UNUSUAL CLINICAL PRESENTATION OF RELAPSE IN PATIENT WITH ACUTE LYMPHOBLASTIC LEUKEMIA.

Acute lymphoblastic leukemia is a disease, which is more common in children. We report a clinical case of a patient aged 25. Thirty-two months before his last admission in Hematology clinic, acute pre- B lymphoblastic leukemia had been diagnosed and treated till March 2012. In September 2013 after bone marrow aspiration, flow cytometric analysis, trepan biopsy and biopsy of the kidney had been carried out, the patient was diagnosed with first late relapse, involving bone marrow and kidney. A second remission was achieved using Berlin- Frankfurt– Munster chemotherapy [BFM] and allogenic stem cell transplantation was performed

Modified Approach Using Mentha arvensis in the Synthesis of ZnO Nanoparticles—Textural, Structural, and Photocatalytic Properties

Zinc oxide arouses considerable interest since it has many applications—in microelectronics, environmental decontaminations, biomedicine, photocatalysis, corrosion, etc. The present investigation describes the green synthesis of nanosized ZnO particles using a low-cost, ecologically friendly approach compared to the classical methods, which are aimed at limiting their harmful effects on the environment. In this study, ZnO nanoparticles were prepared using an extract of Mentha arvensis (MA) leaves as a stabilizing/reducing agent, followed by hydrothermal treatment at 180 °C. The resulting powder samples were characterized by X-ray diffraction (XRD) phase analysis, infrared spectroscopy (IRS), scanning electron microscopy (SEM), and electron paramagnetic resonance (EPR). The specific surface area and pore size distribution were measured by the Brunauer–Emmett–Taylor (BET) method. Electronic paramagnetic resonance spectra were recorded at room temperature and at 123 K by a JEOL JES-FA 100 EPR spectrometer. The intensity of the bands within the range of 400–1700 cm−1 for biosynthesized ZnO (BS-Zn) powders decreased with the increase in the Mentha arvensis extract concentration. Upon increasing the plant extract concentration, the relative proportion of mesopores in the BS-Zn samples also increased. It was established that the photocatalytic performance of the biosynthesized powders was dependent on the MA concentration in the precursor solution. According to EPR and PL analyses, it was proved that there was a presence of singly ionized oxygen vacancies (V0+) and zinc interstitials (Zni). The use of the plant extract led to changes in the morphology, phase composition, and structure of the ZnO particles, which were responsible for the increased photocatalytic rate of discoloration of Malachite Green dye

MDS-344: Pevonedistat Plus Azacitidine vs Azacitidine Alone in Higher-Risk Myelodysplastic Syndromes (MDS): Efficacy and Safety Results from Study P-2001 (NCT02610777)

Pevonedistat, an investigational, first-in-class NEDD8-activating enzyme inhibitor, disrupts protein homeostasis, leading to cancer cell death. For patients with higher-risk MDS ineligible for transplant, real-world data reveal median overall survival (OS) is 11–15 months with treatment, yet no novel treatments have been approved in a decade. Patients with higher-risk MDS/chronic myelomonocytic leukemia or low-blast acute myeloid leukemia (AML) naive to hypomethylating agents were randomized 1:1, receiving pevonedistat (20 mg/m2 intravenously [IV], days 1, 3, 5) + azacitidine (75 mg/m2 IV/subcutaneously, days 1–5, 8, 9) (n=58) or azacitidine alone (n=62) in 28-day cycles until unacceptable toxicity, relapse, AML transformation, or progression. The study was powered for event-free survival (EFS: time from randomization to death/AML transformation, whichever occurred first). This report focuses on higher-risk MDS, including their cytogenetic and genetic characterization. In patients with higher-risk MDS (n=67/120), baseline characteristics were balanced between arms. EFS was longer with pevonedistat+azacitidine vs azacitidine (median 20.2 vs 14.8 months; HR 0.54; 95% CI 0.29–1.00; p=.045). For patients with high-risk MDS assessed using the Cleveland Clinic model formula (n=16/arm), median EFS was 20.2 vs 11.7 months (HR 0.39; 95% CI 0.17–0.90; p=.023); median OS was 24.2 vs 14.2 months (HR 0.45; 95% CI 0.19–1.05; p=.056) with pevonedistat+azacitidine vs azacitidine. Overall response rate (complete remission [CR]+partial remission [PR]+hematological improvement, n=59 response-evaluable patients) was 79% with pevonedistat+azacitidine vs 57% with azacitidine, with a CR rate of 52% vs 27% (p=.050); median duration of response (DOR, CR+PR) was 34.6 vs 13.1 months (p=.106). Median (range) time to transformation (pevonedistat+azacitidine [n=5] vs azacitidine [n=9]) was 12.2 (4.6–12.6) vs 5.9 (1.7–14.8) months. Median dose intensity of azacitidine was 98% in both arms. Exposure-adjusted adverse event (AE) rates, normalized by mean cycles dosed, were lower with pevonedistat+azacitidine vs azacitidine. Pevonedistat+azacitidine clinical activity was observed in patients with adverse-risk mutations. In patients with higher-risk MDS, pevonedistat+azacitidine prolonged EFS, delayed AML transformation, nearly doubled CR rate, and tripled DOR vsazacitidine alone. EFS and OS favored pevonedistat+azacitidine vs azacitidine in patients with high-risk MDS. Exposure-adjusted AE rates were lower with pevonedistat+azacitidine vs azacitidine without added myelosuppression