Clonality of multiple uterine leiomyomas.

OBJECTIVE

To study the clonality of uterine leiomyomas, especially the relationship between different nodules in multinodular cases.

METHODS

Genomic DNA was extracted from fresh tissue samples and digested through incubation with Hpa II and amplified through nested polymerase chain reaction for phosphoglycerate kinase (PGK) gene. The products were treated with Bst XI and resolved on agarose gels.

RESULTS

Among the 103 cases examined, 32 (31%) carried the polymorphic Bst XI site at the PGK locus. Eighty-nine tumors from the 29 cases were subjected to the cloning assay. Loss of polymorphism at the PGK locus was found in all tumor nodules, indicating the monoclonality of the tumor. The relationship between multiple tumors was also assessed by comparing their inactivated alleles. Seven nodules from a leiomyosarcoma were found to have originated from a single cell. However, the relationship was found to be more complicated, as demonstrated in 15 cases of multiple leiomyomas. The same inactivated allele was found in all nodules of 8 cases and in most nodules in 2 cases, while totally different inactivation patterns were observed in 5 cases. The difference was not associated with cell proliferation.

CONCLUSIONS

Clonality analysis can be applied to define the clonality of focal or nodular lesions. Uterine leiomyomas are of clonal origin. Multiple uterine leiomyomas may be subtyped into fully independent and aggressive types as well as a mixed type of both.