Abstract
Background
The indications for Poly(ADP-ribose) polymerase (PARP) inhibitor maintenance therapy in platinum-sensitive recurrent ovarian cancer (PSROC) patients varies across nations. The lack of clinical trial evidence and detailed biomarker analysis in the Asian population results in uncertain clinical benefits. Additionally, the absence of long-term safety monitoring data limits the assessment of tolerance to prolonged PARP inhibitor use.
Methods
This prospective, open-label, single-arm, phase IIIb L-MOCA study enrolled Asian patients with high-grade epithelial PSROC across China and Malaysia. Patients received oral olaparib (300 mg) twice daily until disease progression or unacceptable toxicity. The primary endpoint of progression-free survival has been reported previously. A prespecified final OS analysis was conducted at approximately 60% data maturity.
Results
After a median follow-up of 73.4 months, the median OS (mOS) reached 51.0 months (95% CI, 42.7 to 56.1). The mOS was 64.4 months (49.9 to not reach [NR]) in BRCA-mutated patients and 40.9 months (33.3 to 51.0) in BRCA wild-type patients. The mOS was 54.4 months (42.5 to NE) in HRD-positive patients and 34.8 months (28.3 to 46.6) in HRD-negative patients. No new safety signals were identified compared to the primary L-MOCA report. Myelodysplastic syndrome and acute myeloid leukemia (MDS/AML) occurred in 1.3% of patients, and no additional cases were identified after approximately four additional years of follow-up beyond the primary analysis.
Conclusion
Long-term follow-up data from L-MOCA indicates that olaparib maintenance monotherapy shows promising overall survival and tolerable safety profile in Asian PSROC patients, regardless of BRCA or HRD status.
Trial registration
Registry: ClinicalTrials.gov.
Supplementary Information
The online version contains supplementary material available at 10.1186/s13048-026-02144-4.
Keywords: Olaparib, PARP inhibitor, Platinum-sensitive relapsed, Ovarian cancer
Introduction
Poly(ADP-ribose) polymerase (PARP) inhibitors have become integral maintenance options for patients with platinum-sensitive relapsed ovarian cancer (PSROC) [1, 2]. While maintenance PARP inhibition consistently delivers progression-free survival (PFS) benefits, the translation of this efficacy into overall survival (OS) remains discordant. Moreover, there is heterogeneity in long-term prognosis among subgroups defined by different biomarkers, with some non-BRCA-mutated populations showing numerically unfavorable OS trends, underscoring the need for careful benefit-risk reassessment in the recurrent setting [3–5]. These mature OS findings have prompted regulatory standards reassessments in the United States, leading to restrictions of recurrent maintenance indications primarily to BRCA-mutated disease and withdrawal of selected treatment indications [6].
In contrast, maintenance indications for selected PARP inhibitors remain broader in the European Union and China, contributing to regional divergence in clinical practice [7]. This divergence reinforces the need for robust long-term evidence that jointly characterizes mature OS outcomes and late-onset toxicities in cohorts reflective of contemporary practice, particularly beyond the highly selected populations of initial registration trials. Specifically, rare but serious events such as myelodysplastic syndrome/acute myeloid leukemia (MDS/AML) further underscore the importance of extended safety follow-up.
The phase IIIb L-MOCA study evaluated olaparib as maintenance therapy in a multicenter Asian cohort of PSROC patients, a population that was previously underrepresented in earlier studies [8, 9]. The primary analysis previously reported a median PFS of 16.1 months (95% CI, 13.3 to 18.3) with activity across prespecified biomarker subgroups [8]. Here, we report the final OS analysis after a median follow-up of 73.4 months, together with updated secondary efficacy endpoints and long-term safety outcomes, to inform current benefit–risk considerations of prolonged maintenance therapy.
Methods
Study design and participants
L-MOCA (NCT03534453) was a prospective, open-label, single-arm, multicenter, phase IIIb study conducted across 37 centers in China and Malaysia. The study evaluated the efficacy and safety of oral Olaparib at a dose of 300 mg (tablet formulation) twice daily as maintenance monotherapy in patients with PSR OC who had achieved a complete or partial response to their most recent platinum-based chemotherapy.
