We compared immunogenotypic findings in 73 patients with de novo acute myeloid leukemia (AML) and 30 patients with AML developed in myelodysplastic syndrome (AML post MDS) to determine the biological difference between these hematopoietic neoplasias. Lymphoid-associated antigens were detected in 13 patients with de novo AML, four of whom exhibited rearrangement of the immunoglobulin heavy-chain (IgH) gene. T-cell receptor (TCR) gene rearrangements were detected in 10 patients with de novo AML who did not have lymphoid-associated antigens, none of whom carried rearranged IgH. This group included two AML patients with trilineage dysplasia. Neither lymphoid markers nor IgH rearrangement was detected in any of the 30 patients with AML post-MDS; TCR rearrangements were detected in eight out of 30 patients, TCR-beta rearrangements in six out of 30, and TCR-delta rearrangements in five out of 30. The TCR rearrangement without rearranged IgH in some AML post MDS patients might not be due to a common recombinase activity, and this alteration may link to genomic instability. Some patients with de novo AML also showed this pattern, suggesting a close biologic association between AML post MDS and some patients with de novo AML.