Clinical and laboratory features associated with myeloperoxidase expression in pediatric B-lymphoblastic leukemia.


Journal

Cytometry. Part B, Clinical cytometry
ISSN: 1552-4957
Titre abrégé: Cytometry B Clin Cytom
Pays: United States
ID NLM: 101235690

Informations de publication

Date de publication:
07 2021
Historique:
revised: 18 09 2020
received: 25 05 2020
accepted: 30 09 2020
pubmed: 14 10 2020
medline: 8 1 2022
entrez: 13 10 2020
Statut: ppublish

Résumé

B-lymphoblastic leukemia (B-ALL) is the most common childhood malignancy, and its diagnosis requires immunophenotypically demonstrating blast B cell lineage differentiation. Expression of myeloperoxidase (MPO) in B-ALL is well-described and it has been recognized that a diagnosis of mixed phenotype acute leukemia should be made cautiously if MPO expression is the sole myeloid feature in these cases. We sought to determine whether MPO expression in pediatric B-ALL was associated with differences in laboratory, immunophenotypic, or clinical features. We reviewed clinical, diagnostic bone marrow flow cytometry, and laboratory data for all new B-ALL diagnoses at our pediatric institution in 5 years. Cases were categorized as MPO positive (MPO+) or negative (MPO-) using a threshold of ≥20% blasts expressing MPO at intensity greater than the upper limit of normal lymphocytes on diagnostic bone marrow flow cytometry. A total of 148 cases were reviewed, 32 of which (22%) were MPO+. MPO+ B-ALL was more frequently hyperdiploid and less frequently harbored ETV6-RUNX1; no MPO+ cases had KMT2A rearrangements or BCR-ABL1. Although not significantly so, MPO+ B-ALL was less likely than MPO- B-ALL to have positive end-of-induction minimal residual disease studies (9.4 and 24%, respectively), but relapse rates and stem cell transplantation rates were similar between groups. Aberrant expression of other more typically myeloid markers was similar between these groups. In our study cohort, MPO+ B-ALL showed minimal residual disease persistence less often after induction chemotherapy but otherwise had similar clinical outcomes to MPO- B-ALL, with similar rates of additional myeloid antigen aberrancy.

Sections du résumé

BACKGROUND
B-lymphoblastic leukemia (B-ALL) is the most common childhood malignancy, and its diagnosis requires immunophenotypically demonstrating blast B cell lineage differentiation. Expression of myeloperoxidase (MPO) in B-ALL is well-described and it has been recognized that a diagnosis of mixed phenotype acute leukemia should be made cautiously if MPO expression is the sole myeloid feature in these cases. We sought to determine whether MPO expression in pediatric B-ALL was associated with differences in laboratory, immunophenotypic, or clinical features.
METHODS
We reviewed clinical, diagnostic bone marrow flow cytometry, and laboratory data for all new B-ALL diagnoses at our pediatric institution in 5 years. Cases were categorized as MPO positive (MPO+) or negative (MPO-) using a threshold of ≥20% blasts expressing MPO at intensity greater than the upper limit of normal lymphocytes on diagnostic bone marrow flow cytometry.
RESULTS
A total of 148 cases were reviewed, 32 of which (22%) were MPO+. MPO+ B-ALL was more frequently hyperdiploid and less frequently harbored ETV6-RUNX1; no MPO+ cases had KMT2A rearrangements or BCR-ABL1. Although not significantly so, MPO+ B-ALL was less likely than MPO- B-ALL to have positive end-of-induction minimal residual disease studies (9.4 and 24%, respectively), but relapse rates and stem cell transplantation rates were similar between groups. Aberrant expression of other more typically myeloid markers was similar between these groups.
CONCLUSION
In our study cohort, MPO+ B-ALL showed minimal residual disease persistence less often after induction chemotherapy but otherwise had similar clinical outcomes to MPO- B-ALL, with similar rates of additional myeloid antigen aberrancy.

Identifiants

pubmed: 33048471
doi: 10.1002/cyto.b.21966
doi:

Substances chimiques

BCR-ABL1 fusion protein, human 0
Core Binding Factor Alpha 2 Subunit 0
Oncogene Proteins, Fusion 0
TEL-AML1 fusion protein 0
Peroxidase EC 1.11.1.7
Fusion Proteins, bcr-abl EC 2.7.10.2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

446-453

Informations de copyright

© 2020 International Clinical Cytometry Society.

Références

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Auteurs

Eric McGinnis (E)

Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.

David Yang (D)

Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.

Nicholas Au (N)

Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Division of Hematopathology, British Columbia Children's Hospital, Vancouver, Canada.

Douglas Morrison (D)

Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Division of Hematopathology, British Columbia Children's Hospital, Vancouver, Canada.

Kate M Chipperfield (KM)

Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Division of Hematopathology, British Columbia Children's Hospital, Vancouver, Canada.

Audi F Setiadi (AF)

Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Division of Hematopathology, British Columbia Children's Hospital, Vancouver, Canada.

Lorraine Liu (L)

Division of Hematopathology, British Columbia Children's Hospital, Vancouver, Canada.

Angela Tsang (A)

Division of Hematopathology, British Columbia Children's Hospital, Vancouver, Canada.

Suzanne M Vercauteren (SM)

Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Division of Hematopathology, British Columbia Children's Hospital, Vancouver, Canada.

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