Detailed eligibility criteria and study design has been published previously [8]. Briefly, eligible participants were women aged ≥ 18 years with relapsed, high-grade serous or high-grade endometrioid PSR epithelial ovarian, primary peritoneal, or fallopian tube cancer, with an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1. Patients were required to have received at least two prior lines of platinum-based chemotherapy and to have platinum sensitive relapse, defined as progression at least six months after the last dose of platinum. Key exclusion criteria included prior treatment with a PARP inhibitor, and adequate organ and bone marrow function was required within 28 days before the first dose.
The study complied with the Declaration of Helsinki and Good Clinical Practice guidelines. The trial protocol and its amendments were approved by the Chinese national regulatory authority and ethics committees at each participating center [(2018)-(3)-No.4 for the leading site]. All patients provided written informed consent prior to enrollment.
Procedures
Patients received oral olaparib 300 mg twice daily until disease progression (radiologically confirmed by investigators per Response Evaluation Criteria in Solid Tumors version 1.1 [RECIST v1.1]) or intolerable toxicity. At screening, blood and or archival or newly obtained tumor tissue were collected for biomarker testing, including assessment of BRCA status in tumor with germline testing when available, and evaluation of homologous recombination status with the ACTHRD™ assay [10, 11].
Tumor assessments were performed by investigators according to RECIST v1.1 at baseline, every 12 weeks until week 72, and every 24 weeks thereafter until objective disease progression. Clinical evaluations, laboratory tests, and adverse event monitoring were conducted at scheduled visits throughout treatment. Adverse events were graded using the National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. Dose interruptions and reductions were permitted to manage toxicity. Continuation of treatment beyond progression was allowed clinically justified by the investigator discretion and provided patients did meet other discontinuation criteria. After treatment discontinuation, subsequent anticancer therapies were recorded.
Study endpoints and assessments
The primary endpoint was investigator-assessed PFS per RECIST v1.1. Results of the primary analysis, along with safety and tolerability data, have been published previously [8]. Secondary endpoints included OS, time from first dose to second progression (PFS2), time to first subsequent treatment or death (TFST), time to study treatment discontinuation or death (TDT), and time to second subsequent treatment or death (TSST). Prespecified exploratory analyses evaluated olaparib efficacy by BRCA mutation or HRD status. Efficacy was further analyzed by number of prior treatment lines in a subgroup analysis.
Key safety endpoints included the incidence and severity of treatment-emergent adverse events (TEAEs) and serious TEAEs, graded according to the CTCAE version 4.0, per investigator’s assessment. AEs of special interest, including myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), and new primary malignancies, were actively monitored during treatment and survival follow-up.
Statistical analysis
Sample size determination and PFS analysis was detailed in previous publication [8]. The final analysis of OS was prespecified upon reaching approximately 60% event maturity. Efficacy and safety were evaluated in the full analysis set, defined as all patients who received at least one dose of Olaparib. Descriptive statistics were employed to summarize the data using and time-to-event endpoints were analyzed using Kaplan–Meier method. Statistical analyses were performed using SAS version 9.4 (SAS, Cary, NC).
Results
Patient characteristics
Between March 2018 and December 2020, 225 patients were enrolled, of whom 224 received Olaparib and comprised the full analysis set. Baseline characteristics are summarized in Table S1 and have been described previously [8]. The representativeness of study participants is shown in Table S2. In summary, the study included exclusively female patients, with a median age of 54.0 years [interquartile range (IQR), 50.0–61.5], the majority of whom were Chinese [91.5% (n = 205), Malaysia 8.5% (n = 19)]. Among the participants, 47.3% had BRCA mutations (106 of 224). Of the 190 patients evaluated for HRD status, 65.8% were identified as HRD positive (125 of 190). As of the January 20, 2025 data cutoff (DCO), 207 patients (92.4%) had discontinued treatment, primarily due to disease progression (139 patients, 62.1%), and a total of 157 patients (70.1%) had exited the study.
