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Article

Is Genetic Testing of HER2-Negative Metastatic Breast Cancer Patients Implemented into Clinical Practice? A Retrospective Analysis

Department of Obstetrics and Gynecology, Division of General Gynecology and Gynecologic Oncology, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria
*
Author to whom correspondence should be addressed.
J. Clin. Med. 2026, 15(9), 3433; https://doi.org/10.3390/jcm15093433
Submission received: 19 October 2025 / Revised: 15 April 2026 / Accepted: 20 April 2026 / Published: 30 April 2026
(This article belongs to the Section Oncology)

Abstract

Background/Objectives: Genetic testing in Human Epidermal Growth Factor Receptor 2-negative (HER2−) metastatic breast cancer (mBC) is necessary to enable optimal treatment choices including poly(ADP-ribose)polymerase inhibitors (PARPis). The present study evaluated the implementation of genetic testing in a real-world setting to reveal and subsequently allow targeting of potential inadequacies and risk factors for low testing frequency. Methods: We performed a retrospective analysis including HER2− mBC patients treated at a single academic center starting from 10 April 2019 (date of European Medicines Agency (EMA) approval of Olaparib for germline breast cancer gene mutant (gBRCAm) HER2− mBC) to 7 September 2021. The primary objective of the study was to evaluate the rate of HER2− mBC patients that were recommended to undergo genetic testing by the multidisciplinary tumor board (MTB). The secondary objective was to identify factors that were associated with a higher likelihood of having undergone genetic testing. Results: In total, 47.6% (109 of 229) of HER2− mBC patients had been recommended to undergo genetic testing by the MTB. Of these informed patients, 89.0% (97 of 109) underwent genetic testing, of which 11.6% (11 of 95) had a germline BRCA mutation (gBRCAmut) and were eligible for PARPi treatment. In multivariate analysis, younger age (p-value: 0.0007), hormone receptor positive (HR+)/HER2− subtype (p-value < 0.0001) and positive family history for breast and ovarian cancer (p-value: 0.0001) were significantly associated with the performance of genetic counseling. Conclusions: The present study demonstrated low genetic counseling rates of HER2− mBC patients, especially in individuals without specific risk factors for hereditary breast cancer. Informed patients showed a high willingness to undergo genetic testing. Genetic testing revealed targetable mutations in over 10% of tested patients.

1. Introduction

In breast cancer gene (BRCA)-deficient breast tumors with malfunctioning homologous recombination, poly(ADP-ribose)polymerase inhibitors (PARPis) prevent the repair of single-strand deoxyribonucleic acid (DNA) breaks resulting in the accumulation of double-strand breaks and stalled DNA replication forks subsequently leading to tumor cell death [1].
The two pivotal trials OlympiAD and EMBRACA demonstrated a significantly longer median progression free survival (PFS) with the PARPis Olaparib and Talazoparib versus treatment of physicians choice (TPC) with consistent results across various subgroups [2,3].
No benefit in overall survival (OS) with Olaparib or Talazoparib versus TPC was observed. Yet, significant cross-over following progression from placebo to PARPi might have confounded OS results [4,5].
In both OlympiAD and EMBRACA significant improvement in patient-reported quality of life with a greater delay in time to clinically meaningful deterioration was reported by patients receiving a PARPi versus TPC [2,6].
Up to 10% of patients with metastatic Human Epidermal Growth Factor Receptor 2-negative (HER2−) breast cancer (mBC) have a BRCA mutation (BRCAmut) with an even higher prevalence (>30%) in triple negative breast cancer (TNBC) and are therefore eligible for PARPi treatment [7,8,9,10]. Notably, more patients with a BRCAmut have hormone receptor positive (HR+), HER2− disease as this subtype is more prevalent compared to TNBC.
The advent of PARPis has led to their inclusion in all established international treatment guidelines and the recommendation for genetic testing in HER2− mBC patients [11,12,13].
Furthermore, international guidelines include platinum agents (cisplatin and carboplatin) as preferred treatment options in recurrent unresectable or mTNBC with a BRCAmut [12].
Preclinical studies demonstrated a high sensitivity of cells lacking functional BRCA1 or BRCA2 to cisplatin owing to the formation of covalent crosslinks in the DNA and an impaired ability to repair this damage in the absence of homologous recombination [14,15].
The TNT phase III study showed significant improvements in the objective response rate (ORR) (68% versus 33%, p = 0.03) and PFS (6.8 versus 4.8 months, p = 0.03) with carboplatin versus docetaxel in germline BRCA mutant (gBRCAm) recurrent, locally advanced or mBC [16]. The interaction between the treatment effect regarding the ORR (p = 0.01) as well as PFS (p = 0.03) and BRCA status was significant [17]. Notably, it is not clear how platinum agents compare with PARPis and should be sequenced in this setting [12].
Given the advent of platinum salts as well as PARPis in BRCAm HER2− mBC timely genetic testing in these patients is of high importance to allow adequate treatment [2,3,18,19,20,21,22]. Optimal therapeutic decisions are of particular importance in HR+/HER2− BC with a BRCAmut as this patient population has shown decreased OS compared to BRCA wild-type (WT) (BRCA1m: p = 0.0008; BRCA2m: non-significant) [23].
Yet, testing rates in these patients have been reported suboptimal varying between 16.7% to 97% [24,25,26,27] and being lowest in older patients, those with HR+ mBC and those without a known family history of breast or ovarian cancer [28]. Furthermore, in a real-world international study including the USA, France, Germany, Italy, Spain and the UK BRCA 1/2mut testing rates were significantly less frequent in the European countries than in the USA [28].
The present study evaluated the implementation of genetic testing in a real-world academic setting as well as factors associated with a higher likelihood of having undergone genetic testing. With this study potential deficiencies in genetic testing are revealed which will in the future allow the introduction of measures to increase genetic testing and specifically target populations at risk for low testing rates.

