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Between 1948 and 1984, autopsies were performed on 305 patients with primary carcinomas of the cervix, endometrium, ovaries, fallopian tubes, vulva, and vagina. Skeletal metastases were detected premortem and at autopsy in 49 cases (16.1%): cervix, 20 (40.8%); endometrium, 17 (34.7%); ovary, 7 (14.3%); vulva, 4 (8.2%); fallopian tube, 1 (2%). There were no cases of osseous metastasis from vaginal carcinoma. The incidence and sites of metastasis from these gynecologic carcinomas were correlated with their clinical and histopathologic classifications. This clinicopathologic study, based on autopsy data, demonstrates that osseous metastases are not uncommon, are significantly greater than clinically appreciated, and correlate with advanced anatomic stage and histopathologic type and grade.

Treatment failure for intraepithelial neoplasia of the uterine cervix following electrocautery, cryosurgery, or carbon dioxide laser therapy is related primarily to incomplete eradication of the lesion. This may be due to the depth of crypt involvement, the linear extent, or the location of the abnormal epithelium. In view of this, the extent (depth and linear extent) and the location of cervical intraepithelial neoplasia (CIN) in 319 cervical cone specimens were analyzed. There is a significant correlation between the severity and the extent of the change. The mean depths of CIN I, II, and III were 0.42 +/- 0.28, 0.93 +/- 0.71, and 1.35 +/- 1.15 mm, respectively. The mean linear extents for CIN I, II, and III were 4.10 +/- 2.84, 5.84 +/- 4.13, and 7.60 +/- 4.32 mm, respectively. To eradicate 99.7% of CIN III lesions, it is necessary to destroy the tissue up to 4.80 mm in depth and of sufficient linear extent. While most lesions (87.2%) involved the transformation zone, 9.7% were higher in the cervical canal and 3.1% were located in the ectocervix. Appropriate cytologic samples, endocervical curettage, and colposcopic examination should be employed in evaluating the CIN, and strict criteria should be followed in selecting the patients for conservative management.

This paper details several studies of the effect of a single progestin, megestrol acetate, in patients with persistent endometrial hyperplasia and recurrent or persistent endometrial adenocarcinoma. Results of these studies indicate that megestrol acetate inhibits recurrence of adenomatous and atypical hyperplasia as well as adenocarcinoma in situ. These diseases when left untreated often progress to invasive adenocarcinoma. Additional studies presented here show that megestrol acetate is effective in the treatment of endometrial adenocarcinoma in inoperable patients and increases survival in patients with recurrent endometrial cancer.

In this study, 59 vulvar intraepithelial squamous neoplasms (8 atypia and 51 carcinoma in situ) and 33 invasive squamous carcinomas were analyzed for their nuclear DNA content using Feulgen microspectrophotometry. Four cases of atypia had a polyploid DNA distribution. The remaining 4 cases of atypia and all cases of carcinoma in situ had an aneuploid pattern, and nearly two thirds of these had high ploidy stem cells (greater than 3N). This is in contrast to the low ploidy stem cells (less than 3N) seen in 70% of the invasive carcinomas and in 82% of the intraepithelial neoplasms in the vicinity of invasive carcinomas. This observation suggests that not all vulvar intraepithelial neoplasms have the same propensity to become invasive. Invasive carcinomas of comparable size and depth of invasion with low ploidy stem cells had a higher frequency of lymph node metastasis than those having high ploidy stem cells. The significance of nuclear DNA findings related to gynecologic neoplasms is discussed.

In the past few years there have been a number of reports correlating a high frequency of herpes simplex virus type 2(HSV-2) infection with lesions of the uterine cervix. These studies have used a clinical history of herpetic infection or the demonstration of herpetic antibodies in the cancer patients. The present study was performed to evaluate any possible carcinogenic activity of the formalin-inoculated herpes simplex virus type 2 in the reproductive tract of the female mouse. This approach to the study was selected because of previous experience with a model system of carcinogenesis of the cervix uteri using coal tar hydrocarbons. Cytologic and histologic preparations from experimental animals and controls are presented to demonstrate the mucosal alterations and tumors observed in the animals. Noninvasive lesions of the cervix were identified in 76.8% and invasive adenocarcinoma detected in 30.2% of the mice.

