhibitors, a class of oral maintenance drugs given after initial treatment. It is not one uniform test, and the laboratory and timing can affect your treatment options. ### If my germline BRCA test is positive, do I still need HRD testing? No. If you have a positive germline BRCA1 or BRCA2 mutation, additional HRD testing is considered obsolete because the germline result already answers the question. A positive germline result means you are considered HRD positive and eligible for maintenance therapy with olaparib, so further testing would not change that decision. ### My germline test was negative. Can HRD testing still help me? Yes. If germline testing for BRCA1 and BRCA2 is negative, HRD testing can be pursued as a second test in a two-step procedure, immediately after the negative result. It may show whether your tumor has a genomic instability signature that predicts PARP inhibitor benefit. Ideally, HRD testing should be done at the same time as germline testing. ### Which types of ovarian cancer qualify for HRD testing? HRD testing is particularly relevant for high-grade serous, endometrioid, and clear cell epithelial ovarian carcinoma, and ovarian carcinosarcoma, following the WHO classification of 2014. All forms of low-grade epithelial ovarian carcinoma are not eligible for further HRD testing. Your tumor type should be confirmed before testing is arranged. ### What tissue sample is needed for a reliable HRD result? An adequate sample should be at least 5 mm in diameter with at least 30% tumor cells. If a lymph node metastasis is used, the tumor cell count can be low because of many immune cells and may fall below 10%, making the result less reliable. If tumor tissue cannot be obtained during surgery, minimally invasive biopsies may be taken. ### What does it mean if my HRD result is close to the cutoff? Results near the threshold are not always a clear answer. The 95% confidence intervals for test cutoffs are generally not reported, so the precision of each cutoff is uncertain. A result just above or just below the cutoff should be discussed in an interdisciplinary setting among pathologists, gynecologic oncologists, and other specialists, considering your clinical context. ### Can I have HRD testing if my cancer has come back or I already had PARP inhibitors? If your disease has recurred or was previously treated, HRD testing may not be reliable because changes in tumor cells and the tumor microenvironment could affect the significance of results. Patients who already received PARP inhibition or other immunogenic therapy during ovarian cancer treatment should be excluded from testing outside clinical trials. If an HRD test was already done in a recurrence setting, there is no need to reevaluate. ### When should a patient with advanced ovarian cancer seek a second opinion about HRD testing and PARP inhibitor maintenance therapy? A second opinion is worth considering when the HRD result falls close to the test cutoff, since the 95% confidence intervals for cutoffs are generally not reported and precision around the threshold is uncertain. It also helps when the assay used lacks its own progression-free and overall survival data, when the tissue sample is under 5 mm or below 30% tumor cells, or when testing is proposed for recurrent disease, after neoadjuvant chemotherapy, or for a low-grade tumor, where testing is not recommended. Diagnostic Detectives Network provides independent expert second opinions. ## Source Information **Original article title:** Intergroup-statement: statement of the german ovarian cancer commission, the North-Eastern German Society of gynecological Oncology (NOGGO), AGO Austria and AGO Swiss regarding the use of homologous repair deficiency (HRD) assays in advanced ovarian cancer. **Authors:** Chinczewski L, Harter P, Heukamp L, Mayr D, Grimm C, Heinzelmann-Schwarz V, Wimberger P, Mahner S, Braicu IE, Schmitt W, Denkert C, Sehouli J. **Publication:** Archives of Gynecology and Obstetrics (2025), volume 311, pages 1445–1450. DOI: 10.1007/s00404-025-07991-y. Published online 12 March 2025. Received 30 January 2025; accepted 21 February 2025. **Article type:** Position Statement. Open Access under a Creative Commons Attribution 4.0 International License. **Lead author affiliation:** Department for Gynecology, Campus Virchow-Klinikum, Charité–Universitätsmedizin Berlin, Berlin, Germany. Co-authors are affiliated with institutions in Germany (Essen, Hamburg, Munich, Dresden, Marburg), Austria (Vienna), and Switzerland (Basel). **Conflict of interest disclosure:** the statement reports advisory board and honorary relationships with Myriad MyChoice, GSK, ESAI, and NOGGO e.V. **Note:** This patient-friendly article is based on peer-reviewed research. --- Publisher: Diagnostic Detectives Network (https://diagnosticdetectives.com) — independent multi-expert medical second opinions, worldwide, private-pay. Author byline: Anton Titov, MD, PhD. 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