# Outcomes of First-Line PARP Inhibitor Therapy in Ovarian Cancer: A Multicenter Retrospective Analysis

**Authors:** Baris Koksal, Hasan Cagri Yildirim, Deniz Can Guven, Fatih Kose, Gorkem Koymen, Ozlem Ozdemir, Ugur Ozberk, Efnan Algin, Murad Guliyev, Nebi Serkan Demirci, Ozkan Alan, Ahmet Baklaci, Bilgin Demir, Ozlem Topkaya, Necdet Uskent, Kadriye Bir Yucel, Orhun Akdogan, Bahadir Koylu, Fatih Selcukbiricik, Irem Bilgetekin, Kaan Helvaci, Ahmet Unal, Huseyin Salih Semiz, Teoman Sakalar, Nadiye Sever, Ceren Mordag Cicek, Gamze Gokoz Dogu, Sedat Biter, Ertugrul Bayram, Canan Yildiz, Hacer Demir, Ismail Bayrakci, Bulent Erdogan, Mehmet Emin Kalender, Halil Goksel Guzel, Banu Ozturk, Berkan Karabuga, Ozturk Ates, Emine Bihter Cetin, Mustafa Sahbazlar, Ali Inal, Veli Sunar, Fatma Bugdayci Basal, Esra Asik, Atila Yildirim, Nejat Emre Oksuz, Yuksel Urun, Erdinc Nayir, Sema Turker, Sercan On, Ali Aytac, Serkan Menekse, Yasemin Bakkal Temi, Kazim Uygun, Elif Sahin, Merve Keskinkilic, Zafer Arik

PMC · DOI: 10.3390/jcm15041657 · 2026-02-22

## TL;DR

This study examines how well PARP inhibitors work as first-line treatment for ovarian cancer in real-world settings, showing good results for patients with BRCA mutations.

## Contribution

The study provides real-world evidence on the effectiveness and safety of first-line PARP inhibitors in ovarian cancer patients.

## Key findings

- Patients with pathogenic BRCA mutations experienced longer progression-free survival compared to those with likely pathogenic variants.
- Olaparib and niraparib showed durable progression-free survival benefits in real-world clinical practice.
- Treatment with PARP inhibitors had manageable safety profiles, with hematologic toxicities being the most common adverse events.

## Abstract

Background: Poly(ADP-ribose) polymerase (PARP) inhibitors have been established as a first-line maintenance therapy in advanced epithelial ovarian cancer (EOC) following platinum-based chemotherapy. While phase III trials have demonstrated significant progression-free survival (PFS) benefits with olaparib and niraparib, real-world data remain limited. Methods: This retrospective, multicenter real-world study included 179 patients with newly diagnosed epithelial ovarian treated with first-line maintenance olaparib or niraparib across 33 centers in Türkiye between January 2014 and March 2025. Clinical, pathological, and molecular data—including BRCA (Breast Cancer Susceptibility Gene) mutation status, origin, and variant classification—was collected. The primary endpoint was PFS, and secondary endpoints included overall survival (OS) and safety. Survival outcomes were analyzed using Kaplan–Meier methods. Results: Of 179 patients, 110 received olaparib and 69 received niraparib. BRCA mutations were present in 88.3% of patients, while 11.7% had unknown HRD status. Median follow-up was 16.5 months, and median PFS was not reached. Estimated PFS rates for the overall cohort were 91.0% at 6 months, 83.0% at 12 months, and 64.0% at 24 months. In the olaparib cohort, BRCA-mutant patients demonstrated PFS rates of 89%, 78%, 73%, and 64% at 6, 12, 18, and 24 months, respectively. In the niraparib cohort, corresponding PFS rates among BRCA-mutant patients were 87% at 6 months and 75% at 12 months. Patients harboring pathogenic BRCA variants experienced longer PFS compared with those with likely pathogenic variants. Any-grade adverse events occurred in 73.7% of patients, and grade 3–4 events in 29.6%, with hematologic toxicities predominating. Dose interruptions were more frequent with niraparib, while treatment discontinuation rates were low in both groups. No cases of myelodysplastic syndrome or acute myeloid leukemia were observed. Conclusions: In this large multicenter real-world cohort, first-line maintenance therapy with olaparib and niraparib provided durable PFS benefit in patients with advanced EOC, particularly among those with pathogenic BRCA mutations, confirming their effectiveness and manageable safety profiles in routine clinical practice.

## Linked entities

- **Genes:** Brca2 (BRCA2, DNA repair associated) [NCBI Gene 37916]
- **Diseases:** ovarian cancer (MONDO:0005140), myelodysplastic syndrome (MONDO:0018881), acute myeloid leukemia (MONDO:0015667)

## Full-text entities

- **Genes:** BRCA1 (BRCA1 DNA repair associated) [NCBI Gene 672] {aka BRCAI, BRCC1, BROVCA1, FANCS, IRIS, PNCA4}, BRCA2 (BRCA2 DNA repair associated) [NCBI Gene 675] {aka BRCC2, BROVCA2, FACD, FAD, FAD1, FANCD}, MUC16 (mucin 16, cell surface associated) [NCBI Gene 94025] {aka CA125}, PARP1 (poly(ADP-ribose) polymerase 1) [NCBI Gene 142] {aka ADPRT, ADPRT 1, ADPRT1, ARTD1, PARP, PARP-1}
- **Diseases:** Breast Cancer Susceptibility Gene (MESH:D001943), OC (MESH:D010051), events (MESH:D002318), thrombocytopenia (MESH:D013921), FIGO stage III disease (MESH:D007676), toxicities (MESH:D064420), anemia (MESH:D000740), death (MESH:D003643), neutropenia (MESH:D009503), Hematologic toxicities (MESH:D006402), acute myeloid leukemia (MESH:D015470), myelodysplastic syndrome (MESH:D009190), nausea (MESH:D009325), IV disease (MESH:D020432), fatigue (MESH:D005221), EOC (MESH:D000077216), Tumor (MESH:D009369), disease (MESH:D004194), injury to (MESH:D014947)
- **Chemicals:** Niraparib (MESH:C545685), Olaparib (MESH:C531550), platinum (MESH:D010984)
- **Species:** Homo sapiens (human, species) [taxon 9606], Meleagris gallopavo (common turkey, species) [taxon 9103]
- **Cell lines:** SOLO1 — Mus musculus (Mouse), Hybridoma (CVCL_C7RB)

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Source: https://tomesphere.com/paper/PMC12942131