Molecular evidence for the independent origin of extra-ovarian papillary serous tumors of low malignant potential

Background: Molecular data suggest that peritoneal tumors in women with adv anced-stage ovarian papillary serous adenocarcinoma are monoclonal in origi n. Whether the same is true for ovarian tumors of low malignant potential i s not known. We compared peritoneal and ovarian tumors from women with adva nced-stage ovarian papillary serous tumors of low malignant potential to de termine whether the peritoneal tumors arose from the same clone as the ovar ian tumors. Methods: We studied the clonality of 73 peritoneal and ovarian tumors from 18 women with advanced-stage ovarian papillary serous tumors of low malignant potential. Formalin-fixed, paraffin-embedded tumors and repr esentative normal tissues were sectioned and stained with hematoxylin-eosin , representative sections from separate tumors were manually microdissected , genomic DNA was extracted from the microdissected tumors, and the polymer ase chain reaction was used to amplify a CAG polymorphic site in the human androgen receptor locus on the X chromosome to determine the inactivation p attern of the X chromosome and the clonality of the tumors. Results: The pa ttern of X-chromosome inactivation could be determined from the tumors of 1 3 of 18 patients. Of the 13 patients, seven (54%) had nonrandom inactivatio n of the X chromosome, and six of the seven had different inactivation patt erns in the peritoneal and ovarian tumors. Three of these patients also had different patterns of nonrandom X-chromosome inactivation in tumors from e ach ovary. The remaining six patients had random patterns of X-chromosome i nactivation in the peritoneal and ovarian tumors. Conclusions: Our data sug gest that peritoneal and ovarian tumors of low malignant potential arise in dependently.