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Approximately 25% of the pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cases are genetically unclassified. More thorough elucidation of the pathobiology of these genetically unclassified (‘B-other’) cases may identify novel treatment options. We analyzed gene expression profiles of 572 pediatric BCP-ALL cases, representing all major ALL subtypes. High expression of  STAP1 , an adaptor protein downstream of the B-cell receptor (BCR), was identified in  BCR-ABL1 -like and non- BCR-ABL1 -like B-other cases. Limma analysis revealed an association between high expression of  STAP1  and BCR signaling genes. However,  STAP1  expression and pre-BCR signaling were not causally related: cytoplasmic Igμ levels were not abnormal in cases with high levels of  STAP1  and stimulation of pre-BCR signaling did not induce  STAP1  expression. To elucidate the role of STAP1 in BCP-ALL survival, expression was silenced in two human BCP-ALL cell lines. Knockdown of  STAP1  did not reduce the proliferation rate or viability of these cells, suggesting that  STAP1  is not a likely candidate for precision medicines. Moreover, high expression of  STAP1  was not predictive for an unfavorable prognosis of  BCR-ABL1 -like and non- BCR-ABL1 -like B-other cases. Remarkably,  DUX4 -rearrangements and intragenic  ERG  deletions, were enriched in cases harboring high expression of  STAP1 .

High STAP1 expression in DUX4-rearranged cases is not suitable as therapeutic target in pediatric B-cell precursor acute lymphoblastic leukemia