Ovarian endometrioid carcinomas with sertoliform features (SECs) are infrequent and often misinterpreted as sex cord-stromal tumors. The clinicopathologic features and immunohistochemical expression of keratin, epithelial membrane antigen (EMA), inhibin, and estrogen and progesterone receptors were evaluated in 13 cases of SEC. The women were 41 to 89 years of age (mean, 60 yr) with abdominal enlargement secondary to a unilateral ovarian mass as the most frequent clinical presentation. One patient displayed virilization. At presentation, 10 patients were Stage I, one was Stage II and two were Stage III. The tumors were composed of compact anastomosing cords and small tubules embedded within a fibrous stroma. Nuclear features were Grade 1 or 2 in all but one tumor. Areas of conventional endometrioid carcinoma were observed in 12 cases. An adenofibromatous component comprising 5 to 60% of the lesion was present in seven cases. All 12 cases examined immunohistochemically were positive for keratin and EMA and negative for inhibin with focal, luteinized stromal cells positive for inhibin in 10 cases. Estrogen and progesterone receptors were positive in 10 and 11 cases, respectively. Follow-up on 6 of 10 patients with Stage I and the one patient with Stage II disease displayed no evidence of disease 10 to 120 months (mean, 57 mo). Progressive disease and death occurred at 12 and 72 months only in the two women with Stage III disease, one of which had an associated serous carcinoma in the contralateral ovary. Adequate sampling, a careful search for areas of conventional endometrioid carcinoma, and immunohistochemical studies (including EMA, keratin, and inhibin) are helpful in the evaluation of ovarian tumors with sex cord-stromal features. SEC should be considered a well-differentiated endometrioid carcinoma despite the presence of a solid, sex cord-like proliferation, with a good prognosis when confined to the ovary.
"It has not been pathologically defined as to what part of the components resembling SCST is supposed to be contained for the diagnosis of this variant. Reportedly, the proportions of components resembling SCST in the entire tumor vary considerably, ranging from 30 to 100% . In our review, too, the proportions ranged from 20 to 80%. "
[Show abstract][Hide abstract] ABSTRACT: The 4 present cases with endometrioid adenocarcinoma (EMA) of the ovary were characterized by estrogen overproduction and resemblance to sex cord-stromal tumor (SCST). The patients were all postmenopausal, at ages ranging from 60 to 79 years (av. 67.5), who complained of abdominal discomfort or distention and also atypical genital bleeding. Cytologically, maturation of the cervicovaginal squamous epithelium and active endometrial proliferation were detected. The serum estrogen (estradiol, E2) value was preoperatively found to be elevated, ranging from 48.7 to 83.0 pg/mL (av. 58.4). In contrast, follicle stimulating hormone was suppressed to below the normal value. MR imaging diagnoses included SCSTs such as granulosa cell tumor or thecoma for 3 cases because of predominantly solid growth, and epithelial malignancy for one case because of cystic and solid structure. Grossly, the solid part of 3 cases was homogeneously yellow in color. Histologically, varying amounts of tumor components were arranged in solid nests, hollow tubules, cord-like strands and cribriform-like nests in addition to the conventional EMA histology.
In summary, postmenopausal ovarian solid tumors with the estrogenic manifestations tend to be preoperatively diagnosed as SCST. Due to this, in the histological diagnosis, this variant of ovarian EMA may be challenging and misdiagnosed as SCST because of its wide range in morphology.
[Show abstract][Hide abstract] ABSTRACT: Summary We present a case of Sex Cord Tumor of the ovary with undifferentiated areas in a 24 years-old female that was presented as cystic mass. We review the literature getting loose the diagnostic and prognos- tic aspects.
[Show abstract][Hide abstract] ABSTRACT: Atypical proliferative (borderline) endometrioid tumors (APTs) and well-differentiated endometrioid carcinomas of the ovary constitute a spectrum of morphologically diverse proliferative tumors. There is currently no agreement on the criteria for distinguishing them. We report the clinicopathologic features of 56 proliferative endometrioid tumors focusing on the criteria for invasion, the clinical significance of microinvasion and cytologic atypia, and prognosis. Endometriomas, adenofibromas, adenosarcomas and moderately to poorly differentiated carcinomas were excluded, as were patients with concurrent endometrioid carcinoma of the endometrium. The tumors were classified as atypical proliferative tumor (APT) (33 tumors), APT with intraepithelial carcinoma (high-grade cytology in a tumor lacking stromal invasion) (three tumors), APT with microinvasion (invasion <5 mm) (five tumors), and invasive carcinoma (invasion > or = 5 mm) ( 15 tumors). All tumors were confined to the ovary (stage I). In 50 patients, the tumor involved one ovary, and in three patients, the tumors were bilateral. The predominant growth pattern was adenofibromatous in 29 tumors and glandular or papillary in 27 tumors. In 8 (24%) of 41 APTs, areas of benign adenofibroma were identified, and in 13 (87%) of 15 carcinomas, areas of associated APT were identified. Stromal invasion was manifested by confluent glandular growth in all 15 invasive carcinomas and all tumors with microinvasion. Destructive infiltrative growth was also present in 2 (13%) of 15 carcinomas. Confluent glandular growth was the most common manifestation of stromal invasion and therefore served as the best criterion for the diagnosis of carcinoma. Squamous differentiation was observed in 24 tumors, and mucinous differentiation was seen in 20 tumors and was most often seen in APTs. Endometriosis was present in 14 patients with APTs and one patient with carcinoma. Four patients had hyperplasia or atypical hyperplasia of the endometrium. One patient with an APT had a concurrent peritoneal serous neoplasm. Twenty-one patients had available clinical follow-up. Twenty (95%) of 21 patients, including six with invasive carcinoma, two with microinvasion, one with intraepithelial carcinoma, and 11 with APT were alive with no evidence of disease with a mean follow-up of 47 months. One patient with carcinoma had recurrent tumor after 46 months and was alive 40 months after resection of the recurrent tumor. In this large series of proliferative endometrioid tumors, all were stage I and only one patient had a recurrence. Most carcinomas contained evidence of a precursor APT, and in some APTs, an associated benign adenofibroma was identified. Microinvasion or intraepithelial carcinoma occurred in 19% of APTs. This finding likely reflects the various stages of endometrioid carcinogenesis in the ovary. For clinical management, we suggest that these tumors be divided into two categories-APTs and well-differentiated carcinoma-because based on the available data, cytologic atypia and microinvasion appear not to affect the prognosis.
American Journal of Surgical Pathology 11/2000; 24(11):1465-79. DOI:10.1097/00000478-200011000-00002 · 5.15 Impact Factor
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