Salvage combination chemotherapy with floxuridine, dactinomycin, etoposide, and vincristine (FAEV) for patients with relapsed/chemoresistant gestational trophoblastic neoplasia

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Abstract

Background: Although most patients with gestational trophoblastic neoplasia (GTN) are cured by conventional chemotherapy, some develop drug resistance or relapse. The use of new combination drugs has been studied to treat those with resistant or relapsed disease. We evaluated the results of floxuridine, dactinomycin, etoposide, and vincristine (FAEV) chemotherapy in patients with relapsed/chemoresistant GTN. Patients and methods: Clinical data and outcome of the patients with relapsed/chemoresistant GTN from 1 January 2005 to 30 June 2008 were retrospectively reviewed. Eligible patients had received at least one cycle of FAEV chemotherapy. The primary end points were response rate and toxicity of FAEV regimen; the secondary end point was assessment of clinical predictors of response. Results: In total, 91 patients were included. Fifty-five of these patients (60.4%) achieved serologic complete remission (SCR), 29 patients had no response, 7 patients experienced recurrent grade ≥3 or intolerable toxicity. SCR of FAEV chemotherapy was significantly associated with number of previous chemotherapy regimens (≤2) in multivariate analysis (P = 0.005). The most serious adverse events were greater than or equal to grade 3 neutropenia (26.4%), febrile neutropenia (6.6%), and greater than or equal to grade 3 thrombocytopenia (3.3%). Conclusion: FAEV is an effective regimen with manageable toxicity for patients with relapsed/chemoresistant GTN. Further studies of this regimen are warranted. © The Author 2011. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved.

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Feng, F., Xiang, Y., Wan, X., Geng, S., & Wang, T. (2011). Salvage combination chemotherapy with floxuridine, dactinomycin, etoposide, and vincristine (FAEV) for patients with relapsed/chemoresistant gestational trophoblastic neoplasia. Annals of Oncology, 22(7), 1588–1594. https://doi.org/10.1093/annonc/mdq649

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