Efficacy
At DCO, the median follow-up duration was 73.4 months (IQR, 60.4–75.2), corresponding to 56.7% maturity in overall survival data (127/224 events). The median OS was 51.0 months (95% confidence interval [CI], 42.7–56.1) (Fig. 1A; Table 1). Among 223 patients with confirmed BRCA mutation status, the median OS was 64.4 months (49.9–not reached [NR]) in BRCAm tumors and 40.9 months (33.3–51.0) in BRCAwt tumor (Fig. 1B; Table 1). Within the BRCA mutated subgroups, the median OS was 57.6 months (49.9–NR ) for germline mutations and not reached (NR; 29.4–NR) for somatic BRCA1/2 mutations. By HRD status among the 151 patients with assessment, the median OS was 54.4 months (42.5–NR) in HRD-positive patients and 34.8 months (28.3–46.4) in HRD-negative patients (Table 1; Fig. 1C). In patients with both biomarkers available, the median OS was 64.4 months (43.5–NR) in HRD-positive/BRCAm patients, while HRD-positive/BRCAwt patients demonstrated a median OS of 42.5 months (32.8–73.0).
Fig. 1.
KM curves of OS in the FAS (A), in subgroups stratified by BRCA mutation status (B) and HRD status (C)
Table 1.
Subgroup analysis of OS
| Patients with events, n/N (%) | Median OS, months (95% CI) | |
|---|---|---|
| Overall | 127/224 (56.7) | 51.0 (42.7 to 56.1) |
| By BRCA mutation statusa | ||
| BRCAm | 51/106 (48.1) | 64.4 (49.9 to NE) |
| BRCAwt | 75/117 (64.1) | 40.9 (33.3 to 51.0) |
| By HRD statusa, b | ||
| HRD-positive | 65/125 (52.0) | 54.4 (42.5 to NE) |
| HRD-positive +BRCAm | 34/71 (47.9) | 64.4 (43.5 to NE) |
| HRD-positive +BRCAwt | 31/54 (57.4) | 42.5 (32.8 to 73.0) |
| HRD-negative | 20/26 (76.9) | 34.8 (28.3 to 46.4) |
| By prior lines of anticancer therapy | ||
| 2L | 80/144 (55.6) | 54.6 (43.3 to 67.5) |
| BRCAm | 31/67 (46.3) | NR (51.9 to NE) |
| BRCAwt | 49/77 (63.6) | 43.1 (33.3 to 55.6) |
| > 2L | 47/80 (58.8) | 39.5 (30.1 to 53.6) |
| BRCAm | 20/39 (51.3) | 44.6 (29.3 to NE) |
| BRCAwt | 26/40 (65.0) | 38.0 (24.9 to 51.0) |
2L, second-line; HRD, homologous recombination deficiency; IC, immune cell; mut, mutation; NE, not evaluable; NR, not reached; OS, overall survival; wt, wildtype
aHRD status and BRCA mutations were detected in tumor tissue; 39 patients had unknown HRD status and 1 patient had unknown BRCA mutation status
b219 patients provided informed consent for HRD testing, of which 190 patients had residual DNA available for HRD assay; 39 patients tested had unknown status
Median OS was 54.6 months (43.3–67.5) in patients who had received two prior lines of therapy, and 39.5 months (930.1–53.6) in those with more than two prior lines of therapy (Fig. 2A; Table 1). Among patients with two prior lines, the median OS was NR (51.9–NR) in those with BRCA mutations, and 43.1 months (33.3–55.6) in those with BRCAwt tumor (Fig. 2B; Table 1). Among patients with more than two prior lines, the median OS was 44.6 months (95% CI, 29.3–NR) in those with BRCA mutations and 38.0 months (24.9–51.0) in those with BRCAwt.
Fig. 2.
