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

Abstracts Clinical Lymphoma, Myeloma & Leukemia October 2022 S290 achieved irrespective of BCR::ABL1 levels. Co n clusio n s: ddPCR proved highly sensitive and accurate. Total hands-on time was approximately 2 hrs, and time from sample to results was 2 days. Therefore, ddPCR may be integrated into diagnostic algorithms of CML (and Ph + ALL) patients as a convenient first-level screening tool for mutations impacting TKI selection. Keywords: CML, chronic myeloid leukemia, droplet digital PCR (ddPCR), BCR- ABL1 kinase domain mutations CML-187 Association of Molecular Remission With Eutos and ELTS Risk Scores Among CML Patients in the Armenian Cohort Lusine Harutyunyan MD 1 , Arusyak Ivanyan MD 1 , Narine Ghazaryan MD, PhD 1,2 , Astghik Voskanyan MD 1,3 , Karen Meliksetyan MD 1 , Anahit Ter-Grigoryan MD, PhD 1 , Lusine Sahakyan BS, PhD 1 , Maria Badikyan MD 1 , Nare Martirosyan MD 1 , Samvel Danielyan MD, PhD 1 , Yervand Hakobyan MD, PhD 1,4 1 Hematology Center aft. Prof. R. Yeolyan, Yerevan, Armenia. 2 Laboratory of Toxinology and Molecular Systematics, Institute of Physiology, Yerevan, Armenia. 3 Immune Oncology Research Institute, Yerevan, Armenia. 4 National Institute of Health, Transfusion Medicine Department, Yerevan, Armenia Current research focusing on chronic myeloid leukemia (CML) includes a prediction of treatment outcomes with risk scores and the possibility of treatment-free remission (TFR) with regular molecular monitoring. In Armenia, a low-income country, regular molecular monitoring and monitoring-based treatment has been underway since January 2021. Yet, since 2003, frontline Imatinib therapy was performed among all CML patients. Ponatinib and Nilotinib have been available since 2018. The aim of this retrospective study is to evaluate the association of molecular response with EUTOS and ELTS risk status. The data was taken from Hematology Center after prof. R. Yeolyan (Molecular Biology Department, Blood Disease Registry and Armenian CML Database). The study includes 234 newly-diagnosed CML patients during 2010-2020. Frontline therapy was performed with Imatinib in all patients, of whom 23 switched it to other TKI based on qRT-PCR results. Statistical analysis was performed by SPSS 22. The scores were measured only on the basis of CML Database, which is still being completed. EUTOS was evaluated in 114 patients: 4 (3.5%) high and 110 (96.5%) low risk. ELTS was measured in 110 patients: 16 (14.5%) high, 34 (30.9%) intermediate, and 60 (54.5%) low risk. Of the 4 high-risk patients with EUTOS, 1 achieved MR4, 1 had MR5, 1 had MR4.5, and one reached no MR. Of the 110 low-risk Eutos patients, 28 had MMR, 9 had MR4, 13 had MR5, 24 had MR4.5, and 36 reached no MR. Among 16 high-risk patients with ELTS, MMR was obtained in 3 patients, MR4 in 1, MR5 in 3, MR4.5 in 2, and 7 patients did not reach MR. Among 34 intermediate-risk patients with ELTS, MMR was achieved in 9 patients, MR4 in 4, MR5 in 5, MR4.5 in 8, and 8 achieved no MR. Of the 60 patients at low risk for ELTS, 16 patients achieved MMR, 4 patients MR4, 4 patients MR5, 15 patients MR4.5, and 21 patients did not reached MR. Overall, in the Armenian cohort, CML patients achieved MR regardless of their risk status with EUTOS and ELTS. However, based on the small number of high-risk patients, further analysis is needed for a definitive conclusion. Keywords: CML, molecular monitoring, treatment free remission, treatment outcomes, TKIs CML-216 Hypereosinophilia Syndrome With FIP1L1-PDGFRA Transcript Revealed by Cardiac Involvement Siali Nadjat MD, Benlazar Mohamed PhD CHU Sidibelabbes, Sidibelabbes, Algeria I n troductio n : Hypereosinophilic syndrome (HES) is defined by eosinophilia greater than 1.5 G/L persisting for more than 6 months and associated with specific visceral damage (cardiac, neurological, pulmonary, etc.), after elimination of “classic” causes of hypereosinophilia. A myeloproliferative variant of HES is associated with the fusion of the FIP1L1 and PGDFR  genes, resulting in the constitutive activation of a receptor with tyrosine kinase activity. We report a case revealed unexpectedly by cardiac involvement (a mitral valve disease). Obser v atio n : A 25-year-old man with no particular history, allergies, or cardiovascular risk factors was hospitalized in the cardiology department for sudden-onset precordialgia associated with low-grade fever. The clinical examination: a general state preserved asthenic, nocturnal fever with precordialgia, and stage IV splenomegaly. ECG: unremarkable; heart echo: a thickened mitral valve with moderate mitral leakage, with rupture of the chords giving moderate grade II mitral insufficiency. Three blood cultures taken at the time of the fever peak came back sterile. FNS: anemia reduced to 9 g/dL normochromic normocytic aregenerative, activated thrombocytopenia to 124 G/L, hyperleukocytosis to 65,000/mm 3 , including 81% of eosinophilic polynuclear cells (52,650 elements/mm 3 ) without myelemia. Myelogram: a very rich smear with eosinophilic hyperplasia at all stages of maturation. A thoraco-abdominopelvic CT scan showed heterogeneous splenomegaly with parenchymal involvement in centro-lobular ground glass, predominantly apical with areas of geographical somatic vertebral bone condensation staged in the dorsolumbar and pelvis. A corticosteroid test was negative, and a molecular cytogenetic study revealed the FIP1L1-PDGFRA fusion transcript in 88% of cells with a rearrangement of the locus at 4q12. The patient was put on imatinib 100 mg/day for 15 days then 200 mg/ day with prophylactic anticoagulation. The evolution was favorable with a normalization of the FNS after 20 days. After 6 months of treatment, a FISH was requested, having objectified the complete disappearance of the cytogenetic anomaly. Co n clusio n s: Chronic eosinophilic leukemia with FIP1L1-PDGFRA can be serious and fatal in the event of diagnostic delay and the nature of the affected organ. Patients with clinical manifestations consistent with HES should be investigated for evidence of clonality of hematopoiesis and a search for a T-lymphocyte population for treatment decisions. Keywords: CML, hypereosinophilia, FLIP1L1, PDGFRA