Myeloproliferative neoplasms with concurrent BCR-ABL1 translocation and JAK2 V617F mutation: a multi-institutional study from the bone marrow pathology group.

TitleMyeloproliferative neoplasms with concurrent BCR-ABL1 translocation and JAK2 V617F mutation: a multi-institutional study from the bone marrow pathology group.
Publication TypeJournal Article
Year of Publication2018
AuthorsSoderquist CR, Ewalt MD, Czuchlewski DR, Geyer JT, Rogers HJ, Hsi ED, Wang SA, Bueso-Ramos CE, Orazi A, Arber DA, Hexner EO, Babushok DV, Bagg A
JournalMod Pathol
Volume31
Issue5
Pagination690-704
Date Published2018 05
ISSN1530-0285
KeywordsAged, Aged, 80 and over, Antineoplastic Agents, Bone Marrow, Bone Marrow Neoplasms, Disease Progression, Enzyme Inhibitors, Female, Fusion Proteins, bcr-abl, Humans, Janus Kinase 2, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Male, Middle Aged, Multi-Institutional Systems, Mutation, Myeloproliferative Disorders, Primary Myelofibrosis, Retrospective Studies
Abstract

Myeloproliferative neoplasms arise from hematopoietic stem cells with somatically altered tyrosine kinase signaling. Classification of myeloproliferative neoplasms is based on hematologic, histopathologic and molecular characteristics including the presence of the BCR-ABL1 and JAK2 V617F. Although thought to be mutually exclusive, a number of cases with co-occurring BCR-ABL1 and JAK2 V617F have been identified. To characterize the clinicopathologic features of myeloproliferative neoplasms with concomitant BCR-ABL1 and JAK2 V617F, and define the frequency of co-occurrence, we conducted a retrospective multi-institutional study. Cases were identified using a search of electronic databases over a decade at six major institutions. Of 1570 patients who were tested for both BCR-ABL1 and JAK2 V617F, six were positive for both. An additional five patients were identified via clinical records providing a total of 11 cases for detailed evaluation. For each case, clinical variables, hematologic and genetic data, and bone marrow histomorphologic features were analyzed. The sequence of identification of the genetic abnormalities varied: five patients were initially diagnosed with a JAK2 V617F+ myeloproliferative neoplasm, one patient initially had BCR-ABL1+ chronic myeloid leukemia, while both alterations were identified simultaneously in five patients. Classification of the BCR-ABL1-negative myeloproliferative neoplasms varied, and in some cases, features only became apparent following tyrosine kinase inhibitor therapy. Seven of the 11 patients showed myelofibrosis, in some cases before identification of the second genetic alteration. Our data, reflecting the largest reported study comprehensively detailing clinicopathologic features and response to therapy, show that the co-occurrence of BCR-ABL1 and JAK2 V617F is rare, with an estimated frequency of 0.4%, and most often reflects two distinct ('composite') myeloproliferative neoplasms. Although uncommon, it is important to be aware of this potentially confounding genetic combination, lest these features be misinterpreted to reflect resistance to therapy or disease progression, considerations that could lead to inappropriate management.

DOI10.1038/modpathol.2017.182
Alternate JournalMod Pathol
PubMed ID29327708
PubMed Central IDPMC6008160
Grant ListK08 HL132101 / HL / NHLBI NIH HHS / United States
Related Faculty: 
Julia Geyer, M.D.

Pathology & Laboratory Medicine 1300 York Avenue New York, NY 10065 Phone: (212) 746-6464
Surgical Pathology: (212) 746-2700