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

Abstract

Introduction
Homologous recombination deficiency (HRD) is a key biomarker in the management of high-grade serous ovarian cancer (HGSOC), guiding treatment decisions, particularly regarding the use of poly(ADP-ribose) polymerase inhibitors (PARPi). As multiple HRD assays are available, each with distinct methodologies and cutoff values, the interpretation and clinical application of HRD testing remain complex. This intergroup statement, endorsed by the German Ovarian Cancer Commission, NOGGO, AGO Austria, and AGO Swiss, aims to provide guidance on the indications, appropriate use, and limitations of HRD testing in ovarian cancer.

Materials and methods
The statement is based on an interdisciplinary review of available literature, clinical trial data, and expert consensus. The recommendations focus on the current landscape of HRD assays, their clinical applicability, and practical considerations regarding the optimal timing and indications for testing.

Results and discussion
Various HRD assays, including established commercial tests and emerging academic-clinical approaches, are reviewed in this statement. The document outlines key eligibility criteria for HRD testing in ovarian cancer, emphasizing its relevance in specific histological subtypes and clinical scenarios. Additionally, exclusion criteria are defined, highlighting cases where HRD testing may not be appropriate due to insufficient clinical validation or lack of therapeutic implications. Finally, the statement discusses the pathological minimum requirements for tissue samples used in HRD testing, ensuring adequate sample quality and tumor content for reliable results.

Conclusion
HRD testing is a valuable tool for personalizing ovarian cancer treatment, particularly in identifying patients who may benefit from PARPi therapy. However, assay selection, timing, and result interpretation require careful consideration. This statement provides a structured approach to optimize HRD testing, aiming to improve clinical decision-making and patient outcomes.

Full text

Vol.:(0123456789)
Archives of Gynecology and Obstetrics (2025) 311:1445–1450
https://doi.org/10.1007/s00404-025-07991-y
POSITION STATEMENT
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
LukasChinczewski1 · PhilippHarter2· LukasHeukamp3· DorisMayr4· ChristophGrimm5·
ViolaHeinzelmann‑Schwarz6· PaulineWimberger7· SvenMahner8· IoanaElenaBraicu1· WolfgangSchmitt9·
CarstenDenkert10· JalidSehouli1
Received: 30 January 2025 / Accepted: 21 February 2025 / Published online: 12 March 2025
© The Author(s) 2025
Abstract
Introduction Homologous recombination deficiency (HRD) is a key biomarker in the management of high-grade serous ovar-
ian cancer (HGSOC), guiding treatment decisions, particularly regarding the use of poly(ADP-ribose) polymerase inhibitors
(PARPi). As multiple HRD assays are available, each with distinct methodologies and cutoff values, the interpretation and
clinical application of HRD testing remain complex. This intergroup statement, endorsed by the German Ovarian Cancer
Commission, NOGGO, AGO Austria, and AGO Swiss, aims to provide guidance on the indications, appropriate use, and
limitations of HRD testing in ovarian cancer.
Materials and methods The statement is based on an interdisciplinary review of available literature, clinical trial data, and
expert consensus. The recommendations focus on the current landscape of HRD assays, their clinical applicability, and
practical considerations regarding the optimal timing and indications for testing.
Results and discussion Various HRD assays, including established commercial tests and emerging academic-clinical
approaches, are reviewed in this statement. The document outlines key eligibility criteria for HRD testing in ovarian cancer,
emphasizing its relevance in specific histological subtypes and clinical scenarios. Additionally, exclusion criteria are defined,
highlighting cases where HRD testing may not be appropriate due to insufficient clinical validation or lack of therapeutic
implications. Finally, the statement discusses the pathological minimum requirements for tissue samples used in HRD test-
ing, ensuring adequate sample quality and tumor content for reliable results.
Conclusion HRD testing is a valuable tool for personalizing ovarian cancer treatment, particularly in identifying patients
who may benefit from PARPi therapy. However, assay selection, timing, and result interpretation require careful considera-
tion. This statement provides a structured approach to optimize HRD testing, aiming to improve clinical decision-making
and patient outcomes.
