Clinical Lymphoma, Myeloma & Leukemia, Vol.22, Suppl.2 - October 2022

Abstracts Clinical Lymphoma, Myeloma & Leukemia October 2022 S202 Backgrou n d: Patients with multiple myeloma (MM) have an increased risk of developing second malignancies, especially myeloid neoplasms (t-MDS/AML). However, little is known about the occurrence of lymphoid malignancies, in particular acute lymphoblastic leukemias (ALLs). Methods: We retrospectively analyzed the disease characteristics and outcomes of patients diagnosed with ALL following MM who presented to the MD Anderson Cancer Center between 2005 and 2018. Results: A total of 9 patients were identified. The majority of patients were female (88%). The median age at the time of MM diagnosis was 6 7 years (range, 48– 7 4) and 7 5 years (range, 54–85) at the time of diagnosis of ALL. All patients were receiving lenalidomide as part of MM therapy when they developed ALL. The median time from the diagnosis of MM to ALL diagnosis was 6.8 years (range, 0.33–9.86). All patients were diagnosed with Philadelphia chromosome–negative B-ALL, with a median blast percentage in the bone marrow of 83% (range, 45–100). Of the 9 patients, 3 had complex karyotype with monosomy 13/trisomy 4,5,9,15, 4 patients had a detected mutation of TP53, and 1 patient showed MLL rearrangement. Treatment of B-ALL consisted of a mini-hyper-CVD regimen (n=3) or mini- hyper-CVD + inotuzumab (n=6); 6 patients received blinatumomab as part of the consolidation therapy. Eight patients achieved CR after induction therapy. All patients during ALL diagnosis were MM free; however, 1 patient relapsed with MM after completion of ALL therapy. The median OS from the time of ALL diagnosis was 2. 7 years (range, 0.46–5.21). Co n clusio n s: B-ALL can occur in patients with MM with a median latency of 6.8 years. All patients were receiving lenalidomide at the time of diagnosis of ALL. All patients in our series had Ph-neg B-ALL, and 4/9 had a concomitant TP53 mutation. Keywords: ALL, lenalidomide, ALL post-MM, second primary malignancy ALL-350 Characterization of Acute Lymphoblastic Leukemia in the Pediatric Mexican Mestizo Population Carlos Cortes-Penagos PhD 1,2 , Carlos Alonso- Muñoz BS 1 , Milton Naranjo-Mendoza BS 1 , Victor Alfedro Pérez-Contreras M.S 1 1 Laboratorios MENDEL, Morelia, Mexico. 2 Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Mexico Co n text: Acute lymphoblastic leukemia (ALL) is the most common neoplasm of lymphoid progenitor cells in pediatric populations. ALL cases can be broadly classified as B-cell or T-cell. B-cell ALL (B-ALL) has many genetic subtypes characterized by major chromosomal alterations. Flow cytometry and biomarkers identification provide information about the subtype of ALL and can be correlated with the patient’s prognosis. Based on reactivity with antigens present on the surface or in the cytoplasm of leukemia cells, B-ALL can be divided into 4 subtypes according to its stage of differentiation: pro-B, common B, pre-B, and immature B subtypes. Objecti v e: This study aims to establish the association of the molecular biomarkers TCF3-PBX1 t(1;19), rearrangement of MLL t(4;11), BCR-ABL1 t(9;22), and ETV6-RUNX1 t(12;21) with ALL subtypes according to its stage of differentiation. D esig n : The study includes a retrospective analysis of laboratory data results from the Mexican mestizo pediatric population diagnosed with ALL during a 3-year period (2018–2021), referred to Mendel laboratories from different health institutions. Patie n ts or Other Participa n ts: Ninety ALL cases, age range 0–1 7 years, were classified by immunophenotype and tested by PCR for the biomarkers TCF3- PBX1, rearrangement of MLL, BCR-ABL1, and ETV6-RUNX1. Mai n Outco m e Measures: The biomarkers tested were expected to be present in most of the cases (>50%) regardless of the differentiated ALL subtype. Results: B-cell ALL represented 92.2% of the cases (83); the prevailing subtype was pre-B with 51.1% of all cases. The biomarkers TCF3-PBX1, rearrangement of MLL, BCR-ABL1, and ETV6-RUNX1 were present in at least one case in the subtype pro-B. ETV6-RUNX1 was identified as the only marker in common B-ALL. Seventy-one percent of the cases showed no presence of the 4 biomarkers tested and correspond to quadruple negative cases. Co n clusio n s: The biomarkers TCF3-PBX1, rearrangement of MLL, BCR-ABL1, and ETV6-RUNX1 are decisive in establishing the prognosis of patients with any of the ALL-B subtypes and enable the definition of a stratified treatment. The absence of these markers prevails in the study population, so it is essential to include other recently described mutations in laboratory determinations. Ack n owledge m e n ts: Laboratorios MENDEL, Morelia Michoacán. México. Keywords: ALL, neoplasm, biomarker, translocation ALL-373 Immunophenotype of MRD Cells as an Additional Prognostic Marker Yulia Davydova MD, PhD, Irina Galtseva MD, PhD, Nikolay Kapranov MD, PhD, Ksenia Nikiforova MD, Olga Gavrilina MD, PhD, Yulia Chabaeva MD, PhD, Galina Isinova MD, PhD, Ekaterina Kotova MD, Hunan Julhakyan MD, PhD, Elena Parovichnikova MD, PhD National Medical Research Center for Hematology, Moscow, Russian Federation Co n text: Measurable residual disease (MRD) is an independent prognostic factor in acute lymphoblastic leukemia (ALL). However, the impact of the immunophenotype of MRD cells on survival has not been studied. Objecti v e: To determine the significance of the immunophenotype of MRD cells detected at the end of induction in patients with ALL. D esig n : This study included data from 2016 to 2022 for 26 7 patients enrolled in the Russian multicenter study RALL-2016 (NCT03462095). MRD was assessed on day 7 0 in patients with complete remission. Patie n ts a n d Methods: MRD was assessed in 94 B-ALL and 77 T-ALL patients. Analysis of MRD was performed by 6–11-color flow cytometry. CD19, CD34, CD10, CD20, CD38, CD45, and CD58 were analyzed to detect MRD in all B-ALL patients. CD 7 , CD3 surface , CD3 cytoplasmic , CD4, CD8, CD5, CD99, and CD45 were analyzed to detect MRD in T-ALL patients. The expression of these antigens was assessed relative to normal bone marrow cells and transformed into a numeric score. A dendrogram was constructed using the “ward.D” method in R 3.4.4. Relapse-