Placental site trophoblastic tumor is a rare variant of trophoblastic disease. The malignant form of this disease with metastasis and death is even more infrequent, as is evident from only five cases in the literature. A 30-year-old black woman who died from this disease is presented. Patients with metastases are at extremely high risk with no reported survivors and must be treated aggressively with chemotherapy and cytoreductive surgery. This type of trophoblastic tumor apparently exhibits a different biologic behavior as compared with choriocarcinoma.

Previous studies at this laboratory showed that repeated application of inactivated herpes simplex virus type 2 to the mouse cevix produced premalignant and malignant lesions. In the present study mice were inoculated with inactivated herpes simplex virus type 2 or control solution and Freund's adjuvant by intraperitoneal and subcuaneous routes before exposure of the cervix to inactivated virus. It appears that immunization with inactivated virus conferred a protection against the induction of cervical carcinoma.

Forty-nine cases of ovarian endometrioid carcinoma with squamous foci were reviewed. Of particular interest was the biologic behavior of the neoplasms in relation to the appearance of the epithelium. As previously noted for the analogous uterine endometrial tumors, the ovarian adenosquamous lesions occurred later in life, were more advanced, were associated with less differentiated adenocarcinomatous components, and had a poorer prognosis. The five-year survival rate for patients with adenosquamous endometrioid ovarian carcinoma was 21% in comparison with the 90% survival found in patients with ovarian endometrioid adenocanthoma.

Cellular samples obtained by vaginal scrapings from 204 women exposed to diethylstilbestrol (DES) in utero were evaluated and compared with samples collected from a like number of controls. Several different sampling methods were evaluated. Vaginal scrapings contained columnar cells existing alone or in combination with squamous metaplastic cells and less frequently were characterized only by metaplastic cells. None of the control samples contained columnar cells and only 1 of 200 control samples contained metaplastic cells. The cellular findings in the offspring of women exposed to DES in utero varied in relation to age. Cellular abnormalities were demonstrated in 90.4% of women having scrapings of visible lesions and in 88.1% of women studied by 4-quadrant vaginal scrapings in the absence of clinical disease. Of 58 women with histopathologically proven adenosis, 57 (98.3%) had similar cellular abnormalities. Abnormalities were demonstrated in squamous epithelial cells of the vagina in 8 (3.9%) of the women exposed to DES in utero, and in 5 of these women there were similar changes in the uterine cervix. Only 2 (0.9%) of the women had cellular changes suggesting dysplasia of the vagina.

Cytomegalovirus and Chlamydia trachomatis are prevalent sexually transmissible pathogens. They produce persistent infections of the cervix and have been associated with cervical neoplasia. Cytomegalovirus has also been shown to induce transformation of cells in culture. Because of the high prevalence of genital infections with these pathogens and evidence that they may have oncogenic effects on the cervix, cytomegalovirus (strain AD-169) and C. trachomatis (serovar LGV-2) were tested for oncogenicity in a mouse model in which induction of cervical neoplasia by repeated exposure to inactivated herpes simplex viruses has been demonstrated previously. Cotton tampons, saturated with UV-inactivated cytomegalovirus, C. trachomatis, or corresponding control fluids, were inserted into the vaginas of virgin C57 mice 3 times a week. Smears of vaginal aspirates for cytological examination were obtained every 5 weeks. After 75-90 weeks of exposure, the mice were sacrificed and serial sections of their reproductive tracts were examined. Cervical dysplasia was detected by histological examination in 51% and cervical carcinoma in 10% of mice exposed to cytomegalovirus. In control mice, in contrast, dysplasia developed in 3% and carcinoma in none. The progression from normal cervical epithelium to dysplasia to carcinoma observed with cytomegalovirus exposure was similar to that observed previously in this model after exposure of mice to herpes simplex virus types 1 and 2. The frequencies of cervical abnormalities in mice exposed to C. trachomatis or corresponding control fluid were low, and differences between the two groups were not statistically significant. These data indicate that strain AD-169 of cytomegalovirus is oncogenic for the mouse cervix and suggest that the LGV-2 serovar of C. trachomatis is not.