Poly(ADP‐ribose)polymerase inhibitors‐associated myeloid neoplasms: a retrospective study from the French Network of Pharmacovigilance centres.

The distribution of genetic mutations affects seven out of 20 patients (35%), mainly related to I TP53 i (six patients, 30%), I TET2 i (two patients, 10%) and I DNMT3A i (two patients, 10%). During the long-term follow-ups of randomized controlled trials (RCTs), some cases of therapy-associated myeloid neoplasms (t-MNs), including myelodysplastic syndrome (t-MDS) and acute myeloid leukaemia (t-AML), were reported both in the poly(ADP-ribose)polymerase inhibitors (PARPi) and control arms. For the 21 patients, t-MNs occurred after a median latency period of 18-2 (IQR 10-0-30-0) months following first PARPi exposure. Among them, 113 out of 32 662 patients (0-3%) with OC experienced t-MNs after a mean time from first primary cancer diagnosis of 5-3 years for t-MDS ( I n i = 47 patients) and 4-5 years for t-AML ( I n i = 66 patients), with an overall standardized incidence ratio of 5-8 (4-8-6-9).8 Our shorter latency may be linked to an underlying clonal haematopoiesis as I TET2 i and I DNMT3A i mutations were frequently found. [Extracted from the article]