Intravenous anti-D treatment for immune thrombocytopenic purpura.

the TCR d gene rearrangements in AML show the same pattern as those in T-ALL,4 and occur more frequently in immature AML3,6 or in lymphoid antigen–(CD2, CD4, or CD7) positive (Ly1) AML.4 Because myeloid/NK cell precursor acute leukemia can be recognized as immature AML or Ly1 AML, the existence of the Dd2-Jd1 pattern of TCR d gene rearrangement in myeloid/NK cell precursor acute leukemia is consistent with reports in the literature. We therefore maintain our conclusion that myeloid/NK cell precursor acute leukemia constitutes a distinct hematolymphoid disease entity. However, the NK cell precursor is, in a way, a T-cell precursor, because both T cells and NK cells have been shown to be derived from the same myeloid antigen–positive progenitor.7 Therefore, TCR d chain gene rearrangement in myeloid/NK cell precursor acute leukemia might reflect some characteristics of T-cell precursor origin. It might thus be possible for a differentiation pathway of T/NK cell and myeloid lineage to be identified as a result of investigation of the biological significance and underlying mechanism of the TCR d gene rearrangements in immature AML.