Journal of Clinical Oncology · 2014 · 14 citations · 0 references
MedicineOncologyPharmacologyCancer PharmacologyMetastasisMolecular OncologyMalignant NeoplasmsMetastatic Disease TreatmentOncology PharmacologyTargeted Cancer TherapyTargeted TherapyTherapy Response AssessmentAdrenal Carcinoma EvaluationClinical Activity ScoringClinical Trial ReportsErlotinib TherapyFibroblast Growth Factor Receptor AlterationsFibroblast Growth Factor Receptor SignalingRecist CriteriaStudy Phase
4588 Background: Dovitinib is a novel targeted therapy that inhibits the fibroblast growth factor receptor (FGFR). Preclinical studies have pointed to a major role of this pathway in adrenocortical carcinoma (ACC) thus we aimed to test its clinical activity in this tumor. Methods: A phase II proof of concept trial was designed. Based on a two-stage Gehan model 15 patients needed to be included to show a treatment efficacy of at least 15% (probability of Type I error α = 0.05, power [1 – β] = 0.8). Main inclusion criteria was advanced non-resectable ACC, histologically confirmed, with no prior therapy other than mitotane. Primary endpoint was response rate (RR) by RECIST 1.1 centrally assessed. Dovitinib was administered at 500mg daily dose 5 days on 2 days off for 6 months. Continuation of therapy was permitted at physician criteria. A translational substudy looking for biomarkers of efficacy was also scheduled. Results: From January 2012 to August 2012, 17 patients (5 male and 12 female) were included. Median age was 53 years (range 26–72); ECOG was 0–1 in 15 patients, 2 in one patient and N/A in one patient. Grade 3–4 adverse events deemed as related to the drug were: rash (6%), asthenia (12%), diarrhea (6%), GGT elevation (18%), nausea (6%),hypertriglyceridemia (6%), hypertension (6%), hyperkalemia (6%). No toxic death was reported. After a median follow-up of 5.2 months (range 2.27–21) one partial response has been observed. Median PFS was 1.8 months (95%CI [1.35–2.25]), however clinical benefit has been achieved in 30% of patients with long lasting stable disease (>6 months) in 23%. One patient remains on dovitinib 21 months after initiating therapy. We sequenced 409 tumor suppressor genes and oncogenes frequently mutated in cancer (Ion AmpliSeq Comprehensive Cancer Panel) in 9 FFPE tumor samples. Putative variants are currently being validated by Sanger sequencing and will presented at the meeting. Conclusions: Though primary endpoint was not reached, dovitinib showed activity in a subpopulation of ACC patients. The ongoing molecular identification of such subpopulation will be key in order to prompt further investigation. Clinical trial information: NCT01514526.