Abstracts Clinical Lymphoma, Myeloma & Leukemia September 2023 S314 venetoclax (experimental arm) or placebo + azacitidine + venetoclax (control). Randomization will be stratified by age, cytogenetic risk group, and geographic region. Patients are eligible if aged ≥75 years or 18−74 years with specific comorbidities. Prior antileukemic therapy for AML is not allowed. Magrolimab will be administered intravenously with an initial 1 mg/kg priming dose on days 1 and 4 to mitigate on-target anemia. The dose will then be escalated to 15 mg/kg on day 8, then 30 mg/kg on days 11 and 15 and then weekly for 5 doses, followed by every other week beginning 1 week after the fifth weekly 30 mg/kg dose. Placebo will be dosed at the same frequency as magrolimab. Venetoclax will be administered orally at 100 mg on day 1, 200 mg on day 2, then 400 mg daily starting on day 3, in 28-day cycles. Azacitidine will be given intravenously or subcutaneously at 75 mg/m2 on days 1−7, or days 1−5 and 8−9. Treatment will continue until disease progression, relapse, loss of clinical benefit, unacceptable toxicity, or other discontinuation criteria. Dual primary endpoints are complete remission (CR) rate within 6 treatment cycles and overall survival. Secondary endpoints include duration of CR, transfusion independence, event-free survival, and safety. Results: Trial in progress. Conclusions: As of May 2023, patient enrollment is ongoing at ~130 active sites. Clinical trial information: NCT05079230. Funding: Gilead Sciences, Inc. Keywords: AML, phase III, magrolimab, azacitidine, anti-CD47, acute myeloid leukemia, ENHANCE-3 AML-581 Factors Associated With Survival in Secondary Acute Myeloid Leukemia in Colombia Claudia Sossa MD1,2,3, Virginia Abello MD4,3, Luis Salazar MD1,2,3, Ángela Peña MD1,5,3, Henry Idrobo MD6,3, Jheremy Reyes MD7,3, William Mantilla MD8,3, Guillermo Quintero MD9,3, Rigoberto Gómez MD10,3, Kenny Galvez MD11,3, Mario Correa MD12,3, Paola Guerrero MD13,3, Lina Gaviria MD14,3, Carlos Bermudez MD15,3, Pau Montesinos MD16, Miguel Sanz MD16, Diana Marcela Cuervo, MD4,3 1Clínica FOSCAL, Floridablanca, Colombia. 2Universidad Autónoma de Bucaramanga, Floridablanca, Colombia. 3Asociación Colombiana de Hematología y Oncología, Bogotá, Colombia. 4Hospital San José, Bogotá, Colombia. 5Programa para el Tratamiento de Enfermedades Hemato-Oncológicas de Santander, Floridablanca, Colombia. 6Centro Médico Julián Coronel, Cali, Colombia. 7Clínica Los Nogales, Bogotá, Colombia. 8Fundación Cardioinfantil, Bogotá, Colombia. 9Fundación Santa Fe de Bogotá, Bogotá, Colombia. 10Hematooncólogos SA, Cali, Colombia. 11Hospital Pablo Tobón Uribe, Medellín, Colombia. 12Clínica Nuestra Señora de los Remedios, Cali, Colombia. 13Clínica Imbanaco, Cali, Colombia. 14Hospital Universitario San Vicente Fundación, Medellín, Colombia. 15Centro de Investigaciones Clínica San Diego, Bogotá, Colombia. 16Hospital Universitario La Fe, Valencia, Spain Context: The management of secondary acute myeloid leukemia (s-AML) is challenging because its characteristics predict a poor prognosis. In Colombia, there is a paucity of evidence regarding outcomes in this subgroup of patients. Objective: To determine the factors associated with survival in patients with s-AML in Colombia. Design: Secondary analysis nested in the bidirectional multicenter observational registry of hematologic malignancies in Colombia (RENEHOC), from 2009 to February 2023. Main Outcome Measures: Overall survival (OS) and disease-free survival (DFS). Results: 85 adults diagnosed with s-AML were included; 53% were male with a median age of 66 years (IQR:22–88). Additionally, 64.5% had ECOG<2, splenomegaly (19.5%), anemia (85.1%), and abnormal karyotype (50%). The most common types of s-AML were myelodysplastic neoplasm (MDN)-AML (32.5%) and t-AML (28.8%). 44.7% of patients received non-intensive chemotherapy, 43.5% received intensive chemotherapy (IC), and 11.7% received best supportive care. There were statistically significant differences in age (P=0.0001), ECOG (P=0.001), leukocytes (P=0.007), creatinine (P=0.007), and bilirubin (P=0.03) according to therapeutic approach. During induction, 26.8% died, and 86.5% achieved complete response (CR)/complete response with incomplete count recovery (Cri), of which 36.3% underwent allogeneic hematopoietic stem cell transplantation, and 100% of this group had received IC. OS was 14.98% (95% CI, 7.09–25.63), and DFS was 17.2% (95% CI, 7.61–30.03). According to the therapeutic approach, OS was 35.6% (95% CI, 17.54–54.58) for IC, and according to s-AML type, it was 4.9% (95% CI, 0–20.21) for MDN-AML and 20.6% (95% CI, 4.42–45.05) for t-AML. Finally, DFS, in line with the therapeutic approach, was 35.17% (CI 95%, 16.17–54.91) for CI, and according to s-AML type, it was 7.94% (CI 95%, 0–29.56) for MDS-AML and 26.75% (CI 95%, 5.47–54.96) for t-AML. Conclusions: Patients with s-AML have low CR/CRi rates and high mortality rates Keywords: AML, acute myeloid leukemia, secondary acute myeloid leukemia, survival, Colombia, HSCT, allo-HSCT AML-583 Evaluation of Sirtuins and TP53 Gene Expression and Their Impact on Prognosis in Acute Myeloid Leukemia Piotr Strzałka MD1, Kinga Krawiec MD1, Dariusz Jarych MSc2, Aneta Wiśnik MSc3, Magdalena Góralska MSc3, Michał Soin MSc3, Damian Mikulski MD1, Magdalena Czemerska MD PhD1, Izabela Zawlik MD PhD4, Agnieszka Pluta MD PhD1, Agnieszka Wierzbowska MD PhD1 1Department of Hematology, Medical University of Lodz, Multidisciplinary Provincial Centre of Traumatology and Oncology Nicolas Copernicus in Lodz, Lodz, Poland. 2Laboratory of Immunobiology of Infections, Institute of Medical Biology, Polish Academy of Sciences, Lodz, Poland. 3Multidisciplinary Provincial Centre of Traumatology and Oncology Nicolas Copernicus in Lodz, Lodz, Poland. 4Laboratory of Molecular Biology, Centre for Innovative Research in Medical and Natural Sciences, College of Medical Sciences, University of Rzeszow, Rzeszow, Poland Background: Sirtuins are a family of histone deacetylases with 7 representatives (SIRT1-7), which affect numerous cellular processes. They also have regulatory functions by influencing other proteins, such as p53. Their role in acute myeloid leukemia (AML) has not
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