2. Patients and Methods

The primary objective of the present study was to evaluate the rate of HER2− mBC patients treated at a single academic center in Austria that were recommended to undergo genetic testing by the multidisciplinary tumor board (MTB). The secondary objective of the study was to evaluate factors that were potentially associated with a higher likelihood of having undergone genetic testing including age, BC subtype, treatment line for the metastatic setting and family history.
Age and treatment line were assessed at the time of genetic counseling or if genetic counseling was not performed at the time of last follow-up. BC subtype was assessed according to the latest tumor biopsy. Positive family history was defined as the occurrence of multiple cancer cases in one family line or special situations including at least three BC cases; at least two BC cases with one case occurring prior to 51 years of age; at least two ovarian cancer cases; at least one BC and one ovarian cancer case; at least one woman with breast and ovarian cancer; at least one case with bilateral BC with the first diagnosis prior to 51 years of age; at least one male BC case; a known mutation in BRCA1, BRCA2, ATM, BARD1, BRIP1, CHECK2, PALB2, RAD51C or RAD51D in the family; a personal history of early-stage HER2− BC with high risk of recurrence; or high-grade epithelial ovarian cancer.
We included all HER2− mBC patients treated at the Department of Obstetrics and Gynecology of the Medical University of Vienna, Austria, starting from 10 April 2019 (date of European Medicines Agency (EMA) approval of Olaparib for gBRCAm HER2− mBC) to 7 September 2021. Metastatic disease was assessed centrally by computer tomography (CT) and biopsy of a metastasis in the course of routine clinical care. There were no exclusion criteria.
We conducted a retrospective chart review and assessed whether genetic counseling was recommended by the MTB and testing was subsequently performed, as well as patient and disease characteristics.
At the study site genetic counseling and blood collection for germline genetic testing were conducted by a gynecologist trained in genetic counseling. In the course of genetic testing 18 genes including ATM, BARD1, BRCA1, BRCA2, BRIP1, CDH1, CHEK2, EPCAM, MLH1, MSH2, MSH6, PALB2, PMS2, PTEN, RAD51C, RAD51D, STK11 and TP53 were evaluated using next-generation sequencing (NGS). In one patient of the study genetic testing was solely performed on tumor tissue (somatic testing).
In the course of a subsequent study all patients who had not been advised to undergo genetic testing by the MTB as well as patients who had been recommended to undergo genetic testing by the MTB but had not for an unknown reason were contacted and invited to undergo genetic testing (end of patient recruitment: 8 May 2024). The testing rates of these patients are presented in the present manuscript to allow thorough discussion of patients’ acceptance to undergo genetic testing. Information on genetic test results of these patients and uptake of PARPi treatment is still pending at the time of manuscript preparation and will be presented elsewhere.
Statistical analysis was done using R version 4.3.2 and package viridis version 0.6.4. Categorical data are presented by absolute and relative frequencies, whereas numerical data are aggregated by mean and standard deviation (SD). Differences between groups were tested with a chi-squared test for the former and Student’s t-test for the latter. ‘Genetic testing: yes/no’ was modeled by logistic regression with age, HR+/HER2− subtype, family history and treatment line as independent variables. A p-value below 0.05 is viewed as statistically significant.

