PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11890573

Poorly differentiated endometrial sarcoma with clear cell features.

M Fukunaga
View original source ↗Export metadata ↓

Abstract

A case of poorly differentiated endometrial sarcoma with clear cell features in a 46-year-old female is presented. A 9 x 8 x 6 cm, transmural, white solid tumor in the uterine fundic wall was characterized histologically by infiltrative growth and a solid arrangement of tumor cells with clear cytoplasm. The tumor showed vascular invasion, moderate to severe cellular atypia, mitotic activity of 20 per 10 high-power fields and necrosis. It was immunohistochemically positive for vimentin and negative for CAM5.2, epithelial membrane antigen, desmin, alpha-smooth muscle actin, muscle actin, estrogen and progesterone receptors. Electron microscopy showed that the clear cytoplasm was attributed to the presence of numerous dilated mitochondria and lipid droplets. Flow cytometry showed a diploid phenotype. Pathologists should be aware of the existence of this type of endometrial sarcoma with clear cells and should not confuse it with other neoplasma showing clear cell features.

Explore related subjects

Endometrial NeoplasmsFemaleHumansMiddle AgedSarcomaCase ReportsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Fukunaga. 2001. Poorly differentiated endometrial sarcoma with clear cell features.. https://doi.org/10.1034/j.1600-0463.2001.d01-134.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Molecular genetic defects in endometrial carcinomas: microsatellite instability, PTEN and beta-catenin (CTNNB1) genes mutations.

PURPOSE: The present study aims to assess the incidence of microsatellite instability (MSI) and mutations in the PTEN and beta-catenin (CTNNB1) genes in endometrial carcinomas and to analyze the detected defects in these factors in relation to each other and to the clinico-pathological features of tumors. MATERIALS AND METHODS: In a series of 56 endometrioid endometrial carcinomas, the status of MSI was determined using nine polymorphic markers, and mutations in all exons of the PTEN gene and in exon 3 of the CTNNB1 gene were evaluated by SSCP and sequencing methods. RESULTS: Microsatellite instability was found in 18 carcinomas (32.1%, MSI+); the remaining 38 tumors were microsatellite stable (MSI-). In 15 cases (26.8%), a loss of heterozygosity (LOH) at the studied microsatellite markers also occurred. In 29 carcinomas (51.8%), mutations were found in the PTEN gene and in nine tumors (16.1%) in the CTNNB1 gene. PTEN mutations occurred significantly more frequently in MSI+ than in MSI- tumors (77.8 vs. 39.5%, p = 0.007), but, except for one, none of them was attributable to MSI. In contrast, incidence of CTNNB1 mutations in MSI+ and MSI- tumors no significantly differed between themselves (16.7 vs. 15.8%, p = 0.760). Interestingly, mutations in the CTNNB1 gene most frequently coexisted with mutations in the PTEN gene (7/9, 77.8%). However, this finding requires future verification on a larger group of cases. The incidence of MSI and PTEN, but not CTNNB1 mutations, was significantly more common in poorly, than in well-to-moderately, differentiated tumors (G3 vs. G1 + G2; p = 0.042, 0.039 and 0.958, respectively). CONCLUSION: We conclude that most frequently occurring mutations in the PTEN gene may be a key event for the tumorigenesis of endometrioid endometrial carcinomas, while coexistence or absence of microsatellite instability or mutations in the CTNNB1 gene may reflect the heterogeneity of molecular mechanisms contributing to the development of these tumors.

Endometrial Neoplasms↗
PubMed2007

Physical activity and endometrial cancer risk: a review of the current evidence, biologic mechanisms and the quality of physical activity assessment methods.

OBJECTIVES: To (1) determine the nature of the association between physical activity and endometrial cancer risk; (2) assess the contribution of variation in the quality of physical activity measurement to inconsistencies in study results; and (3) review the biologic mechanisms that might mediate possible effects of physical activity on risk. METHODS: We reviewed and summarized all published epidemiologic studies examining physical activity and endometrial cancer risk, and evidence relating to possible biologic mechanisms. We assigned each study a quality score for physical activity measurement. RESULTS: Fourteen of the 18 studies showed a convincing or possible protective effect of physical activity on endometrial cancer risk, with an average relative risk reduction of around 30%. A dose-response relation was observed in 7 of 13 studies. The quality score was not related to the observed strength of association or the presence of a dose-response relation. There was epidemiologic and biologic evidence that vigorous activity, as well as light and moderate intensity activities, such as housework, gardening or walking for transportation, may reduce risk. CONCLUSIONS: Physical activity probably has a protective role in endometrial cancer development. More epidemiologic and biologic evidence is needed to make conclusive recommendations on optimal types, characteristics or time periods of physical activity.

Endometrial Neoplasms↗
PubMed2007

Immunoprofile of endocervical and endometrial stromal cells and its potential application in localization of tumor involvement.

To evaluate and compare the immunophenotype of endocervical and endometrial stromal cells and to asses its potential application in tumor localization. Paraffin sections of benign endocervix (n = 24), benign endometrium (n = 33), endocervical adenocarcinoma (n = 9), endometrial carcinoma (n = 13), and endometrial hyperplasia (n = 16) were stained with antibodies to CD10, Wilms Tumor-1, CD34, smooth muscle actin, and factor XIIIa by immunohistochemistry. In 16 cases, lower uterine segment was also available. Immunoreactivity of stromal cells was recorded as positive (>/=50% staining), focally positive (>/=5%-<50%) or negative (<5%). Endocervical stromal cells (ECSC) in either benign or malignant cervical epithelial lesions were predominantly CD34/CD10 (CD34 dominant immunophenotype). Endometrial stromal cells (EMSCs) in either benign or malignant epithelial lesions were primarily CD34/CD10 (CD10 dominant immunophenotype). Expression of Wilms Tumor-1 was decreased in EMSC of the EMCA when compared to their counterpart in endometrial hyperplasia. There was no differential expression of smooth muscle actin and factor XIIIa identified between ECSC and EMSC. The immunophenotypes of the ECSC and EMSC overlapped in the lower uterine segment. The functional status of the endometrium had no effect on the immunoprofile. The pattern of CD34 and CD10 immunostaining in stromal cells might be helpful in determining tumor involvement in uterine and cervical sites.

Endometrial Neoplasms↗