KM curves of OS by prior lines of anticancer therapy (A), and by BRCA mutation status prior lines of anticancer therapy (B)
The investigator-assessed median PFS was 16.2 months (12.5–18.2), consistent with the primary analysis (Table 2). Overall, 153 patients (68.3%) received subsequent therapy (Table S3). The median TDT was 13.7 months (95% CI, 9.8 to 15.8) (Table 2), with 15.2% (95% CI, 10.8 to 20.2), 8.5% (95% CI, 5.3 to 12.6), and 7.5% (95% CI, 4.5 to 11.5) of patients remaining on treatment at 36, 60, and 72 months, respectively. The median TFST was 18.3 months (95% CI, 16.0 to 20.9) (Table 2), with 30.0% (95% CI, 24.1 to 36.2), 21.5% (95% CI, 16.2 to 27.2), and 20.9% (95% CI, 15.8 to 26.6) of patients free from subsequent treatment or death at 36, 60, and 72 months, respectively. The median PFS2 was 29.4 months (95% CI, 26.2 to 32.8), with a PFS2 rate of 39.2% (95% CI, 32.6 to 45.7) at 36 months, 24.4% (95% CI, 18.7 to 30.5) at 60 months, and 22.5% (95% CI, 17.0 to 28.6) at 72 months. The median TSST was 34.0 months (95% CI, 30.3 to 41.4); where 47.9% (95% CI, 41.1 to 54.5), 32.7% (95% CI, 26.4 to 39.1), and 32.1% (95% CI, 25.8 to 38.6) of patients were free from second subsequent treatment or death at 36, 60, and 72 months, respectively.
Table 2.
Updated efficacy endpoints
| Endpoint | Patients with events, n/N (%) | Median, months (95% CI) |
|---|---|---|
| PFS | 171/224 (76.3) | 16.2 (12.5, 18.2) |
| By BRCA statusa | ||
| BRCAm | 75/106 (70.8) | 20.1 (16.4 to 26.1) |
| BRCAwt | 95/117 (81.2) | 11.0 (8.3 to 15.8) |
| By HRD statusa, b | ||
| HRD-positive | 92/125 (73.6) | 16.6 (14.3 to 22.1) |
| HRD-positive + BRCAm | 48/71 (67.6) | 20.1 (14.5 to 27.5) |
| HRD-positive +BRCAwt | 44/54 (81.5) | 15.8 (6.9 to 20.9) |
| HRD-negative | 23/26 (88.5) | 9.2 (7.5 to 13.8) |
| By prior lines of anticancer therapy | ||
| 2L | 106/144 (73.6) | 17.6 (15.8 to 22.1) |
| > 2L | 65/80 (81.3) | 11.0 (7.5 to 15.6) |
| TDT | 207/224 (92.4) | 13.7 (9.8 to 15.8) |
| TFST | 172/224 (76.8) | 18.3 (16.0 to 20.9) |
| PFS2 | 162/224 (72.3) | 29.4 (26.2 to 32.8) |
| TSST | 144/224 (64.3) | 34.0 (30.3 to 41.4) |
aHRD status and BRCA mutations were detected in tumor tissue; 39 patients had unknown HRD status and 1 patient had unknown BRCA mutation status
bHRD tested in 219 patients who provided informed consent, of which 190 patients had residual DNA available for HRD assay; 39 patients tested had unknown status
2L, second-line; HRD, homologous recombination deficiency; PFS, progression free survival; PFS2, time from first dose to second progression ; TDT, time to Olaparib discontinuation or death; TFST, time to first subsequent therapy or death; TSST, time to second subsequent treatment or death; wt, wildtype
Safety
In the full analysis set, the median total exposure time to olaparib was 418.5 days (IQR 170.0-799.0), accompanied by a median daily dose of 588.4 mg/day (IQR 506.5-597.1). TEAEs of any grade occurred in 98.7% (n = 221) of patients, with the primary occurrences being anemia (n = 165, 73.7%), nausea (n = 121, 54.0%), and reduced white blood cell count (n = 106, 47.3%) (Table 3). Grade ≥ 3 TEAEs were reported in 49.1% (n = 110) of patients, with the most common ones being anemia (n = 54, 24.1%), decreased neutrophil count (n = 31, 13.8%), and decreased white blood cell count (n = 20, 8.9%). A total of 220 patients (98.2%) experienced treatment-related TEAEs of any grade, as evaluated by the investigator; among them, 99 cases (44.2%) were of grade ≥ 3. Serious TEAEs were observed in 60 patients (26.8%); among them, 40 cases (17.9%) were treatment-related, with anemia (n = 23, 10.3%) and myelosuppression (n = 5, 2.2%) being the most frequently reported treatment-related serious TEAEs (according to preferred terms). The remaining hematological TEAEs in ≤ 10% of patients are presented in Table S4.