Keywords Gynecological oncology· Ovarian cancer· Homologous recombination deficiency testing· Maintenance
therapy· Intergroup statement
Denition ofHRD andHRD testing
Genomic instability (GIS) is one of the most common causes
of tumorigenesis [1]. There are several DNA repair systems
that play a significant role in maintaining genomic stability.
If there is an imbalance or malfunction in these systems,
often due to mutations, the genome exhibits instability. One
of these DNA repair systems is the homologous recombina-
tion repair (HRR) system. When double strand breaks and
interstrand cross-links (ICL) occur during genomic replica-
tion, the HRR system respond to these mutations with its
proteins for repair.
Extended author information available on the last page of the article
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1446 Archives of Gynecology and Obstetrics (2025) 311:1445–1450
Defects in HRR pathway due to (epi-) genetic events
may result in the phenotype of homologous repair defi-
ciency (HRD), indicating the inability to repair DNA
double-strand breaks. If HRD occurs, GIS can be pro-
moted. GIS may manifest as genomic loss of heterozygo-
sity (gLOH), telomeric imbalance (TAI) and large-scale
transitions (LST).
Especially in the tumorigenesis of high-grade serous
ovarian cancer (HGSOC), the HRR system plays a sig-
nificant role. Germline and somatic mutations within
the breast-cancer gene (BRCA) 1 and BRCA 2 are mainly
responsible for HRR pathway defects. Approximately 13
to 15% of patients with HGSOC show a germline mutation
in BRCA1/2, and up to 3–7% show somatic mutations [2,
3]. However, besides BRCA1 and 2, there are other genes
involved that may lead to HRD, such as BRCA1-associated
RING domain 1 (BARD1), BRCA-interacting protein 1
(BRIP1), checkpoint kinase 1 (CHEK1), checkpoint kinase
2 (CHEK2), family with sequence similarity 175, mem-
ber A (FAM175A), nibrin (NBN), partner and localizer of
BRCA2 (PALB2), RAD51 paralog C (RAD51C), RAD51
paralog D (RAD51D), and many more.
The clinical impact of these malfunctions in the
HRR pathway was demonstrated by the introduction of
poly(adenosine diphosphate [ADP]–ribose) polymerase
(PARP) inhibitors (PARPi). The PARPi block base exci-
sion repair, which leads to the accumulation of single-
strand breaks during DNA replication. This ultimately
results in a collapse of the repair system and the formation
of double-strand breaks. In cells with HRD, these breaks
cannot be adequately repaired, leading to synthetic letality
in the presence of PARPi.
The efficacy of PARPi in maintenance therapy for
HGSOC has been demonstrated in several studies, includ-
ing those utilizing different drugs such as Olaparib mono-
therapy in the SOLO1 study, the combination of Olaparib
and bevacizumab in the PAOLA1 study, and Niraparib
monotherapy in the PRIMA trial, which led to EMA and
FDA approval [4–7].
The BRCA germline mutations were the first to be
understood as an indicator for the effective use of PARPi.
The PAOLA1 trial showed that not only patients with path-
ogenic BRCA1/2 mutations but also those with genomic
instability measured by the Myriad MyChoice assay ben-
efited from maintenance therapy with Olaparib. Therefore,
the importance of other HRD-related genes is emphasized,
and their inclusion in regular testing for patients with ovar-
ian cancer (OC) is warranted. This would enable clinicians
to make well-grounded clinical decisions regarding the use
of PARPi. The aim of this statement is to simplify clini-
cians’ decision-making regarding indications and correct
conduct of HRD testing in patients with OC based on cur-
rent knowledge.
Landscape oftests andits choice
There are different tests available for the determining of
HRD status. Principally, there are three different catego-
ries for the determining HRD:
(1) Next-generation sequencing (NGS) assays: These
assays analyze genomic DNA to detect mutations
in genes associated with HRD, such as BRCA1 and
BRCA2, as well as other HRD-related genes.
a. Genetic Testing: mutations in the BRCA1 and
BRCA2 genes are well-established indicators of
HRD, particularly in breast and ovarian cancers.
