Adenosarcoma of the uterus: a clinicopathologic, DNA flow cytometric, p53 and mdm-2 analysis of 11 cases

Eleven patients with uterine adenosarcoma diagnosed between 1970 and 1995 w ere evaluated according to DNA ploidy, S-phase fraction, p53 and mdm-2 expr ession, and traditional clinical and pathological prognostic factors, such as tumor stage, grade and mitotic index. DNA flow cytometric analysis and i mmunohistochemical staining for p53 and mdm-2 were performed on paraffin-em bedded archival tissue from the uterine tumors. The patients ranged in age from 41 to 90 years (median, 76 years). Only one patient was premenopausal at the time of diagnosis and five (45%) were nulliparous. One patient had r eceived previous pelvic irradiation for anal squamous carcinoma. Six of the tumors (55%) were pure adenosarcoma and five (45%) were adenosarcoma with sarcomatous overgrowth. Nine patients had a stage I tumor and two had a sta ge II tumor. Among the six adenosarcomas we found three DNA diploid tumors, two DNA aneuploid tumors, and one DNA multiploid tumor. All adenosarcomas had an S-phase fraction less than 10%, except one that was not assessable. None was p53 positive and only one overexpressed mdm-2. All five adenosarco mas with sarcomatous overgrowth were DNA aneuploid, three (60%) had an S-ph ase fraction >10%, two (40%) were p53 positive, and one (20%) overexpressed mdm-2. Five of the eleven patients suffered recurrences, and three (60%) o f these developed lung metastases. During the observation period four (36%) patients (2 adenosarcomas and 2 adenosarcoma with sarcomatous overgrowth) died of disease, three patients died of intercurrent disease without recurr ence, and the remaining four are alive with no evidence of disease. The ove rall five-year survival rate for all stages was 69%; for patients with AS i t was 80%, while for those with adenosarcoma with sarcomatous overgrowth it was 50%. There were no variables which correlated with survival. In conclu sion, we found hat the typical adenosarcoma had a tendency to be of low sta ge, have a lower mitotic rate and an S-phase fraction <10%. On the other ha nd, adenosarcomas with sarcomatous overgrowth were of high grade, had a hig h mitotic rate, and were DNA aneuploid with an S-phase fraction >10%. None of the variables studied correlated with survival. Tumors that were p53-pos itive or overexpressed mdm-2 did not behave worse than their negative count erpart. All patients who recurred with distant metastases died of disease.