3. Results

3.1. Demographics

In total, 229 patients with a HER2− mBC were included in the study. The mean age of the study population was 64 ± 13 years. A total of 21.0% of patients had a positive family history for breast and/or ovarian cancer. The majority of patients (76.4%) had a HR+, HER2− mBC. Patients were on average on the second treatment line for the metastatic disease at the time of study inclusion (see Table 1).

3.2. Genetic Testing Rates

A total of 47.6% (109 of 229) of HER2− mBC patients had been advised to undergo genetic testing by the MTB. Of these informed patients, 89.0% (97 of 109) underwent genetic testing.
In total, 11.0% (12 of 109) of informed patients did not undergo genetic testing, 2 of these patients refused genetic testing after counseling, 1 patient died prior to genetic testing and in 9 patients the reason for not having undergone genetic testing was not explicit.
Overall, 52.4% (120 of 229) of HER2− mBC patients had not been recommended to undergo genetic testing by the MTB (see Figure 1).

3.3. Genetic Testing Rates in the Sub-Study

These 120 patients who had not been recommended to undergo genetic testing by the MTB as well as patients who had been advised to undergo genetic testing but had not for unknown reason (n = 9) were contacted in the course of a subsequent study and invited to undergo genetic testing.
In total, 42 of these 129 patients could successfully be contacted. Of these, 83.3% (35 of 42) of patients consented to genetic testing. However, 16.7% (7 of 42) of informed patients refused to undergo genetic testing.
A total of 87 patients in the subsequent study could not be informed and invited to genetic testing due to the following reasons: patient was deceased (n = 57), unsuccessful telephonic outreach (n = 15), change in treating physician (n = 10), immobility (n = 2), decremental state of health (n = 1), intellectual disability (n = 1) and language barrier (n = 1) (see Figure 1).

3.4. Predictors of Genetic Testing

In multivariate analysis the variables younger age (p-value: 0.0007), HR+/HER2− subtype (p-value < 0.0001) and positive family history for breast and ovarian cancer (p-value: 0.0001) were significantly associated with the performance of genetic counseling. Treatment line showed no association with the performance of genetic counseling (p-value 2nd line: 0.2292, p-value 3rd line: 0.68) (see Table 1).

3.5. Genetic Test Results

Genetic test results are shown for the retrospective cohort only. Information on genetic test results of the prospective subsequent study is still pending at the time of manuscript preparation and will be presented elsewhere.
The majority of patients had a WT or Variant of Uncertain Significance (VUS) result (84.2%). The most frequent pathogenic mutation was in the BRCA2 (8.4%), followed by BRCA1 (4.2%), partner and localizer of BRCA2 (PALB2) (1.1%) and Checkpoint kinase 2 (CHEK2) gene (1.1%). In 2 of 97 tested patients the genetic test result was unknown. An overview of genetic test results is displayed in Table 2.

3.6. PARP Inhibitor Treatment

Data on the uptake of PARPi treatment is shown for the retrospective cohort only. Information on the use of PARPis in the prospective subsequent study is still being collected at the time of manuscript preparation and will be published elsewhere.
In total, 11.6% (11 of 95) of tested patients had a gBRCA1/2mut and were therefore eligible for PARPi treatment, 4 patients had a gBRCA1mut and 7 patients a gBRCA2mut. 1 patient had a somatic (s) BRCA2mut (see Table 2).
Overall, 75% (9 of 12) of patients with a gBRCA or sBRCAmut had received treatment with a PARPi. The three patients with a gBRCAmut who had not received a PARPi were on an early treatment line for metastatic disease (1 patient with TN disease on 1st treatment line, 1 patient with HR+ disease on 1st treatment line and 1 patient with HR+ disease on 2nd treatment line).
2 HER2− mBC patients without a gBRCA or sBRCAmut were treated with a PARPi on the basis of compassionate use as well as in the course of a clinical study (see Table 3).

