Clinical Lymphoma, Myeloma & Leukemia, Vol.21, Suppl.1 - September 2021

Clinical Lymphoma, Myeloma & Leukemia September 2021 S313 Abstracts (95%CI: 48. 7 %–52. 7 %) at 1 and 5 years of follow-up, with HR: 2. 7 (95%CI: 1.43–5.32; p<0.01). Co n clusio n : As has been shown in other studies, our analyses agree and show a decrease in survival in older patients (  65 years). It is important to recognize older adult patients with these pathologies to evaluate treatment strategies with new alternatives with which better responses can be achieved with less toxicity. Keywords: AML, acute myeloid leukemia, survival, relapse-free survival AML-448 Overlapping B-Cell Non-Hodgkin Lymphoma with Myeloid Malignancies: A Case Series Ayman Youssef*, Mohamed Badreldein, Ashraf Elghandour, Sara Eshba, Reem Eshra Hematology and BMT unit, Alexandria faculty of medicine, Alexandria, Egypt Co n text: This case series is reported from the cases we give care to in our facility. Objecti v e: The main objective of this study is to highlight the possible co-incidence of myeloid malignancy with mature B cell neoplasm. D esig n : This is a case series. Patie n ts or Other Participa n ts: The case series included 4 patients with mature B-cell neoplasms and developed myeloid malignancy at the time of first presentation without giving any history of previous chemotherapy or radiotherapy exposure. Mai n Outco m es Measures: The main outcome is to report the possible occurrence of this confusing association and to study the biology behind it. Results: We have 4 cases included in this series. Case 1: A 58-year- old male who was diagnosed with chronic myeloid leukemia and showed accelerated profile. His CBC film showed peripheral leukocytosis, which was mistaken initially as a sign of acceleration; however the cell morphology was suspicious. Flow cytometric studies showed a mantle cells phenotype. His cytogenetics showed t(9,11) and extra Philadelphia chromosome. This patient received high-dose cytarabine with tyrosine kinase inhibitors and showed good response. Case 2: A 4 7 -year-old female who was diagnosed with chronic lymphocytic leukemia (CLL) and put under watchful waiting. Then, she developed pancytopenia and appearance of aggressive B symptoms. Bone marrow examination and flow cytometry confirmed the presence of two clones of cells, one of CLL phenotype and the other of myelomonocytic line, and she had normal karyotyping. She received the FLAG protocol and went into remission. Case 3: A32-year-oldmale presentedwith enlarged cervical LNs and peripheral leukocytosis. Excisional LN biopsy confirmed follicular NHL; however, promyelocytes were seen in his peripheral blood smear. Further PML-RARA mutation was detected with FISH, confirming the diagnosis of coinciding acute promyelocytic leukemia. Unfortunately, this patient died during chemotherapy induction from sepsis. Case 4: A 56-year-old male presented with bleeding and anemia. Bone marrow aspiration showed acute myeloid leukemia with dysplastic features. Further trephine biopsy showed a CLL clone. He received induction chemotherapy and died with sepsis. Co n clusio n s: This overlap of hematologic malignancies may suggest that there is a common molecular aberration behind them. Testing for TP53 mutations should have been done together with germline mutations. Keywords: AML, leukemia, lymphoma, TP53, case AML-468 Outcomes of FLT3-Mutated Acute Myeloid Leukemia Patients: A Single- Center, Real-World Experience Mahran Shoukier*, Vamsi Kota, Ravindra Jillella, Mohammad Mian, Jorge Cortes Georgia Cancer Center at Augusta University, Augusta, Georgia, USA Co n text: The FMS-like tyrosine kinase 3 (FLT3) gene confers a poor prognosis in patients with acute myeloid leukemia (AML). Objecti v e: Real-world experience for patients with FLT3 mutations in small academic institutions is scant. D esig n : We reviewed retrospectively FLT3-ITDmutated AML patients fromMarch 2015– December 2019. The median follow-up was 11.2 months [range, 1.2–48.1 months]. Setti n g: All FLT3-ITD mutated AML patients in our institution were included irrespective of allelic frequency. Patie n ts or Other Participa n ts: Twenty-five patients with newly diagnosed FLT3-ITD-mutated AML were identified. I n ter v e n tio n s: FLT3 inhibitors (midostaurin, sorafenib, and gilteritinib) (FLT3is) were administered as a single agent or in combination with cytotoxic chemotherapy (CCT) or low-intensity therapy (LIT) (hypomethylating agents). Mai n Outco m es Measures: We analyzed these patients’ responses to treatment and their outcomes. Results: Ten patients (40%) received CCT and 15 patients (60%) received CCT+FLT3i. The most frequently used FLT3i was midostaurin (12 patients, 48% of all patients). The complete remission rate (CR) and the overall response rate (ORR) (CR+CR with incomplete hematologic recovery [CRi]) were 32% and 84%, respectively. Among the patients who received CCT+FLT3i, CR and OOR were 46% and 93%, respectively. The median duration of response in frontline FLT3-ITD patients who did not receive allogeneic stem cell transplantation (ASCT) was 8 months [range, 1–22 months] (8 7 % received CCT+FLT3i). Ten patients (40%) received an ASCT (8 patients were in CR); two relapsed after ASCT (20%); one received ivosidenib and azacitidine (IDH1 mutation) after ASCT, achieved remission, then received a 2nd ASCT and maintained remission after ASCT. The other one received CCT after ASCT and subsequently died of septic shock. Four patients (40%) received maintenance therapy with FLT3is after ASCT; all of them are still in remission. All patients who did not receive ASCT relapsed; 4 received gilteritinib alone (n=3) or with LIT (n=1) after relapse. CR rate was 25% and CRi 50%; two patients relapsed (50%), and two patients (50%) subsequently received ASCT. The median overall survival for all patients was 9.2 months versus 22.8 months for patients who received ASCT. Co n clusio n s: Combination of FLT3i- based therapy with CCT is effective therapy in FLT3-ITD frontline patients in a real-world setting. Duration of response is short in the absence of ASCT. Keywords: AML, acute myeloid leukemia; FMS- like tyrosine kinase 3, FLT3-ITD, FLT3 inhibitors