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Wang L. et al: Characteristics and Therapy of AML-MRCRESEARCH ARTICLEDOI: 10.4274/tjh.galenos.2021.2021.0009Turk J Hematol 2021;38:188-194Clinical Characteristics and Optimal Therapy of Acute MyeloidLeukemia with Myelodysplasia-Related Changes: A RetrospectiveAnalysis of a Cohort of Chinese PatientsMyelodisplazi İlişkili Değişiklikler Gösteren Akut Myeloid Löseminin Klinik Özellikleri veOptimal Tedavisi: Çinli Hastalar Kohortunun Retrospektif Bir AnaliziLei Wang 1 , Xiaoxia Chu 1 , Jingyao Wang 1 , Licai An 1 , Yinghui Liu 1 , Li Li 2 , Junqing Xu 11Qingdao University Medical College, Affiliated Yantai Yuhuangding Hospital, Department of Hematology, Yantai, China2Linyi Central Hospital, Department of Hematology, Linyi, ChinaAbstractObjective: This study aimed to investigate the clinical characteristicsof acute myeloid leukemia with myelodysplasia-related changes (AML-MRC) according to the 2016 World Health Organization classificationand the preferred therapy for patients with AML-MRC aged 60-75years.Materials and Methods: We retrospectively analyzed differences inclinical data among 190 patients with AML-MRC and 667 patientswith AML not otherwise specified (AML-NOS). We also compareddifferent therapeutic regimens among patients with AML-MRC aged60-75 years.Results: Compared with AML-NOS, patients with AML-MRC hadsignificantly different clinical characteristics as well as worseoverall survival (OS) (9.2 vs. 13.6 months; p<0.001) and completeremission rates (65.3% vs. 76.2%; p=0.005). Multivariate analysisperformed for the whole group (patients with both AML-MRC andAML-NOS) showed that AML-MRC was the independent prognosticfactor (p=0.002). Additional multivariate analysis performed for 190patients with AML-MRC indicated that age (p<0.001) and lactatedehydrogenase (p=0.031) were independent prognostic factors.Compared with the IA/DA regimen [idarubicin and cytarabine (IA) ordaunorubicin and cytarabine (DA)], the DAC+CAG regimen [decitabineand half-dose CAG regimen (cytarabine, aclarubicin, and granulocytecolony-stimulating factor)] was associated with better OS (4.5 vs. 6.2months; p=0.021) in patients aged 60-75 years and categorized intothe unfavorable risk group.Conclusion: AML-MRC cases exhibited worse clinical outcomescompared to AML-NOS. Compared to the IA/DA regimen, theDAC+CAG regimen was the optimal choice for patients with AML-MRC in the unfavorable risk group and aged 60-75 years.Keywords: Acute myeloid leukemia with myelodysplasia-relatedchanges, Clinical characteristics, TherapyÖzAmaç: Bu çalışma, 2016 Dünya Sağlık Örgütü sınıflamasına göremyelodisplazi ilişkili değişiklikler gösteren akut myeloid löseminin(AML-MRC) klinik özelliklerini ve 60-75 yaş arası AML-MRChastalarında tercih edilen tedaviyi araştırmayı amaçlamıştır.Gereç ve Yöntemler: AML-MRC’li 190 hasta ve başka şekildetanımlanmamış AML’li (AML-NOS) 667 hasta arasındaki klinikfarklılıkları geriye dönük olarak analiz ettik. Ayrıca 60-75 yaş arasıAML-MRC’li hastalar arasında farklı terapötik rejimleri karşılaştırdık.Bulgular: AML-NOS ile karşılaştırıldığında, AML-MRC’li hastalar, dahakötü genel sağkalım (GS) (9,22’ye karşı 13,6 ay; p<0,001) ve dahadüşük tam remisyon oranları ile (%65,3’e karşı %76,2; p=0,005) önemliölçüde farklı klinik özelliklere sahipti. Tüm grup (hem AML-MRC hem deAML-NOS’li hastalar) için yapılan çok değişkenli analiz, AML-MRC’ninbağımsız prognostik faktör olduğunu gösterdi (p=0,002). AML-MRC’li190 hasta için yapılan ek çok değişkenli analiz, yaşın (p<0,001) velaktat dehidrogenaz düzeyinin (p=0,031) bağımsız prognostik faktörolduğunu gösterdi. IA/DA rejimi [idarubisin ve sitarabin (IA) veyadaunorubisin ve sitarabin (DA)] ile karşılaştırıldığında, DAC+CAGrejimi [desitabin ve yarım doz CAG rejimi (sitarabin, aklarubisin vegranülosit koloni uyarıcı faktör)] 60-75 yaş arası ve olumsuz riskgrubuna dahil olan hastalarda daha iyi GS ile ilişkili (4,5’e karşı 6,2 ay;p=0,021) bulundu.Sonuç: AML-MRC olguları, AML-NOS’ye kıyasla daha kötü kliniksonuçlar sergilemiştir. IA/DA rejimi ile karşılaştırıldığında, DAC+CAGrejimi, olumsuz risk grubundaki 60-75 yaş AML-MRC’li hastalar içinoptimal seçim olarak bulunmuştur.Anahtar Sözcükler: Myelodisplazi ilişkili değişiklikler gösteren akutmyeloid lösemi, Klinik özellikler, Tedavi©Copyright 2021 by Turkish Society of HematologyTurkish Journal of Hematology, Published by Galenos Publishing HouseAddress for Correspondence/Yazışma Adresi: Junqing Xu, M.D., Qingdao University Medical College,Affiliated Yantai Yuhuangding Hospital, Department of Hematology, Yantai, ChinaPhone : +86-535-18561001682E-mail : xjq7619@126.com ORCID: orcid.org/0000-0002-5687-6760Received/Geliş tarihi: January 6, 2021Accepted/Kabul tarihi: April 29, 2021188