Genetic testing can identify these mutations, and
the presence of such mutations suggests HRD. This
testing can be performed through various methods,
including targeted sequencing, multiplex ligation
dependent probe amplification (MLPA), or next
generation sequencing (NGS).
b. Homologous Recombination Deficiency Score
(HRD Score): some commercial tests, such as the
Myriad myChoice® HRD test, calculate an HRD
score based on multiple genomic markers associated
with HRD. This score is used to predict HRD and
guide treatment decisions.This test includes meas-
ures of GIS such as loss of heterozygosity (LOH),
telomeric allelic imbalance (TAI) and large-sclae
state transitions (LSTs).
(2) Genomic instability assays: these assays measure
genomic instability through various methods, such
as assessing loss of heterozygosity (LOH), telomeric
allelic imbalance (TAI), and large-scale state transi-
tions (LSTs).
a. Loss of Heterozygosity (LOH) Testing: LOH is a
common feature of HRD and is characterized by the
loss of one of the two copies of a gene in a tumor.
LOH testing can identify regions of the genome
where one copy has been lost, indicating HRD
b. Telomeric allelic imbalance (TAI) refers to an imbal-
ance in the lengths of telomeres, which are the pro-
tective caps at the ends of chromosomes, between
the two alleles of a gene. Telomeric allelic imbal-
ance is a form of genomic instability that can be
indicative of defects in DNA repair pathways, such
as homologous recombination repair (HRR), and is
associated with certain types of cancer, including
ovarian cancer.
c. Large-scale state transitions (LSTs) are structural
genomic alterations that occur on a large scale,
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1447Archives of Gynecology and Obstetrics (2025) 311:1445–1450
involving changes in chromosomal structure or
organization. These transitions may include events
such as chromosomal rearrangements, copy number
alterations, or changes in chromosome arm status.
(3) Functional assays: these assays evaluate the function-
ality of HRD repair pathways in cells, often through
laboratory-based experiments or assays measuring the
ability of cells to repair DNA damage (e.g., RAD51
Foci assay).
The following tests are clinically approved and are com-
monly accessible in Germany:
Test name Mechanism HRD-positive Patient’s probe Trial evaluated
Genetic testing
BRACAnalysis CDx test Germline mutation in BRCA1/2 Mutation detectable Blood
HRD-Test
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% [8]
Tumor tissue ATHENA Mono/
ARIEL 2/3/
QUADRA
NOGGO GIS assay [9] Next Generation Sequencing (NGS)
hybrid-capture biomarker assay that
detects BRCA1/2 + 55 fur ther HRR-
relevant genes and structural alterations
to establish GIS
BRCA-mutation or
GIS > 83
Tumor tissue PAOLA-1 cohort
Geneva test [10, 11] OncoScan + number of large-scale state
transitions (nLST)
nLST threshold of 15 Tumor tissue PAOLA-1 cohort
Academic Leuven HRD
test [12]
Targeted sequencing of genome-wide
single-nucleotide polymorphisms and
coding exons of eight HR genes includ-
ing BRCA1, BRCA2, and TP53
Tumor tissue PAOLA-1 cohort
SOPHiA DDM™ Dx
HRD Solution [13]
Detects SNVs and Indels in 28 genes
involved in the HRR pathway, including
BRCA1 and BRCA2
Tumor tissue PAOLA-1 cohort
Illumina TSO 500 Low-WGS for LOH + TAI + LST Tumor tissue PAOLA-1 cohort
BRCA-like classifier
[14]
Discriminate BRCA-associated from spo-
radic cancers by employing the shrunken
centroid algorithm; low-WGS
BRCA-like > 0.5; non-
BRCA-like ≤ 0.5
Tumor tissue PAOLA-1, AGO-TR1
Regarding the cutoff values of each test, we like to under-
line that the 95% CI are generaly not reported and the inter-
pretation of values near the threshold should be discussed
interdisciplary, considering various factors and clinical
context.
Further tests that are not yet been clinically evaluated
regarding progression-free survival (PFS) and overall sur-
vival (OS) but show a high concordance to the Myriad
myChoice (reffered to as bridging) [15, 16] include:
• CytoSNP: Single Nucelotid Polymorphism (SNP) Array
for LOH + TAI + LST.
