W R Hart

Carcinosarcomas of the female genital tract have generally been regarded as a type of sarcoma. Recent evidence suggests, however, that they may be more closely related to carcinoma. The histologic features of 29 carcinosarcomas with documented metastases were analyzed to study the relative importance of the carcinomatous and sarcomatous components and attempt to provide further evidence on the histogenesis of these neoplasms. Patients' ages ranged from 33 to 81 years (mean, 68). The primary tumor originated in the uterus in 17 cases, the ovary in 11, and the fallopian tube in one. Heterologous sarcoma was present in 21 of the primary tumors (72%). Myometrial invasion was present in all 15 of the uterine tumors treated with hysterectomy and consisted only of the carcinomatous component in 12 cases (80%). In two cases, which possibly developed as "collision"-type carcinosarcomas, the myometrium was separately invaded by carcinoma and sarcoma. Myoinvasive tumor consisted solely of sarcoma in one case. Lymphatic-vascular invasion was found in 10 of the primary tumors (eight uterine, two extrauterine) and consisted of pure carcinoma in all instances. The cellular composition of 62 metastases was evaluated. Of these, 51 metastases were diagnosed concurrently with the primary tumor in 21 patients (73%). Eleven metastases were diagnosed from 2 to 26 months after initial treatment. Carcinoma only was found in 43 metastases (70%), both carcinoma and sarcoma in 15 (24%), and sarcoma alone in four (6%). A total of 35 lymph node metastases occurred in 10 cases, consisting of carcinoma alone at 34 sites. The sole example of a purely sarcomatous lymph node metastasis occurred in one of the possible uterine "collision"-type tumors. Intraperitoneal metastases to serosal surfaces or the omentum occurred in 19 cases and consisted of both carcinoma and sarcoma in 14 and carcinoma only in five. Vaginal metastases occurred in four cases and consisted of only carcinoma in two, carcinoma and sarcoma in one and only sarcoma in one. Four patients had distant organ metastases, including one each to the liver (carcinoma only), breast (carcinoma only), bone marrow (sarcoma only), and brain (sarcoma only). Of the 51 concurrent metastases, only carcinoma was present in 37 (73%), both carcinoma and sarcoma in 13 (26%), and sarcoma alone in one. Of the 11 subsequent metastases, carcinoma alone was found in six (55%), sarcoma alone in three (27%), and both carcinoma and sarcoma in two (18%).(ABSTRACT TRUNCATED AT 400 WORDS)

The clinical and pathological features of three personally observed and six previously reported cases of renal cell carcinoma metastatic to the ovary are reviewed. The patients' ages ranged from 39 to 64 (average, 52) years. In five patients the ovarian tumor was discovered first. In four of these patients renal tumors were detected during the initial clinical studies or in the early postoperative period, but in the fifth the renal primary tumor was not detected until 8 years later. The ovarian tumor in two cases was initially misdiagnosed as a primary ovarian clear cell carcinoma. In the remaining four patients the ovarian metastasis was detected 5 months, 12 months, 19 months, and 11 years after a renal tumor had been removed. In two patients the initial clinical manifestations were due to a metastasis of the renal tumor, to the thyroid gland in one and to the vagina in the other. The renal tumors in these nine patients typically were well-differentiated renal cell adenocarcinomas of clear cell type. The ovarian tumors measured from 7 to 18 (average, 12.5) cm in greatest dimension; two of them were bilateral. Grossly they were usually solid or solid and cystic; one was a unilocular cyst with a predominantly smooth lining and a 2.5-cm solid nodule in one area. The solid component of the tumors was typically either uniformly yellow or had focal yellow areas with hemorrhagic foci. Microscopic examination showed a relatively uniform picture in most cases: solid or alveolar nests of epithelial cells with abundant clear cytoplasm or tubules lined by clear cells and containing intraluminal eosinophilic material and extravasated blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoimmune oophoritis is a rare cause of premature ovarian failure. Previous studies of autoimmune oophoritis have detailed the clinical, immunologic, and histologic findings. The gross pathologic features of the involved ovaries have detailed the clinical, immunologic, and histologic findings. The gross pathologic features of the involved ovaries have not been emphasized. Herein, we describe a 35-year-old woman with autoimmune oophoritis who presented with symptoms referable to a right cystic adnexal mass. She underwent a diagnostic laparotomy and right salpingo-oophorectomy for removal of an 8.0-cm-diameter, twisted multicystic ovary. Microscopically, mononuclear inflammatory cells infiltrated multiple follicular and luteal cysts. We have seen two additional patients with histologically verified autoimmune oophoritis who underwent diagnostic laparotomy and oophorectomy because of cystic enlargement of the ovaries. Stimulation of ovarian follicles by elevated levels of pituitary gonadotropins probably causes the cystic changes. Recognition of this aspect of autoimmune oophoritis may help to prevent oophorectomy in patients whose functioning ovarian tissue is already compromised by autoimmune destruction.

ras oncogene mutations appear in over 50% of colon tumors in humans. Studies in animal systems have revealed that ras mutations are also present in preneoplastic lesions, suggesting the possibility of early detection of ras mutation in morphologically normal colon tissues for diagnostic purposes. An Enriched PCR, developed by us, eliminates most of the normal ras alleles prior to amplification; subsequent analysis via RFLP enables the detection of one mutant allele within 10(4) normal alleles. Using the Enriched PCR, we have determined the frequency of mutant ras alleles in normal mucosae and in adenomatous polyps of patients with or without adenocarcinoma. Of the 42 patients who had colon tumors, 15 were found to harbor K-ras oncogene mutation (35%). In two of the 14 cases with mutant K-ras in the tumor tissue we were able to identify mutations in tissues that had been obtained from a site at considerable distance from the tumor (13%); Analysis of 7 adenomas identified one as a carrier of the mutant ras allele (14%). Of 11 normal colonic mucosa obtained from patients without neoplasia, one specimen contained K-ras mutation. Thus, mutated alleles of K-ras may be present, at low frequency, throughout the 'normal appearing' tissue. Cells of normal appearance that harbor such mutation, have the potential to undergo further changes and to develop into the transformed phenotype. Overall, our findings suggest that mutant ras alleles can be detected in preneoplastic mucosa that is morphologically normal, and in adenomas, suggesting the occurrence of an initiation event, and possibly enabling the identification of patients who may be at high risk for developing malignant tumors.