4. Discussion

Referral rates for genetic testing of BC patients who potentially qualify for PARPi treatment or could profit from platinum-based chemotherapy remain suboptimal despite guideline recommendations [11,12,13,24,25,26,27,29,30,31].
In the present retrospective analysis of a single academic center in Austria only 47.6% (109 of 229) of HER2− mBC patients had been recommended to undergo genetic testing by the MTB. Notably, informed patients showed a high acceptance rate to undergo genetic testing, with 93.6% (132 of 141) of patients willing to undergo genetic testing, compared to 6.4% (9 of 141) who refused genetic testing. Comparably low genetic testing rates have been reported by other real-world studies [25,32]. As such an analysis of the Flatiron database revealed that only 16.7% of over 12,000 patients with mBC (86% HR+/HER2− and 14% TNBC) had received genetic testing [32].
Particularly in recent years a significant decline in genetic testing rates has been reported which may be explained by the introduction of new targeted endocrine treatment options such as CDK4/6 inhibitors in HR+/HER2− mBC [28]. A retrospective analysis of BRCA1/2m HER2− mBC patients from the USA, European Union and Israel showed that endocrine therapies were the most prevalent in patients with HR+/HER2− mBC across all treatment lines (62%, 63% and 47% in 1st, 2nd and 3rd treatment line) [33]. In TNBC patients platinum-based chemotherapy was the most common therapy in first- and third-line patients, while non-platinum-based chemotherapy was the most frequent therapy in the second treatment line. The use of PARPis only increased in later treatment lines in both BC subtypes (HR+ subtype: 1st, 2nd and 3rd treatment line: 5%, 11% and 12%; TN subtype: 1st, 2nd and 3rd treatment line: 18%, 44% and 36%) [33].
In comparison, in the present study only 3.9% (9 of 229) of all HER2− mBC patients received PARPis and treatment line showed no association with the performance of genetic counseling in order to identify potential candidates for PARPis in multivariate analysis (p-value second line: 0.2292, p-value third line: 0.68).
The EMA label approves Olaparib as monotherapy for gBRCAm HER2− locally advanced or mBC patients who have previously received chemotherapy in the neoadjuvant, adjuvant or metastatic setting and in case of HR+ mBC were treated prior with endocrine therapy or were considered inappropriate for endocrine therapy. Yet, it is important to note that, the optimal sequencing of PARPis and endocrine-targeted treatments has not been established particularly in view of emerging evidence of better outcomes when PARPis are used earlier in the treatment cascade. As such, an exploratory subgroup analysis of the OlympiAD trial showed a greater OS benefit with the PARPi compared to TPC in the first-line setting, emphasizing the importance of early treatment initiation [4,34]. Likewise, in the phase IIIb LUCY trial median OS was longer in gBRCAm HER2− mBC patients who received first-line Olaparib than in second- or third-line settings [35]. Similar results of improved outcomes in cases of earlier implementation in the therapeutic algorithm were shown for other PARPis as well [36,37].
The indication for PARPis and therefore the need for genetic testing will become increasingly relevant as combinational treatments with other drug classes such as chemotherapy (NCT02163694), programmed cell death 1 (PD-1) or programmed cell death ligand 1 (PD-L1) immune checkpoint inhibitors (NCT02849496) as well as AKT inhibitors are being studied [20,36,37,38,39,40,41,42,43].
Moreover, pathogenic variants in BC susceptibility genes beyond BRCA1/2 are increasingly being considered in clinical trials with targeted therapies emphasizing the need for multigene panels [44,45,46,47]. As such PALB2 mutations have been identified as predictive markers for PARPi treatment [44]. Notably, identification of targetable variants and therefore treatment options were two times more likely following the extension of genetic testing to multigene panels [48,49,50]. Multigene panels for BC may include (but are not limited to) ATM, BARD1, BRCA1, BRCA2, CDH1, CHEK2, NF1, PALB2, PTEN, RAD51C, RAD51D, STK11 and TP53 [12,51].
In the present study—similar to other real-world data—11.6% (11 of 95) of tested patients had a gBRCAmut and were eligible for targeted treatment [7,8]. Notably, one patient had a sBRCA2mut and subsequently received PARPi treatment in the course of a compassionate use program.
There is accumulating evidence to support testing for sBRCA1/2muts as approximately 3% of BCs harbor exclusively sBRCA1/2mut and might benefit from targeted therapy (NCT03344965) [44,52,53,54,55]. Furthermore, tumor testing allows screening for additional alterations and treatment targets [56,57,58].
In the present study, younger age (p-value: 0.0007), HR+/HER2− subtype (p-value < 0.0001) and positive family history (p-value: 0.0001) were significantly associated with the performance of genetic counseling in multivariate analysis. While these parameters have been related with BRCAm BC—it is worth noting that in the PRAEGNANT registry, a German real-world registry for mBC patients, approximately 66% of patients with a BRCA1/2mut did not have a family history of BC [9]. In another study including breast and ovarian cancer patients 39% of BRCAm patients had no family history [59].
Notably, patients with an unknown family history are more likely to undergo BRCAmut testing if they have TNBC compared to HR+/HER2− disease [60]. The effect of BC subtype on genetic testing rates was shown to be especially pronounced in non-academic settings [28,61].
While there is a relatively high prevalence of BRCAmuts in TN subtype, a multinational epidemiologic study among BRCA1mut carriers showed that 22% of tumors were estrogen receptor positive (ER+) and 21% were progesterone receptor positive (PR+), while among BRCA2mut carriers, 77% were ER+ and 64% were PR+ [62]. Therefore, genetic testing must be considered in HR+ disease if other risk factors for hereditary disease are present or PARPis and platinum salts are treatment options.
It is worth noting that the benefit with Olaparib in OlympiAD was independent of HR status [34]. Likewise, the ABRAZO study showed similar response rates to Talazoparib in BRCA1/2mut carriers with mBC independent of subtype (ER+: 29% versus TN: 26%) [63].
In the present study—besides the lack of recommendation by the MTB (52.4% (120/229) of the total patient population) and patients’ refusal to undergo genetic testing (6.4% (9/141) of informed patients)— genetic testing was not performed due to immobility of the patient (1.6% (2/129) of untested patients were not informed and invited to undergo genetic testing) and language barrier of the patient (0.8% (1/129) of untested patients were not informed and invited to undergo genetic testing).
This emphasizes the need to improve education on hereditary breast and ovarian cancer and introduce alternative genetic counseling strategies to increase access to genetic testing.
Notably, genetic counseling by a physician or geneticist is a prerequisite for genetic testing performance. The physician has been shown to have significant impact on whether patients consent to genetic testing [64]. Therefore, improved education of physicians, increasing their awareness of testing indications, clinical consequences and therapeutic options of hereditary breast and ovarian cancer and therefore their perception of the importance of genetic testing might subsequently increase its uptake.
Furthermore, besides mainstream testing approaches, where not only a geneticist but various members of the medical oncology team perform genetic counseling and testing [65], the introduction of digital tools including web-based tools, mobile applications, chatbots, videos and games in the counseling process has been shown to improve access to genetic testing [66,67,68,69,70].
The present study has some limitations. Firstly, due to the retrospective nature, no information on the incentive for genetic testing such as HER2− metastatic disease and/or family history is available. Secondly, the study was performed in a single academic institution. A multinational and institutional setting might lead to different results.

