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. Author manuscript; available in PMC: 2023 Nov 14.
Published in final edited form as: Virchows Arch. 2022 Nov 24;482(1):11–26. doi: 10.1007/s00428-022-03448-8

Table 6.

T-ALL Diagnostic Considerations and Ancillary Testing.

Clinical Information History of CML: consider T-lymphoblastic transformation (rare)
Eosinophilia: consider “myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions,” including FGFR1-r and FLT3-r
Immunophenot yping Flow cytometry ETP ALL, NOS and ETP ALL, BCL11B-a: cytoplasmic CD3+*, CD7 +, CD8−, CD1a−, one or more myeloid/stem cell markers (CD34, CD117, HLA-DR, CD13, CD3, CD11b, CD65), CD4+/−, CD2+/−, CD5 (<75% of blasts)

“Near-ETP T-ALL.”: ETP immunophenotype with ≥75% of blasts CD5+

*T-ALL characteristically expresses cCD3, but a specific level of expression is not required for a diagnosis of T-ALL

Note: Dedicated flow cytometry studies to characterize the neoplastic cells for later MRD monitoring is strongly recommended at diagnosis; however, MRD studies utilize a limited panel of antibodies and do not provide comprehensive immunophenotypic analysis of the blasts.
Immunohistochemis try BCL11B: Positive in a subset of
ETP ALL, BCL11B-a; negative in T-ALL with TXL3::BCL11B (TXL3-r)
LMO2: Possible role for immunohistochemistry in the detection of T-ALLwith LMO2-r
PU.1: needs validation but might be useful for TALL with SPI1-r
Cytogenetics Fluorescence in situ hybridization (FISH) BCL11B breakapart: ETP-ALL with BCL11B-a (subset)
Note: FISH studies will not identify BCL11B-r alterations from enhancer amplification downstream of BCL11B that results in looping of the enhancer to BCL11B
Molecular Diagnostics Clonality studies Recommended at diagnosis to facilitate molecular MRD monitoring

*The presence or absence of a TCR and/or IGH clone cannot utilized for lineage assignment (T-ALL versus B-ALL).

New/provisional Entities in the ICC subclassification are underlined.