s bone marrow revealed a copy-number-neutral loss of heterozygosity at the TP00 locus, suggestive of the homozygous nonsense mutation in the TP00 gene. In addition, the loss of heterozygosity at the TP00 locus was also detected in the dysgerminoma. Conclusions: These results indicated that either the mast cells causing the ASM in this case had originated from the preceding ovarian dysgerminoma as a clonal evolution of a residual tumor cell, which acquired the TP00 mutation, or that both tumors developed from a common cancer stem cell carrying the KIT D000A variation.