Abstracts Clinical Lymphoma, Myeloma & Leukemia September 2023 S340 studied. Objective: To evaluate the clinical features and outcomes CML in AYA. Design: Files of adults with chronic phase CML treated at King Hussein Cancer Centre from 2011 to 2021 were retrospectively reviewed. Patients were grouped according to age into two groups: AYA (age 18–39 years) and Older-Age (age >39 years). Prognostic risk scores, including Sokal, Hasford, European Treatment and Outcome Study (EUTOS) and the EUTOS longterm survival (ELTS) scores, were calculated. Response to tyrosine kinase inhibitors (TKIs) was evaluated by polymerase chain reaction for BCR-ABL and stratified according to the last National Comprehensive Cancer Network guidelines (version 1.2023). Comparisons were done using Fisher’s exact and Student’s T tests. Event-free survival (EFS) and overall survival (OS) were analysed using Kaplan-Meier method. Results: Of the 165 patients, 80 (48.5%) were AYA and 95 (57.6%) were male. The median age of the AYA group was 29 (18–39 years) and 51 (40–79 years) in the Older-Age group. There was no significant difference in the clinical, laboratory, or first line treatment (first or second generation TKIs) characteristics between the two groups. While the Older-Age group had higher frequencies of intermediate Sokal (14.5% vs 46.3%, P≤0.001) and Hasford scores (14.5% vs 56.7%, P≤0.001), the AYA group had higher frequencies of low Sokal (80.6% vs 44.5%) and Hasford (83.9% vs 43.3%, P≤0.001) scores. Both groups had similar EUTOS (P=0.878) and ELTS (P=0.06) risk scores. Achievement of response milestones (TKI sensitive disease) at different time points was comparable in both groups. At a median follow-up of 46.5 (9–223) months, there was no significant difference between both groups in EFS (5-year EFS 60.2% vs 64.7% P=0.565) or OS (5-year OS 90% vs 89.8%, P=0.619). Conclusion: CML patients tend to present at a younger age in our population. Compared to older CML patients, AYA patients presented with similar clinical and laboratory features but had lower risk disease. EFS and OS were comparable between both groups. Keywords: CML, AYA, risk scores CML-398 Responses With Asciminib Continue to Deepen Over Time in Patients With Chronic Myeloid Leukemia in Chronic Phase (CML‑CP) After ≥2 Prior Tyrosine Kinase Inhibitors (TKIs) in the Phase III ASCEMBL Study Michael Mauro MD1, Andreas Hochhaus MD2, Timothy Hughes MD3, Delphine Rea MD4, Carla Boquimpani MD5, Yosuke Minami MD6, Jane Apperley MD7, Valentin Garcia-Gutiérrez MD8, Shruti Kapoor MS9, Noemi Espurz MD10, Vishal Dhamal MS11, Jorge Cortes MD12 1Memorial Sloan Kettering Cancer Center, New York, USA. 2Universitätsklinikum Jena, Jena, Germany. 3South Australian Health and Medical Research Institute and University of Adelaide, Adelaide, Australia. 4Hôpital Saint-Louis, Paris, France. 5HEMORIO, State Institute of Hematology Arthur de Siquiera Cavalcanti, Rio de Janeiro, Brazil. 6National Cancer Center Hospital East, Kashiwa, Japan. 7Centre for Haematology Imperial College London, London, United Kingdom. 8Servicio de Hematología, Hospital Universitario Ramón y Cajal (IRYCIS), Madrid, Spain. 9Novartis Pharmaceuticals Corporation, East Hanover, USA. 10Novartis Pharma AG, Basel, Switzerland. 11Novartis Healthcare Private Limited, Hyderabad, India. 12Georgia Cancer Center, Augusta, USA Context: In ASCEMBL, after ≥2 years of follow-up, asciminib continued to demonstrate superior efficacy and better safety and tolerability than bosutinib in patients with CML-CP previously treated with ≥2 TKIs. Objective: Characterize the efficacy of asciminib over time and versus bosutinib through exploratory analyses. Methods: Adults with CML-CP previously treated with ≥2 TKIs were randomized 2:1 to asciminib, 40 mg twice daily, or bosutinib, 500 mg once daily. Results: Of 18 patients on asciminib with BCR::ABL1IS >1% by week 24 who continued to receive asciminib, the probability of BCR::ABL1IS ≤1% (95% CI) was 22.2% (6.5%–43.6%) by 1 year and 38.9% (16.4%–61.0%) by 2 years. Of 56 patients on asciminib without major molecular response (MMR) by week 24 who continued to receive asciminib, the probability of MMR (95% CI) was 17.9% (9.1%–29.0%) by 1 year and 37.9% (25.1%–50.6%) by 2 years. Overall MMR rates at week 96 were higher with asciminib versus bosutinib, respectively, regardless of the last prior TKI and the reason for its discontinuation (intolerance or resistance): imatinib, 55.6% vs 14.3%; nilotinib, 40.9% vs 35.7%; dasatinib, 37.1% vs 10.5%; radotinib, 50.0% vs 0%; and ponatinib, 20.0% vs 11.8%. MMR at week 96 with asciminib versus bosutinib in patients resistant to all prior second-generation (2G) TKIs was 34.3% vs 7.7% (1 prior 2G TKI); 35.0% vs 16.7% (≥2 prior 2G TKIs). Cumulative incidence of MMR by week 96 was higher with asciminib versus bosutinib, respectively, in patients with baseline BCR::ABL1IS ≥10% (28.4% vs 12.6%) and <10% (62.1% vs 40.7%), in patients who discontinued their prior TKI due to lack of efficacy (33.2% vs 9.4%), and by line of randomized therapy (third: 45.9% vs 33.3%; fourth: 40.9% vs 24.8%). Conclusions: Responses with asciminib continued to deepen over time. Patients who continued asciminib beyond week 24 could still achieve MMR by later time points. Overall MMR rates at week 96 were higher with asciminib than bosutinib regardless of the last TKI or reason for its discontinuation and in patients resistant to all prior 2G TKIs. Efficacy of asciminib after treatment failure with 2G TKIs supports a new standard of care for patients with CML-CP. Keywords: CML, asciminib, TKI, ASCEMBL, phase III CML-415 Comparative Study Between Brand and Generic Imatinib Mesylate Using Molecular Genetic Analysis on CML Libyan Patients Reem Hammad BSc1,2, Abdulfatah Gabj PhD3 1Tripoli University Hospital, Tripoli, Libya. 2Libyan Academy of Postgraduate Studies, Janzor, Libya. 3Tripoli University, Tripoli, Libya Background: Chronic myeloid leukemia (CML) is a hematological malignancy characterized by the presence of the Philadelphia chromosome, resulting in the abnormal fusion protein BCR-ABL1. Imatinib, a tyrosine kinase inhibitor, has revolutionized the treatment of CML. However, the availability of generic versions
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