Table 3.
Summary of TEAEs
| N (%) | Olaparib (N = 224) | |
|---|---|---|
| Any grade TEAE | 221 (98.7) | |
| Grade ≥ 3 | 110 (49.1) | |
| Treatment-related TEAE | 220 (98.2) | |
| Grade ≥ 3 | 99 (44.2) | |
| Any serious TEAE | 60 (26.8) | |
| Treatment-related serious TEAE | 40 (17.9) | |
| Any TEAE leading to dose modification | 143 (63.8) | |
| Treatment-related TEAE leading to dose modification | 135 (60.3) | |
| Any TEAE leading to dose reduction | 90 (40.2) | |
| Treatment-related TEAE leading to dose reduction | 89 (39.7) | |
| Any TEAE leading to treatment discontinuation | 29 (12.9) | |
| Treatment-related TEAE leading to treatment discontinuation | 28 (12.5) | |
| Any TEAE occurring in > 10% of patients, n (%) | Any grade | Grade ≥ 3 |
| Nausea | 121 (54.0) | 1 (0.4) |
| Anemia | 165 (73.7) | 54 (24.1) |
| White blood cell count decreased | 106 (47.3) | 20 (8.9) |
| Platelet count decreased | 76 (33.9) | 8 (3.6) |
| Neutrophil count decreased | 98 (43.8) | 31 (13.8) |
| Vomiting | 57 (25.4) | 5 (2.2) |
| Leukopenia | 56 (25.0) | 8 (3.6) |
| Upper respiratory tract infection | 43 (19.2) | 4 (1.8) |
| Neutropenia | 42 (18.8) | 11 (4.9) |
| Decreased appetite | 41 (18.3) | 0 |
| Aspartate aminotransferase increased | 33 (14.7) | 1 (0.4) |
| Alanine aminotransferase increased | 33 (14.7) | 2 (0.9) |
| Cough | 28 (12.5) | 0 |
| Nasopharyngitis | 26 (11.6) | 0 |
| Asthenia | 24 (10.7) | 0 |
| Dizziness | 25 (11.2) | 2 (0.9) |
| Lymphocyte count decreased | 25 (11.2) | 4 (1.8) |
| Thrombocytopenia | 23 (10.3) | 6 (2.7) |
SAE, serious adverse event; TEAE, treatment emergent adverse event
Dose adjustments due to TEAEs were observed in 143 patients (63.8%), with 90 of them (40.2%) requiring a reduction in dosage. TEAEs led to the discontinuation of treatment in 29 patients (12.9%) and resulted in death in one patient (0.4%) due to AML. At the time of the final analysis, MDS or AML occurred in 3 patients (1.3%), with no increase in incidence compared to the primary analysis [8].
Discussion
The recurrent maintenance landscape for PARP inhibitors is characterized by consistent PFS benefit but less consistent OS findings. The final OS results of Study 19 are encouraging for PSR OC patients receiving Olaparib, irrespective of their BRCA1/2 mutation status [5]. However, extended follow-up from ENGOT-OV16/NOVA showed that in the non–germline BRCA cohort, OS outcomes were similar between niraparib and placebo. The final OS analysis of ARIEL3 also did not demonstrate a clear OS benefit from rucaparib in the HRD or overall populations [3, 4]. Interpretation of OS in this setting is complicated by subsequent therapies and post-progression PARP inhibitor use. Prolonged exposure also warrants careful monitoring for delayed hematologic toxicities, supporting the value of extended safety follow-up. In this context, the prespecified final analysis of the phase IIIb L-MOCA trial provides long-term outcomes for olaparib maintenance in a comprehensive multicenter Asian PSROC cohort with a median follow-up exceeding 73.4 months, providing essential clinical data and evidence for the benefits of PARP inhibitors in the OS of the entire PSROC patients. Median OS reached 51.0 months at 56.7% event maturity, and OS estimates remained clinically meaningful across prespecified biomarker and clinical subsets, including BRCA mutation, HRD status and number of prior lines of chemotherapy. Updated secondary time-to-event endpoints, including PFS2, TFST, and TSST, further supported durable disease control beyond first progression.
