PS1050 MARKER CHROMOSOME IS A STRONG POOR PROGNOSIS FACTOR AFTER ALLOGENEIC HSCT FOR AML PATIENTS

• Published in: HemaSphere 2019-06, Vol.3 (S1), p.475-n/a
• Main Authors: Fuse, K., Tanaka, T., Uemura, S., Tamura, S., Suwabe, T., Katagiri, T., Ushiki, T., Shibasaki, Y., Satou, N., Yano, T., Kuroha, T., Hashimoto, S., Furukawa, T., Narita, M., Sone, H., Masuko, M.
• Format: Article
• Language: English
• ISSN: 2572-9241; 2572-9241
• DOI: 10.1097/01.HS9.0000562496.27488.92

Background: A marker chromosome (MC) is a fragmented chromosome whose origin cannot be identified from an existing autosomal or sex chromosome. Recently, MC was found to result from chromothripsis. Chromothripsis is a catastrophic phenomenon by which chromosomes are shattered into tens to hundreds of fragments, and half of the cases are related to TP53 gene mutation. MC is a relatively common abnormality and its incidence in acute myeloid leukemia (AML) is approximately 15%. Although AML with MC was reported to have a poor prognosis after intensive chemotherapy, the influence of MC on the outcome after allo‐HSCT for AML is unclear. Aims: We evaluated the outcomes of AML patients with MC after allo‐HSCT in comparison with other chromosomal abnormalities such as monosomal karyotype (MK), complex karyotype (CK) and existing sub‐clone (SC). Methods: This retrospective analysis included 166 AML patients who received allo‐HCT in our study group between 1990 and 2017. The median age of the patients at allo‐HCT was 38 years old. The median follow‐up period was 2.0 y.According to the revised Medical Research Council (rMRC) criteria for cytogenetic risk categories, 26 (15.7%), 104 (62.7%) and 36 (21.7%) patients were categorized as favorable‐, intermediate‐ and adverse‐risk, respectively. Results: MC was detected in 14 (8.4%) of 166 patients. Eleven (78.6%) had adverse‐risk karyotypes. CK, MK and SC were observed in 26 (16.3%), 20 (12.0%) and 23 (13.9%) patients, respectively. The median age of AML with MC (AML/MC+, n = 14) and AML without MC (AML/MC‐, n = 152) patients was similar (38.5 y vs 38 y, P = 0.812). Twelve AML/MC+ patients (85.7%) received allo‐HCT at an advanced stage and 10 (71.4%) demonstrated primary induction failure. Compared with AML/MC‐ patients, AML/MC+ patients had a higher coexistence rate of CK (85.7% vs. 9.9%, p