• Affymetrix OncoScan: Single Nucelotid Polymorphism
(SNP) Array for LOH + TAI + LST.
• OncoMine: Shallow Whole Genome Sequencing (low-
WGS) for LOH-Score.
• AmoyDX: low-WGS HRD focus panel for the detection
of BRCA1/2 mutation and GIS and many more.
Real-world data have shown that a genomic loss of het-
erozygosity (gLOH) (> 16%) und GIS (> 42) exhibit a sig-
nificant overlap and are clinically comparable regarding the
time to treatment discontinuation (TTD) [17].
Statement
(1) Since patients are considered HRD positive and thus
eligible for maintenance therapy with olaparib either
with a germline or somatic BRCA1/2 mutation OR GIS
positivity both GIS and BRCA1/2 status has to be evalu-
ated together for a conclusive result.
(2) Since GIS is a continuous marker to which a hard cutoff
is applied, ideally all assays used to stratify patients for
treatment decisions should have shown effectiveness by
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1448 Archives of Gynecology and Obstetrics (2025) 311:1445–1450
providing clinical PFS and ideally OS data. However,
in most settings, these data are not available due to
limited access to clinical trial specimens.
(3) A number of assays with their specific cutoffs have also
been evaluated and validated with tissue samples of the
PAOLA1 clinical trial, made available by the ENGOT/
ARC AGY [18]. For some of these assays, PFS and OS
data are available, and survival curves show highly
comparable results with comparable Hazard ratios
[9, 11, 18, 19]. Therefore, it is recommended to uti-
lize assays for which a significant clinical benefit, and
comparable PFS and OS advantages have been shown
on samples from the PAOLA-1 trial or other clinical
trials looking at outcome in HRD/HRP population.
When isit appropriate totest forHRD inOC,
andwhenisit notrecommended?
All patients diagnosed with ovarian cancer should undergo
genetic counseling and testing for BRCA1/BRCA2 and other
BRCA -related genes as recommended by guidelines. This
testing is typically included in a broad standardized panel
of the most common mutations associated with hereditary
cancer syndromes.
The following criteria should be considered for further
testing HRD in ovarian cancer:
• Contextual relevance: the inclusion of the HRD test must
be made wihin 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
used orally.
• Negative germline mutations: if germline mutations for
BRCA1/2 alone tested by human genetics are negative,
HRD can be persued as second test in a two-step proce-
dure. This can be performed immediately following a
negative result for germline mutations. Ideally, HRD test-
ing should be performed simultaneously with germline
testing.
• Primary setting: HRD testing should ideally be con-
ducted after the initial diagnosis using tumor tissue. If
tumor tissue can not be obtained during cytoreductive
surgery, multiple minimally invasive biopsies should
be taken to gather sufficient material. The selection of
biopsy anatomic sites should prioritize obtaining a high
tumor sample size to optimize the results (further infor-
mation below). Tissue can be collected via laparoscopy
or interventional radiology.
• Histological subtypes: HRD testing is particularly rel-
evant for histological subtypes such as high-grade serous,
endometrioid, and clear cell epithelial ovarian carcinoma,
as well as ovarian carcinosarcoma, following the WHO
classification of 2014 (p53-mutated).
The following criteria are not eligible for further HRD
testing:
• Positive germline mutation for BRCA : the use of addi-
tional HRD testing is obsolete.
• Recurrent disease or previously treated ovarian cancer:
there is a lack in clinical and preclinical trials on this
topic. HRD testing may not be reliable in the setting of
recurrent disease or pretreated cancer, as 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 from clinical trials. However, therapies in
other preexisting cancer sites are not part of this exclu-
sion. If in recurrent disease a previous HRD test has
been done, there is no need to reevaluate HRD again.