Regulatory decisions for PARP inhibitor maintenance in PSROC remain heterogeneous across regions. Since late 2022, the FDA has restricted recurrent maintenance indications primarily to BRCA-mutated disease, whereas broader labels have been retained in the European Union and China [7, 12]. Due to ethical reasons and the priority of enhancing patient benefits, L-MOCA study was designed without a control arm, incorporating the entire PSROC population in the treatment arm. Because patients receiving placebo had shorter PFS than those receiving PARPi [13–15]. In China, randomized data from the phase III NORA trial provides relevant regional context, with hazard ratios for OS, mid-term endpoints, including CFI, TFST, and PFS-2 favoring niraparib over placebo in both germline BRCA–mutated and non–germline BRCA subgroups [16]. Importantly, NORA enrolled patients exclusively in the second-line maintenance setting, whereas L-MOCA included a substantial proportion of heavily pretreated patients, with 35.7% having received three or more prior lines of chemotherapy. In L-MOCA, median OS was 64.4 months in BRCA-mutated disease and 40.9 months in BRCA wild-type disease. The clinical benefit of olaparib in BRCA-mutated subgroups were numerically comparable with SOLO2 trials, which reported mOS of 51.7 months in the BRCAm subgroup receiving olaparib [17]. In addition, prospective evidence specifically targeting the HRD-negative subgroup of Chinese PSROC patients remains limited. We additionally assessed OS by HRD status, where median OS was numerically longer in HRD-positive than in HRD-negative disease (54.4 vs. 34.8 months). The findings are in agreement with the results of the OPINION trial that included HRD testing. Specifically, the median overall survival (OS) rates were 40.1 months for the HRD-positive subgroup, which includes the sBRCAm subgroup; 37.4 months for the HRD-positive subgroup excluding the sBRCAm subgroup; and 31.4 months for the HRD-negative subgroup [18]. It is important to emphasize that L-MOCA is a Phase IIIb, single-arm study targeting a broader Asian PSROC population, rather than a biomarker-selected trial enriched based on HRD status. In this research, HRD status was defined only as a predefined exploratory stratification factor and not as an inclusion or exclusion criterion. Additionally, one should be aware that the count of HRD-negative patients in this study is relatively small, therefore, associated findings should be interpreted cautiously. Nevertheless, due to the limited availability of clinical trials focused on HRD testing in patients with PSROC undergoing PARP inhibitor treatment, our study offers meaningful implications for the use of Olaparib among PSROC patients with different HRD statuses, particularly in Asian cohorts. Although cross-trial comparisons should be interpreted cautiously, and considering the maximization of benefits for PSROC patients, a single-arm study design was employed in this study. Long-term follow-up from L-MOCA adds evidence that extended survival can be observed alongside PARP inhibitor maintenance in broader Asian PSR OC populations.
Long-term tolerability is central to current benefit-risk assessment of PARP inhibitor maintenance. As of the data cut-off, the safety profile of olaparib remained consistent with that reported at the primary analysis, and no new safety signals emerged with extended follow-up [8]. The overall safety profile was consistent with the established olaparib experience reported in global studies such as Study 19 and SOLO2 studies [5, 17]. Dose interruption and reduction were common in our cohort and represent an integral component of long-term management during maintenance therapy. MDS or AML occurred in 1.3% of patients after extended follow-up. Reported incidences of MDS/AML have varied across randomized maintenance trials in recurrent ovarian cancer (e.g., SOLO2 8%, NORA 1.7%, and ARIEL3 4%). This study reports a lower incidence of MDS/AML compared to the SOLO-2 trial. Previous research has indicated that factors such as germline BRCA mutations and history of platinum-based chemotherapy exposure are significant risk factors for MDS/AML [19–20]. Our study features a lower proportion of gBRCAmut patients receiving Olaparib compared to the SOLO-2 trial (41.1% vs. 100%) and a smaller percentage of patients who had received more than two lines of chemotherapy (35.7% vs. 44%). In addition, a higher percentage of patients in our study required dosage reductions (40.2% vs. 28%). These differences may contribute to the relatively low rates of MDS/AML observed in the L-MOCA trial. Importantly, after approximately four additional years of follow-up beyond the primary analysis, no new MDS/AML cases were identified, supporting the stability of this key long-term safety signal with prolonged observation. Overall, our study provides long-term follow-up and safety data for olaparib, demonstrating that olaparib toxicity can typically be managed through dose adjustments guided by the protocol, and long-term treatment is feasible in Asian population.
