Most women with ovarian cancer experience disease relapse, presenting numerous treatment challenges for clinicians. Maintenance therapy in the relapsed setting aims to extend the time taken for a cancer to progress, thus delaying the need for additional treatments. Four therapies are currently approved in the USA for secondline maintenance treatment of platinum sensitive, recurrent ovarian cancer: one antivascular endothelial growth factor agent (bevacizumab) and three poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitors (olaparib, niraparib, and rucaparib). In addition to efficacy, maintenance therapies must have a good tolerability profile and no significant detrimental impact on quality of life, as patients who receive maintenance are generally free from cancer related symptoms. Data from key bevacizumab trials (OCEANS, NCT00434642; GOG-0213, NCT00565851; MITO16B, NCT01802749) and PARP inhibitor trials (Study 19, NCT00753545; SOLO2, NCT01874353; NOVA, NCT01847274; ARIEL3, NCT01968213) indicate that bevacizumab and the PARP inhibitors are effective in patients with platinum sensitive, recurrent ovarian cancer but differ in their tolerability profiles. In addition, the efficacy of PARP inhibitors is dependent on the presence of homologous recombination repair deficiency, with patients with the deficiency experiencing greater responses from treatment compared with those who are homologous recombination repair proficient. Allowing for caveats of cross trial comparisons, we advise that clinicians account for the following points when choosing whether and when to administer a secondline maintenance treatment for a specific patient: presence of a homologous recombination repair deficient tumor; the patient’s baseline characteristics, such as platelet count and blood pressure; mode of administration of therapy; and consideration of future treatment options for thirdline and later therapy.
- ovarian cancer
- poly(adenosine diphosphate-ribose) polymerase inhibitor
- treatment outcome
- anti-vascular endothelial growth factor agent
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Correction notice Since this paper was first published online a middle initial has been added to Robert Coleman's name.
Contributors All authors contributed to the conception of this manuscript, and the collection and interpretation of published data. All authors drafted, reviewed, and provided their comments on this manuscript, and approved the final version.
Funding Medical writing support was funded by AstraZeneca and Merck & Co Inc.
Competing interests RA: consultancy/advisory (AstraZeneca, Clovis, Pfizer, Puma, Tesaro, VBL therapeutics). RC: integration panel (DOD-CDMRP); grant review committee (NCCN); consultancy/advisory (Clovis Oncology, Esperance Pharmaceuticals, Genentech/Roche); travel/accommodation/expenses (Amgen, Array BioPharma, AstraZeneca/MedImmune, Bayer, Clovis Oncology, GOG, Research to Practice, Merck, Millennium, Roche/Genentech, New Mexico Cancer Center, University of California, Irvine, University of Cincinnati Cancer Center, University of Miami); research funding (Abbott/AbbVie, Array BioPharma, AstraZeneca/MedImmune, Clovis Oncology, Esperance Pharmaceuticals, Johnson & Johnson, Merck, OncoMed, Roche/Genentech). SNW: consulting (AstraZeneca, Clovis, Merck, MediVation, Ovation, Pfizer, Roche/Genentech, Takeda, Tesaro); research support (AstraZeneca, ArQule, Bayer, Clovis, Cotinga Pharmaceuticals, Novartis, Roche/Genentech, Tesaro).
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
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