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At least 289 records · Page 16Linked to original sources
PubMed1998

[Mixed uterine mesodermal sarcoma in the population of southern Israel in the years 1996-1971--clinical and pathological characteristics].

During 1971-1996, 17 patients with mixed mesodermal uterine tumors were treated. Average age at diagnosis was 67.3 years, 12/17 were of European and 5/17 of Afro-Asian extraction. The overall 5-year survival was 21%. 10/17 patients had mixed mesodermal tumors with a heterologous mesenchymal element, and 7/17 had a homologous mesenchymal element (carcinosarcoma). 6/17 had another primary malignancy, including breast cancer (3/17), bilateral metachronous breast tumor (2/17), and malignant lymphoma of the neck region (2/17). All 3 with breast cancer had previously been treated with tamoxifen. I had simultaneous mesodermal tumor and ovarian thecoma. Simultaneous autoimmune manifestations occurred in 2/17, including thrombocytopenic purpura in 1, and myasthenia gravis in another. Mesodermal tumor of the uterus is a relatively rare malignancy with aggressive behavior and poor prognosis. It also had unusual associations with other primary tumors, hormonal treatment, and autoimmune manifestations.

Aged↗
PubMed1997

[Endometrial carcinoma with polycystic ovaries. Report of two cases in women younger than 40 years old].

Endometrial carcinoma is rare in women under 40 years of age. The incidence in this age group has been variously reported to be from 1% to 8% of all cases of endometrial carcinoma. Women at high risk, as a result of excess estrogenic stimulation are those with polycystic ovaries, long-standing estrogen users and functioning granulosa cell tumors and thecomas. We report two cases of young women with endometrial carcinoma and polycystic ovaries (Stein-Leventhal syndrome).

Adult↗
PubMed1998

[Cytomorphological diagnosis of granulosa cell tumor of the ovary].

The cytology of granulosa cell tumor in children and adults is studied. Cytological smears of ascitic fluid and fresh tissue smears were examined. The tumor was diagnosed in 9 patients aged 11 to 73 years. All patients had symptoms of hyperestrogenia. Adequate treatment of the condition requires the tumor to be differentiated from other tumors (thecoma, low-grade and small-cell carcinomas, carcinoid, yolk-sac tumor, and lymphoma) before or during surgery.

Adolescent↗
PubMed1998

Inhibin expression in ovarian tumors and tumor-like lesions: an immunohistochemical study.

We investigated 203 ovarian tumors and tumor-like lesions for inhibin expression using a monoclonal anti-inhibin alpha antibody. Inhibin was present in the tumor cells in all 14 primary adult granulosa cell tumors (4 luteinized) plus 3 metastatic, all 10 primary juvenile granulosa cell tumors plus 1 metastatic, 10 of 11 thecomas, 3 of 11 fibromas, 4 of 11 sclerosing stromal tumors, 6 of 11 Sertoli cell tumors (1 oxyphilic), 7 of 11 Sertoli-Leydig cell tumors, 1 gynandroblastoma, 10 primary ovarian sex cord tumors with annular tubules plus 2 metastatic, 8 of 9 steroid cell tumors, both pregnancy luteomas, 1 of 2 unclassified sex cord tumors, 2 of 5 gonadoblastomas, 9 of 10 female adnexal tumors of probable wolffian origin, and in the non-neoplastic stroma of many carcinomas and germ cell tumors. The tumor cells were inhibin-negative in 10 fibrosarcomas, 12 small cell carcinomas of hypercalcemic type, 24 germ cell tumors (except for a focus of inhibin-positive syncytiotrophoblast in one case), and 17 ovarian carcinomas. Two of the three inhibin-positive fibromas showed diffuse immunostaining and were associated with evidence of estrogenic activity. Among nine Sertoli-Leydig cell tumors with available clinical data, four that were more than minimally inhibin-positive were accompanied by androgenic manifestations; five inhibin-negative or only minimally positive tumors lacked such evidence. Inhibin immunostaining may be useful in the differential diagnosis of inhibin-positive sex cord tumors versus histologically similar inhibin-negative neoplasms, but inhibin negativity does not preclude a diagnosis of sex cord tumor. The unexpected, common inhibin positivity of female adnexal tumors of probable wolffian origin indicates that inhibin staining cannot be used to differentiate these tumors from Sertoli cell tumors. Inhibin immunostaining is also helpful in identifying potential steroid hormone-secreting cells in the non-neoplastic stromal component of epithelial, germ cell, and other ovarian tumors.

Adnexal Diseases↗
PubMed1982

Fetal and maternal virilization associated with pregnancy. A case report and review of the literature.

A masculinized female infant was born to a mother who had virilizing signs dating from the fourth month of pregnancy. Serum 17 alpha-hydroxyprogesterone, dehydroepiandrosterone, and testosterone levels were all normal in the infant. Maternal testosterone level was markedly elevated one week post partum. Dexamethasone phosphate suppression was normal. Human chorionic gonadotropin stimulation five weeks post partum revealed further elevation of high baseline free and total testosterone levels. Free and total testosterone levels 30 weeks post partum were normal, and all maternal virilizing signs had regressed with the exception of her deepened voice. The child has had no progression of masculinization. The mother is believed to have had a luteoma of pregnancy.

Adult↗
PubMed1981

Surgical management of ovarian cancer.

