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Bone Marrow Morphology Is a Strong Discriminator Between Chronic Eosinophilic Leukemia, Not Otherwise Specified and Reactive

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Bone Marrow Morphology Is a Strong Discriminator Between Chronic Eosinophilic Leukemia, Not Otherwise Specified and Reactive ARTICLE Myeloproliferative DIsorders Bone marrow morphology is a strong Ferrata Storti EUROPEAN discriminator between chronic eosinophilic HEMATOLOGY Foundation ASSOCIATION leukemia, not otherwise specified and reactive idiopathic hypereosinophilic syndrome Sa A. Wang,1 Robert P. Hasserjian,2 Wayne Tam,3 Albert G. Tsai,4 Haematologica 2017 Julia T. Geyer,3 Tracy I. George,5 Kathryn Foucar,5 Heesun J. Rogers,6 Volume 102(8):1352-1360 Eric D. Hsi,6 Bryan A. Rea,7 Adam Bagg,7 Carlos E. Bueso-Ramos,1 Daniel A. Arber,8 Srdan Verstovsek9 and Attilio Orazi3 1Department of Hematopathology, M.D. Anderson Cancer Center, Houston, TX; 2Department of Pathology, Massachusetts General Hospital, Boston, MA; 3Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY; 4Department of Pathology, Stanford University, CA; 5Department of Pathology, University of New Mexico, Albuquerque, NM; 6Department of Laboratory Medicine, Cleveland Clinic, OH; 7Department of Pathology and Laboratory Medicine, the University of Pennsylvania, Philadelphia, PA; 8Department of Pathology and Laboratory Medicine, University of Chicago, IL and 9Department of Leukemia, M.D. Anderson Cancer Center, Houston, TX, USA ABSTRACT hronic eosinophilic leukemia, not otherwise specified can be dif- ficult to distinguish from idiopathic hypereosinophilic syndrome Caccording to the current World Health Organization guideline. To examine whether the morphological features of bone marrow might aid in the differential diagnosis of these two entities, we studied a total of 139 patients with a diagnosis of chronic eosinophilic leukemia, not oth- Correspondence: erwise specified (n=17) or idiopathic hypereosinophilic syndrome [email protected] (n=122). As a group, abnormal bone marrow morphological features, resembling myelodysplastic syndromes, myeloproliferative neoplasm or myelodysplastic/myeloproliferative neoplasm, were identified in 40/139 Received: January 25, 2017. (27%) patients: 16 (94%) of those with chronic eosinophilic leukemia Accepted: May 4, 2017. and 24 (20%) of those with hypereosinophilic syndrome. Abnormal bone marrow correlated with older age (P<0.001), constitutional symp- Pre-published: May 11, 2017. toms (P<0.001), anemia (P=0.041), abnormal platelet count (P=0.002), organomegaly (P=0.008), elevated lactate dehydrogenase concentration doi:10.3324/haematol.2017.165340 (P=0.005), abnormal karyotype (P<0.001), as well as the presence of myeloid neoplasm-related mutations (P<0.001). Patients with abnormal Check the online version for the most updated bone marrow had shorter survival (48.1 months versus not reached, information on this article, online supplements, and information on authorship & disclosures: P<0.001), a finding which was independent of other confounding factors www.haematologica.org/content/102/8/1352 (P<0.001). The association between abnormal bone marrow and shorter survival was also observed in hypereosinophilic syndrome patients alone. In summary, most patients with chronic eosinophilic leukemia, ©2017 Ferrata Storti Foundation not otherwise specified and a proportion of those with idiopathic hyper- Material published in Haematologica is covered by copyright. eosinophilic syndrome show abnormal bone marrow features similar to All rights are reserved to the Ferrata Storti Foundation. Use of published material is allowed under the following terms and the ones encountered in patients with myelodysplastic syndromes, conditions: myelodysplastic/myeloproliferative neoplasm or BCR-ABL1-negative https://creativecommons.org/licenses/by-nc/4.0/legalcode. myeloproliferative neoplasm. Among patients who are currently consid- Copies of published material are allowed for personal or inter- nal use. Sharing published material for non-commercial pur- ered to have idiopathic hypereosinophilic syndrome, abnormal bone poses is subject to the following conditions: marrow is a strong indicator of clonal hematopoiesis. Similar to other https://creativecommons.org/licenses/by-nc/4.0/legalcode, sect. 3. Reproducing and sharing published material for com- myeloid neoplasms, bone marrow morphology should be one of the mercial purposes is not allowed without permission in writing major criteria to distinguish patients with chronic eosinophilic leukemia, from the publisher. not otherwise specified or clonal hypereosinophilic syndrome from those with truly reactive idiopathic hypereosinophilic syndrome. 