Publications by authors named "G Benevolo"
Calreticulin (CALR) mutations are detected in around 20% of patients with primary and post-essential thrombocythemia myelofibrosis (MF). Regardless of driver mutations, patients with splenomegaly and symptoms are generally treated with JAK2-inhibitors, most commonly ruxolitinib. Recently, new therapies specifically targeting the CALR mutant clone have entered clinical investigation.
View Article and Find Full Text PDFThis multicentre phase II study Fondazione Italiana Linfomi (FIL)-bortezomib plus rituximab plus bendamustine (BRB) tested a combination of bendamustine (90 mg/m on days 1-2), rituximab (375 mg/m intravenously on day 1) and bortezomib (1.3 mg/m sc on days 1, 8, 15, 22) every 28 days for six cycles in 38 symptomatic patients with relapsed/refractory Waldenstrom macroglobulinaemia (RR-WM). Moreover, MYD88 and CXCR4 mutations were tested by droplet digital polymerase chain reaction (ddPCR) both at baseline and at the end of treatment in 21 patients.
View Article and Find Full Text PDFArticle Synopsis
- Most patients with myelofibrosis who are treated with ruxolitinib eventually develop intolerance or relapse, leading to poor survival rates after stopping the drug; hence, the study evaluates fedratinib against best available therapy (BAT).
- The FREEDOM2 trial was a phase 3, open-label study involving 201 patients with myelofibrosis who were either intolerant or had relapsed during ruxolitinib treatment, comparing fedratinib to BAT, with the main goal being the rate of spleen volume reduction after 6 cycles.
- At the data cutoff, 36% of patients treated with fedratinib achieved a significant spleen volume reduction by the end of cycle