Turk J Hematol 2021;38:188-194Wang L. et al: Characteristics and Therapy of AML-MRCIntroductionAcute myeloid leukemia with myelodysplasia-related changes(AML-MRC) is a distinct entity first defined by the World HealthOrganization (WHO) in 2008 [1]. The 2016 WHO classificationrevised the myelodysplastic syndrome (MDS)-related cytogeneticabnormalities: del (9q) was removed and patients with mutatedNPM1 or biallelic CEBPA were recategorized as having recurrentgenetic abnormalities [2]. According to recent studies, AML-MRC has a worse prognosis, including lower complete remission(CR) rate and shorter overall survival (OS), compared to AMLnot otherwise specified (AML-NOS) [3,4,5]. Although the IA/DAregimen [idarubicin and cytarabine (IA) or daunorubicin andcytarabine (DA)] and DAC+CAG regimen [decitabine and halfdoseCAG regimen (cytarabine, aclarubicin, and granulocytecolony-stimulating factor)] have often been chosen forchemotherapy, no particular therapy has yet been found tohave therapeutic advantages, especially in patients older than60 years and not eligible for allogeneic hematopoietic stem celltransplantation (allo-HSCT). We retrospectively investigated 190patients with AML-MRC admitted to our hospital and comparedthose cases with AML-NOS for a better understanding of theclinical and biological features. We also compared the IA/DA andDAC+CAG regimens in patients aged 60-75 years to determinethe optimal therapy.Materials and MethodsPatientsOur study was performed based on a cohort of 857 patientsadmitted to our hospital between August 2010 and September2019 with complete data regarding baseline characteristics andtreatment outcomes. These patients were reevaluated as havingAML-NOS or AML-MRC according to the 2016 WHO classificationof myeloid neoplasms and acute leukemia [2], strictly excludingcases of therapy-related myeloid neoplasms and AML withrecurrent genetic abnormalities including mutated NPM1and biallelic CEBPA. Patients who underwent allo-HSCT werealso excluded. Clinical and laboratory data were searched inelectronic medical records. Follow-up information was obtainedfrom electronic records or by contacting family members andwas initialized from the day of diagnosis to October 1, 2020,or the day of death. All subjects provided informed consent incompliance with the Declaration of Helsinki.Morphology AnalysisMorphology analyses of 857 patients were confirmed byat least two morphological experts. Peripheral blood andbone marrow smears were stained using the Wright-Giemsamethod. Cytochemistry was performed using myeloperoxidase,non-specific esterase, sodium fluoride inhibition tests, andperiodic acid-Schiff staining. Dyserythropoiesis was confirmedwhen there were erythroid precursors showing megaloblasticnuclei, karyorrhexis, nuclear fragments, or multinucleation.Dysgranulopoiesis was characterized as polymorphonuclearneutrophils with agranular or hypogranular cytoplasm orwith hyposegmented nuclei (pseudo-Pelger-Hüet anomaly).Dysmegakaryopoiesis was defined as micromegakaryocytesand multiple separated nuclei or monolobed nuclei inmegakaryocytes of all sizes. Patients were categorized as havingAML with multilineage dysplasia (AML-MLD) upon the presenceof dysplasia in ≥50% cells in at least two cell lineages. All casesfulfilled the 2016 WHO criterion of at least 20% blasts in theperipheral blood or bone marrow.Molecular Mutation AnalysisMolecular mutation analyses including CEBPA, NPM1, ASXL1,RUNX1, and Flt3-ITD were obtained for the whole group.Before May 2016, this process was performed by polymerasechain reaction, which was then replaced by high-throughputsequencing.Cytogenetic AnalysisCytogenetic information was obtained for all patients.Chromosome karyotype detection of bone marrow cells wasperformed by short-time culture and G-banding methods.Patients were categorized into an intermediate risk group orpoor risk group based on cytogenetics and molecular mutationas outlined by the 2017 European Leukemia Net (ELN) criteria [6].According to the 2016 WHO criteria [2], when ≥20% peripheralblood or bone marrow blasts are present and prior therapy hasbeen excluded, cytogenetic abnormalities sufficient to diagnoseAML-MRC are as follows: 1) complex karyotype; 2) unbalancedabnormalities of -7/del(7q), del(5q)/t(5q), i(17q)/t(17p), -13/del(13q), del(11q), del(12p)/t(12p), and idic(X)(q13); 3) balancedabnormalities of t(11;16), t(3;21), t(1;3), t(2;11), t(5;12), andt(5;7).TherapyAccording to treatment regimens, patients with AML-MRC aged60-75 years (n=99) were divided into three groups, including anIA/DA group (n=43), DAC+CAG group (n=49), and supportivegroup (n=7). Patients in the IA/DA group were treated with IA(idarubicin, 10-12 mg/m 2 , days 1-3; Ara-C, 100-200 mg/m 2 , days1-7) or DA (daunomycin, 45-60 mg/m 2 , days 1-3; Ara-C, 100-200 mg/m 2 , days 1-7). Patients in the DAC+CAG group receiveddecitabine (20 mg/m 2 , days 1-5), aclarubicin (10-14 mg/m 2 , days4-7), Ara-C (10 mg/m 2 q12h, days 4-10), and granulocyte colonystimulatingfactor [5 µg/kg, days 4-10 or day 4 until white bloodcell (WBC) count was more than 30x10 9 /L]. In the supportivegroup, patients received hydroxyurea to inhibit the proliferationof leukemia cells or only supportive care such as transfusionsof blood products when necessary and anti-infection therapywhen patients had symptoms of infection.189
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