1352 haematologica | 2017; 102(8) BM morphology of CEL,NOS/idiopathic HES Introduction relation to BM morphology. In our previous study,7 with molecular genetic information for patients, we observed Hypereosinophilia is defined by the presence of ≥1.5 some BM features that appeared to be preferentially pres- x109/L eosinophils in the peripheral blood (PB) and may be ent in cases with molecular genetic alterations. In this reactive, neoplastic or idiopathic.1-3 Chronic eosinophilic study, we conducted a thorough review of BM morpholo- leukemia, not otherwise specified (CEL, NOS)4 is a myelo- gy of a large series of CEL, NOS and idiopathic HES cases proliferative neoplasm (MPN), characterized by an expan- collected from seven large medical centers in the USA sion of eosinophils but lacking well-defined molecular using a defined set of morphological criteria, blinded to genetic alterations such as BCR-ABL1 and rearrangements the original diagnosis and molecular genetic data. We used of PDGFRA, PDGFRB, FGFR1 and PCM1-JAK2. In idio- the morphological features to define an “abnormal” BM pathic hypereosinophilic syndrome (HES), there is morphology, and correlated the morphological results tissue/organ damage related to an eosinophilic with clinical and laboratory features, cytogenetics, muta- infiltrate/activation, but the cause of the hypereosinophil- tion data, and patients’ outcomes. We sought to determine ia is unknown. whether morphology can be utilized in the distinction of Due to substantial overlapping of their features, idio- CEL, NOS and clonal HES from truly reactive idiopathic pathic HES was described alongside CEL, NOS in the HES. World Health Organization (WHO) classification mono- graph;4 this categorization remains largely unmodified in the 2016 WHO revision.5 According to the current guide- Methods lines, CEL, NOS, can only be reliably separated from idio- pathic HES by the presence of increased blasts in bone Patients marrow (BM) and/or PB, or proof of clonality. Clonality Cases were collected from MD Anderson Cancer Center, was mainly determined by chromosomal analysis or test- Stanford University Medical Center, Cleveland Clinic, ing for mutations well known to occur in MPN, such as Massachusetts General Hospital, Weill-Cornell Medical College, JAK2, MPL, CALR and KIT. However, these mutations are the Hospital of the University of Pennsylvania and the University uncommon in the eosinophilic diseases.6,7 More recently, of New Mexico between 2005 and 2014. All included patients had 9 next-generation sequencing (NGS) approaches have been persistent hypereosinophilia (≥1.5x10 /L) and did not have acute applied to these eosinophilic disorders. Anderson and col- leukemias, chronic myeloid leukemia, MDS, chronic myelomono- leagues conducted whole-exome sequencing of nine cytic leukemia, systemic mastocytosis, or rearrangements of patients with idiopathic HES8 and identified somatic mis- PDGFRA, PDGFRB, FGFR1 or PCM1-JAK2. For idiopathic HES, sense mutations in three of them. The mutations they every patient had “end-organ damage” according to the definition found involved the spliceosome gene PUF60 and the cad- by the working group on eosinophil disorders.15 Lymphocytic/T- herin gene CDH17. More recently, using NGS with a gene cell variant HES1 was excluded based on the identification of aber- panel targeted to somatic mutations commonly associated rant T cells by flow cytometry with or without TCR gene with myeloid neoplasms, we detected the presence of rearrangement polymerase chain reaction studies. Clinical infor- mutations at a relatively high (≥10%) variant allele fre- mation was retrieved from the electronic medical records. This quency (VAF) in 25-30% of cases of idiopathic HES.7 study was approved by the Institutional Review Boards of all par- These mutations mostly occurred in genes involved in ticipating institutions. DNA methylation and chromatin modification, such as AXSL1, TET2, EZH2, and DNMT3A. While such muta- Bone marrow morphology and histology tions would imply that some idiopathic HES are clonal BM was assessed for the following morphological parameters stem cell neoplasms, they have also been reported in some (Table 1): cellularity; megakaryocyte numbers, morphology and aging individuals without evidence of a myeloid neo- distribution; fibrosis; dysgranulopoiesis; dyserythropoiesis; plasm,9,10 mandating caution in the use of mutations as myeloid:erythroid (M:E) ratio; and eosinophil morphology. PB definitive proof of a neoplastic myeloid process. On the smears were also reviewed for eosinophil morphology and evi- other hand, the detection of mutations by NGS relies on dence of dysgranulopoiesis. Hypercellularity was defined by a cel- the testing panel used, which may vary for the number of lularity at least 20% higher than the age-appropriate cellularity, genes sequenced as well as the depth of sequencing. and overall ≥70% in patients age 50-60 years; ≥60% in patients Although some studies have suggested that abnormal >60 years; and ≥90% in patients <30 years of age. Megakaryocyte eosinophil morphology is
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