In conclusion, this open-label, phase IIIb study, Olaparib maintenance monotherapy showed promising OS and an acceptable safety profile in Asian patients with advanced PSR OC, regardless of BRCAm or HRD status. These findings are consistent with global evidence and strongly support the use of Olaparib in Asian patients with PSR OC.
Supplementary Information
Acknowledgements
We would like to thank the participating patients and their families for making the study possible, and also the investigators and clinical study teams who conducted the study. Medical writing assistance was provided by Pearl Toh, PhD, and Flint Stevenson-Jones, PhD, of Parexel, which was funded by AstraZeneca, Shanghai, China.
Authors’ contributions
X. Liu: Resources, data curation, writing–original draft, writing–review and editing.D. Liu: Resources, data curation, writing–original draft, writing–review and editing.Z. Peng: Resources, data curation, writing–original draft, writing–review and editing.J. Zhu: Resources, data curation, writing–original draft, writing–review and editing.W. Zhao: Resources, data curation, writing–original draft, writing–review and editing.Y. Huang: Resources, data curation, writing–original draft, writing–review and editing.R. An: Resources, data curation, writing–original draft, writing–review and editing.H. Zheng: Resources, data curation, writing–original draft, writing–review and editing.P. Qu: Resources, data curation, writing–original draft, writing–review and editing.L. Wang: Resources, data curation, writing–original draft, writing–review and editing.Q. Zhou: Resources, data curation, writing–original draft, writing–review and editing.D. Wang: Resources, data curation, writing–original draft, writing–review and editing.G. Lou: Resources, data curation, writing–original draft, writing–review and editing.J. Wang: Resources, data curation, writing–original draft, writing–review and editing.K. Wang: Resources, data curation, writing–original draft, writing–review and editing.J. Low: Resources, data curation, writing–original draft, writing–review and editing.B. Kong: Resources, data curation, writing–original draft, writing–review and editing.R. Yin: Resources, data curation, writing–original draft, writing–review and editing.X. Xie: Resources, data curation, writing–original draft, writing–review and editing.J. Liu: Resources, data curation, writing–original draft, writing–review and editing.W. Sun: Resources, data curation, writing–original draft, writing–review and editing.R. Zang: Resources, methodology, writing–original draft, project administration, writing–review and editing.D. Ma: Conceptualization, resources, investigation, methodology, writing–original draft, project administration, writing–review and editing.Q. Gao: Conceptualization, resources, writing–original draft, project administration, writing–review and editing.
Funding
The study was funded by AstraZeneca, Shanghai, China and National Science Foundation of China (#U25A20117).
Data availability
The data supporting the findings of this study are available within the article and its supplementary materials.
Declarations
Ethics approval and consent to participate
The trial protocol and its amendments were approved by the Chinese national regulatory authority and ethics committees at each participating center [(2018)-(3)-No.4 for the leading site]. The study (NCT03534453) complied with the Declaration of Helsinki and Good Clinical Practice guidelines. Informed written consent was obtained from all study participants.
Consent for publication
Not Applicable.
Competing interests
The authors declare no competing interests.
Clinical trial registration number
Footnotes
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Xingzhe Liu, Dan Liu, Zikun Peng, Jianqing Zhu, Weidong Zhao and Yi Huang contributed equally to this work.
Contributor Information
Rongyu Zang, Email: zang.rongyu@zs-hospital.sh.cn.
Ding Ma, Email: dma@tjh.tjmu.edu.cn.
Qinglei Gao, Email: qingleigao@hotmail.com.
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Data Availability Statement
The data supporting the findings of this study are available within the article and its supplementary materials.