If a HRD test has not been done before and if the result
supports the treatment decision making process, it can
be considered to be performed in a recurrence situation
on an individual basis.Tumor tissue obtained after neo-
adjuvant chemotherapy within the primary diagnosis: the
significance of the HRD test in tissue obtained after neo-
adjuvant chemotherapy at the time of primary diagnosis
remains unclear. Tumor necrosis 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 requirements andstardards
forpathological examination
The molecular pathological report should include the fol-
lowing minimal information:
1. Patient identification and short clinical background:
a. Date of initial diagnosis.
b. Date of test performance.
c. Statement of previous administration of systematic
treatment.
2. Details on the assay used:
a. Name of the assay.
b. Assay performance parameters (specification of
mechanism used within the test).
c. Minimal and maximum tumor cell content.
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1449Archives of Gynecology and Obstetrics (2025) 311:1445–1450
d. Listing of all genes covered by test.
e. Sufficiency of sequencing depth (in case of NGS
assays).
f. Cut-off and threshold for a test result.
g. Clear statement on clinical test approval, its eligibil-
ity for HRD testing and name of reference.
3. Details of the specimen taken for testing:
a. Histological diagnosis (confirmation that high-grade
epithelial ovarian cancer is present).
b. Anatomic site of specimen taken.
c. Tumor cell content.
d. Statement on adequacy of sample measurements: an
adequate sample should be at least 5mm in diameter
with at least 30% tumor cell count [20]. CAVE: in
lymph node metastasis the tumor cell count can be
low due to a high amount of immunocompentent
cells (rapidly below 10%).
e. Cut-off definition: if the HRD score lies few points
beneath the medical approval of a certain drug, a
new biopsy to score a higher tumor cell count can
be considered. Moreover, an off-label use of the
drug can be discussed.
4. BRCA1/2 status:
a. Somatic mutation status of BRCA1/2, including
large deletions and information on LOH of BRCA1/2
b. classification of BRCA mutation according to con-
sensus recommendation of the American College of
Medical Genetics and Genomics and the Associa-
tion for Molecular Pathology
5. Genomic instability score as either positive or negative
according to the test specific cut-off or threshold:
6. Final HRD status based on BRCA1/2 mutation status,
GIS and other HRR-relevant genes tested (HRD + vs
HRD-).
7. If applicable, recommendation of specific drug and
name of reference.
Author contributions L.C. wrote the main manuscript text and pre-
pared the tables J.S. made substantial contributions to the conception
or design of the work All authors revised it critically for important
intellectual content and reviewed the manuscript.
Funding Open Access funding enabled and organized by Projekt
DEAL.
Data availability No datasets were generated or analysed during the
current study.
Declarations
Conflict of interests AdBoard Honorary by Myriad MyChoice Honor-
ary by GSK, ESAI and NOGGO e.V.
Open Access This article is licensed under a Creative Commons Attri-
bution 4.0 International License, which permits use, sharing, adapta-
tion, distribution and reproduction in any medium or format, as long
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Authors and Aliations
LukasChinczewski1 · PhilippHarter2· LukasHeukamp3· DorisMayr4· ChristophGrimm5·
ViolaHeinzelmann‑Schwarz6· PaulineWimberger7· SvenMahner8· IoanaElenaBraicu1· WolfgangSchmitt9·
CarstenDenkert10· JalidSehouli1
* Lukas Chinczewski
Lukas.chinczewski@charite.de
1 Department forGynecology, Campus Virchow-Klinikum,
Charité–Universitätsmedizin Berlin, Berlin, Germany
2 Department forGynecology, Klinikum Essen-Mitte, Essen,
Germany
3 Institut für Hämatopathologie Hamburg, Hamburg, Germany
4 Department forPathology, Ludwig-Maximilians-Universität
München, Munich, Germany
5 Department forGynecology, Allgemeines Krankenhaus
Wien, Vienna, Austria
6 Department forGynecology, Universitätsspital Basel, Basel,
Switzerland
7 Department forGynecology, Universitätsklinikum Carl
Gustav Carus Dresden, Dresden, Germany
8 Department forGynecology,
Ludwig-Maximilians-Universität München, Munich,
Germany
9 Department forPathology, Campus Charité Mitte, Charité–
Universitätsmedizin Berlin, Berlin, Germany
10 Department forPathology, Philipps-Universität Marburg,
Marburg, Germany
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