5. Conclusions

The present study—in line with other real-world data—demonstrated suboptimal referral rates of HER2− mBC patients in an academic setting, especially in older patients, those with a HR+ subtype and no family history of breast and ovarian cancer. While young age, TN subtype and positive family history are associated with BRCAm BC–genetic testing should not be limited to these patient populations if additional risk factors for hereditary disease or a potential indication for a PARPi and platinum-based chemotherapy are present. Measures to increase awareness for genetic testing indications as well as new genetic counseling strategies to increase access to genetic testing are needed. Particularly, as the present study demonstrated that patients who had been counseled showed a high willingness to undergo genetic testing which revealed targetable mutations in over 10% of tested patients.

Author Contributions

C.D. conceptualization, data curation, writing of the original draft, reviewing and editing; F.H. formal analysis, reviewing and editing of original draft; C.L. data curation, reviewing and editing; D.G.-K. data curation, reviewing and editing; C.F.S. data curation, reviewing and editing; S.K. data curation, reviewing and editing; A.G. data curation, reviewing and editing; G.P. conceptualization, data curation, writing of the original draft, reviewing and editing. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

The study was approved by the ethics committee of the Medical University of Vienna (EK-Nr.: 1707/2021) on 18 January 2022. The study was performed in accordance with the Declaration of Helsinki.

Informed Consent Statement

Patient consent to participate was waived owing to the retrospective nature of the study.

Data Availability Statement

Research data includes confidential patient information and is therefore unavailable for distribution.

Conflicts of Interest

CD: received research funding from Novartis; honoraria from Stemline, AstraZeneca, Lilly, Gilead and DaiichiSankyo; had consulting/advisory role for Novartis, Stemline and received travel/accomodation/expenses from AstraZeneca, Roche, Novartis, DaiichiSankyo, Pfizer, Stemline; FH: none; CL: none; GKD: none; CFS: received grants from Amgen, Stemline, AZ, Novartis, Gilead, Pfizer, MSD; SK: none; AG: none; GP received grants and honoraria by Pfizer, Roche, Amgen, Lilly, Seagen, Daichii Sankyo, AstraZeneca, Novartis, Accord, Menarini Stemline, MSD and Gilead.