Ovarian cancer represents the second most common cancer of the female reproductive organs. It is usually not associated with significant warning signals that led to early diagnosis. The management is based on adequate surgical staging, removal of as much of the bulk tumor as possible, careful histologic assessment of the primary cancer and its metastases, and appropriate postoperative adjuvant therapy. Stage I cancer confined to one ovary and with a very favorable histology, such as borderline malignant epithelial cancers, dysgerminoma, granulosa cell tumor, and Sertoli-Leydig's cell tumor, may be treated with surgery alone. Stage I epithelial cancers are best treated with a total abdominal hysterectomy, bilateral salpingo-oophorectomy, and adjuvant chemotherapy or radiation therapy. Stage I nonepithelial malignant neoplasms are best treated with a unilateral salpingo-oophorectomy followed by an aggressive combination chemotherapy. Advanced ovarian cancers regardless of the histologic origin of the tissue should be treated with aggressive surgery, including complete removal of the tumor whenever possible followed by adjuvant therapy selected on the basis of the histologic appearance of the tumor. Complete remissions for ovarian cancer should be confirmed by second-look operation prior to discontinuing adjuvant chemotherapy.

Adenocarcinoma↗
PubMed1996

Inactivation of p16/CDKN2 and p15/MTS2 genes in different histological types and clinical stages of primary ovarian tumors.

To define the involvement of p16/CDKN2 and p15/MTS2 inactivation in ovarian tumorigenesis and the association of these inactivation events with histological types and clinical stages of ovarian tumors, we analyzed homozygous deletion and somatic mutation of p16/CDKN2 and p15/MTS2 genes, as well as hypermethylation of the 5'-CpG island of the p16/CDKN2 gene, in 49 primary ovarian tumors and 6 ovarian carcinoma cell lines. We found homozygous deletions of p16/CDKN2 and p15/MTS2 in 6 (12%) and 5 (10%) primary tumors, respectively. Somatic mutation of p16/CDKN2 was found in only 1 primary tumor, but mutation of p15/MTS2 was not detected in any sample. None of the 28 primary tumors or 6 cell lines was hypermethylated at the 5'-CpG island of p16/CDKN2. The incidence of inactivation of p16/CDKN2 in primary tumors was significantly higher in the advanced stages (7 of 29) than in the early stages (0 of 14). Seven of 9 alterations in p16/CDKN2 and p15/MTS2 were observed in serous (3 of 12), endometrioid (3 of 9) and clear-cell (1 of 4) carcinomas. However, only normal sequences of these genes were detected in mucinous carcinomas. Loss of heterozygosity (LOH) at the IFNA locus was detected in 1 of 19 (5%) tumors, but no change at the D9S171 locus was observed in 17 tumors. These results suggest that: (i) homozygous deletion is the main mechanism of inactivation of p16/CDKN2 and p15/MTS2 in ovarian tumorigenesis; (ii) inactivation of p16/CDKN2 and p15/MTS2 may be the histological type-specific events involved in ovarian tumorigenesis; and (iii) inactivation of p16/CDKN2 is potentially involved in the progression of ovarian tumors in advanced stages.

Carcinoma↗
PubMed1997

E-cadherin expression in human epithelial ovarian cancer and normal ovary.

The ovarian surface epithelium (OSE) is the origin of the majority of human ovarian cancers. These adenocarcinomas are characterized by initial local growth followed by spreading into the peritoneal cavity at later stages of tumor progression. The cell-adhesion molecule E-cadherin (E-cad) plays an important role in maintaining tissue integrity. Disappearance or impaired function of E-cad have often been associated with tumor formation and invasion in vivo and in vitro. The cell-specific expression of E-cad was investigated in normal human ovaries (n = 12), in benign (n = 5) and borderline (n = 4) ovarian epithelial tumors and in adenocarcinomas of different stages and histological grades (n = 18), by immunohistochemistry and immunoblotting. An ovarian cancer cell line (NIH-OVCAR3) was used as a reference. The epithelial origin of the cells was confirmed with cytokeratin (AE1/AE3) staining. In normal ovaries, the expression of E-cad was limited to inclusion cysts or deep clefts lined with OSE, whereas no staining of the OSE could be demonstrated at the surface of the ovary. In contrast, benign and borderline tumors uniformly expressed E-cad. This was observed in malignant tumors of all stages despite their degree of differentiation. E-cad was also present in metastasis from such tumors. The cell-specific expression of E-cad in inclusion cysts of normal ovaries and in epithelial layers of borderline tumors indicates a role for E-cad in the early events of the progression to a malignant phenotype. E-cad was not downregulated in later stages of ovarian cancer progression.

Adenocarcinoma, Mucinous↗
PubMed1999

Fine-needle aspiration cytology of malignant fibrothecoma of the ovary.

Fibrothecomas are common, but their malignant counterpart is extraordinarily rare. To the best of our knowledge, this is the first report on the cytologic features of malignant fibrothecoma. We had an opportunity to study it because the 70-yr-old woman refused initial surgery until the tumor reached 22 cm in size and weighed 1, 500 gm. A CT-guided fine-needle aspiration biopsy was obtained from a 5 cm left pelvic mass, which was the second recurrence within 5 yr. The smears showed large fragments of tightly packed, small, oval cells with scanty, eccentric blue cytoplasm (Diff-Quik stain), and finely granular chromatin with small central nucleoli (Ultrafast Papanicolaou stain), transected by delicate blood vessels. The tumor resembled well-differentiated carcinoma, low-grade endometrial stromal sarcoma, and other small oval cell gynecologic neoplasms. Cytodiagnosis of nonepithelial ovarian neoplasms can be difficult. However, it is not impossible, especially for recurrent tumors with previously established histodiagnosis. Diagn. Cytopath. 21:284-286, 1999.

Aged↗