According to Alexander Chan, MD, and colleagues from the Department of Pathology at the Memorial Sloan Kettering Cancer Center, driver gene events are frequent in multipotent progenitor cells in patients with myeloid neoplasms, suggesting that lineage infidelity—where individual blast cells have a cytoplasmic marker of one lineage and a surface marker of a different lineage—may be more common than current knowledge holds.
Thus, Dr. Chan and collaborators examined this phenomenon in myelodysplastic syndrome (MDS) and non–chronic myeloid leukemia (CML) myeloproliferative neoplasms (MPN) and revealed that, while abnormal immature B lineage cells were produced, it was a rare event.
The study, published in Cytometry Part B: Clinical Cytometry, assessed phenotypic lineage infidelity in B- and T-cells based on 1,262 patients with MDS or non–CML MPN enrolled in bone marrow pathology and flow cytometry (FC) studies. When abnormal B-lymphoblast (ABLB) concentrations were identified, the researchers additionally evaluated immature B-cells using a “high sensitivity FC assay for B-lymphoblastic leukemia/lymphoma (B-ALL).”
Nine patients who had low–level ABLB populations with abnormal immunophenotypes were identified. Genetic studies confirmed that some ABLB populations were related to myeloid blasts. Notably, the ABLB populations were stable or disappeared in eight of nine patients, and only one patient progressed to B-ALL.
Given their findings, Dr. Chan theorized that “while presence of ABLB does not necessarily reflect blast crisis, the underlying disease biology of our findings may ultimately be relevant to patient management and warrants further investigation.”