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Figure 1. Study population overview. HER2−: Human Epidermal Growth Factor Receptor 2 negative, mBC: metastatic breast cancer, EMA: European Medicines Agency, gBRCAm: germline breast cancer gene mutant, MTB: multidisciplinary tumor board.
Figure 1. Study population overview. HER2−: Human Epidermal Growth Factor Receptor 2 negative, mBC: metastatic breast cancer, EMA: European Medicines Agency, gBRCAm: germline breast cancer gene mutant, MTB: multidisciplinary tumor board.
Jcm 15 03433 g001
Table 1. Demographic data and predictive markers for genetic testing performance.
Table 1. Demographic data and predictive markers for genetic testing performance.
Patient CharacteristicsTotal Study PopulationRecommendation for Genetic Testingp-Value
Number of Patients
(%, n = 229)
Yes
Number of Patients (%, n = 109)
No
Number of Patients (%, n = 120)
Age, mean ± SD64 ± 1359 ± 13.467.6 ± 11.80.0007
Breast cancer subtype 0.000
- HR+/HER2−76.455.095.8
- TN23.645.04.2
Treatment line
- 1st treatment line52.850.555
- 2nd treatment line17.516.518.30.2292
≥3rd treatment line29.733.026.70.68
- mean ± SD2.0 ± 1.51.0 ± 1.61.0 ± 1.3
Family history 0.0001
- positive21.033.010.0
- negative51.145.056.7
- unknown27.922.033.3
SD: standard deviation, HR+: hormone receptor positive, HER2−: Human Epidermal Growth Factor Receptor 2 negative, TN: triple negative.
Table 2. Genetic test results (only including the 95 patients with a known genetic test result).
Table 2. Genetic test results (only including the 95 patients with a known genetic test result).
Genetic Test ResultNumber of Patients
(%, n = 95)
WT or VUS84.2
BRCA2
1 patient with a somatic mutation (only tumor tissue was tested in this patient.)
8.4
BRCA14.2
PALB21.1
CHEK21.1
WT: wild-type, VUS: variant of uncertain significance, BRCA1/2: breast cancer gene 1/2, PALB2: partner and localizer of BRCA2, CHEK2: Checkpoint kinase 2.
Table 3. PARP inhibitor treatment.
Table 3. PARP inhibitor treatment.
Treatment IndicationAbsolute Number of Patients
Targetable mutations9
- gBRCA1/2mut8
- sBRCA2mut1
No targetable mutations2
- Compassionate use1
- Clinical study1
gBRCAmut: germline breast cancer gene mutation, sBRCAmut: somatic breast cancer gene mutation.
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Deutschmann, C.; Heinzl, F.; Leser, C.; Gschwantler-Kaulich, D.; Singer, C.F.; Kostic, S.; Golescu, A.; Pfeiler, G. Is Genetic Testing of HER2-Negative Metastatic Breast Cancer Patients Implemented into Clinical Practice? A Retrospective Analysis. J. Clin. Med. 2026, 15, 3433. https://doi.org/10.3390/jcm15093433

AMA Style

Deutschmann C, Heinzl F, Leser C, Gschwantler-Kaulich D, Singer CF, Kostic S, Golescu A, Pfeiler G. Is Genetic Testing of HER2-Negative Metastatic Breast Cancer Patients Implemented into Clinical Practice? A Retrospective Analysis. Journal of Clinical Medicine. 2026; 15(9):3433. https://doi.org/10.3390/jcm15093433

Chicago/Turabian Style

Deutschmann, Christine, Florian Heinzl, Carmen Leser, Daphne Gschwantler-Kaulich, Christian F. Singer, Suncica Kostic, Adelheid Golescu, and Georg Pfeiler. 2026. "Is Genetic Testing of HER2-Negative Metastatic Breast Cancer Patients Implemented into Clinical Practice? A Retrospective Analysis" Journal of Clinical Medicine 15, no. 9: 3433. https://doi.org/10.3390/jcm15093433

APA Style

Deutschmann, C., Heinzl, F., Leser, C., Gschwantler-Kaulich, D., Singer, C. F., Kostic, S., Golescu, A., & Pfeiler, G. (2026). Is Genetic Testing of HER2-Negative Metastatic Breast Cancer Patients Implemented into Clinical Practice? A Retrospective Analysis. Journal of Clinical Medicine, 15(9), 3433. https://doi.org/10.3390/jcm15093433

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