Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Uterine sarcomas comprise leiomyosarcoma, endometrial stromal sarcoma, adenosarcoma, undifferentiated endometrial sarcoma, and their variants. Carcinosarcoma is historically classified as sarcoma, but it is now regarded as a metaplastic carcinoma. Uterine sarcomas are rare, and are traditionally staged in the same way as endometrial carcinoma. Because of their different clinical and biological behaviours, the International Federation of Gynecology and Obstetrics introduced a new staging system in 2009 for leiomyosarcoma, endometrial stromal sarcoma and adenosarcoma, and carcinosarcoma, respectively. Following an extensive literature review no good evidence was found to support the modification of the staging system. This is mainly because of the rarity of the sarcomas and the heterogeneity of the reports, the different diagnostic criteria and treatments changing over the decades the retrospective nature and small sample size in most studies, and the lack of uniform pathological review even in large studies. Currently, evidence is still lacking about the use of preoperative imaging for staging purpose, and uterine sarcomas remain to be surgically staged. Total hysterectomy is the cornerstone for both staging and treatment. Newer evidence shows that routine lymphadenectomy and bilateral salpingo-oophorectomy may not be necessary, unless in the presence of extra-uterine spread, suspicious ovaries or lymph nodes, and certain poor histological types, such as undifferentiated endometrial sarcoma and adenosarcoma with sarcomatous overgrowth. More research and data collection are definitely needed in order to verify and further revise the current staging systems.
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PMID:Staging of uterine sarcomas. 2175 16

Carcinosarcoma of the uterus is a rare gynaecological neoplasm, which is also known as malignant mixed mesodermal tumor. Traditionally this tumour has been regarded as a subtype of uterine sarcoma, and its origin remains controversial. The exact nature and prognosis was not clear in the past. It is believed that uterine carcinosarcoma have a Mullerian duct origin and have a capacity to differentiate into various mesenchymal and epithelial components. Regarding the histogensis, various theories have been given; of which 'conversion theory' was broadly accepted. Carcinosarcoma are mostly of monoclonal origin with the carcinomatous component being the driving force. This type of tumor is broadly divided into two groups, homologous and heterologous, depending on the characteristics of the stroma or mesenchymal components of endometrial tissue. It is more frequent in black women and postmenopausal women. Radiation is a possible etiological factor but the exact etiology is not known yet. However, tamoxifen may induce carcinogenesis in some patients. Its clinical feature is very similar to endometrial carcinoma i.e. postmenopausal vaginal bleeding, have a very aggressive behavior and a poor prognosis. This pelvic malignancy is treated by multimodality therapy including surgery, chemotherapy and radiotherapy. Here we are reviewing old concepts about the disease and modern understandings of the origin, classification, pathogenesis and recent advances in the treatment of the uterine carcinosarcoma.
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PMID:Review literature on uterine carcinosarcoma. 2531 23

Carcinosarcoma (CS) of the uterus or ovary is a rare, aggressive and biphasic neoplasm composed of carcinoma and sarcoma elements. Previous genomic studies have identified the driver genes and genomic properties associated with CS. However, there is still no molecular subtyping scheme with clinical relevance for this disease. Here, we sequence 109 CS samples, focusing on 596 genes. We identify four molecular subtypes that resemble those observed in endometrial carcinoma: POLE-mutated, microsatellite instability, copy number high, and copy number low subtypes. These molecular subtypes are linked with DNA repair deficiencies, potential therapeutic strategies, and multiple clinicopathological features, including patient outcomes. Multi-regional comparative sequencing reveals genomic alteration-independent CS cell differentiation. Transcriptome and DNA methylome analyses confirm epithelial-mesenchymal transition as a mechanism of sarcoma differentiation. The current study thus provides therapeutic possibilities for CS as well as clues to understanding the molecular histogenic mechanism of its development.
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PMID:Clinically relevant molecular subtypes and genomic alteration-independent differentiation in gynecologic carcinosarcoma. 3167 74