7e55008a-986c-467e-a379-cbd220f952ff - samples
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ABSTRACT:
PROVIDER: EGAD00001009099 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Uterine carcinosarcoma (UCS) is a form of endometrial cancer simultaneously exhibiting carcinomatous and sarcomatous elements, but the underlying molecular and epigenetic characteristic of this disease is poorly understood. We generated complete DNA methylomes for both the carcinomatous and the sarcomatous components of three UCS samples separated by laser capture microdissection and compared DNA methylomes of UCS with that of normal endometrium as well as methylomes derived from endometrioid carcinoma, serous endometrial carcinoma, and endometrial stromal sarcoma. We identified epigenetic lesions specific to carcinosarcoma, and specific to two components. Hallmarks of DNA methylation abnormality of UCS included global hypomethylation, especially in repetitive elements, and hypermethylation of tumor suppressor gene promoters. Among these, aberrant DNA methylation of MIR200 genes is a key feature of UCS. The carcinoma component of UCS was characterized by hypermethylation of promoters of EMILIN1, NEFM and CLEC14A, genes that are associated with tumor vascularization. In contrast, DNA methylation changes of PKP3, FAM83F and TCP11 were more characteristic of the sarcoma components. Our findings highlight the epigenetic signatures that distinguish the two components of UCS, providing a valuable resource for investigation of these diseases.
2017-03-08 | GSE86505 | GEO
Project description:In this study, we present a case of parotid gland de novo carcinosarcoma. Salivary gland carcinosarcoma (or true malignant mixed tumor) is a rare biphasic neoplasm, composed of both malignant epithelial and malignant mesenchymal components. It is yet unclear whether these two phenotypes occur by collision of two independent tumors or if they are of clonal origin. To analyze the clonality of the different morphologic tumor components, oligonucleotide microarray-based comparative genomic hybridization (oaCGH) was performed on the carcinoma and the sarcoma entity separately. This technique enables a high-resolution, genome-wide overview of the chromosomal alterations in the distinct tumor elements. Analysis of both fractions showed a high number of DNA copy number changes. Losses were more prevalent than gains (82 and 49, respectively). The carcinomatous element displayed more chromosomal aberrations than the sarcomatous component. Specific amplifications of MUC20 (in mesenchymal element) and BMI-1 (in both elements) loci were observed. Overall homology between the two genomic profiles was 75%. DNA copy number profiles of the epithelial and mesenchymal components in this salivary gland carcinosarcoma displayed extensive overlap, indicating a monoclonal origin. Since losses are shared to a larger extent than gains, they seem to be more essential for initial oncogenic events. Furthermore, specific amplifications of a mucin and a Polycomb group gene imply these proteins in the tumorigenesis of carcinosarcomas.
2008-10-01 | GSE12958 | GEO
Project description:Carcinosarcomas of the female genital tract, or GCS, are uncommon but clinically highly aggressive neoplasms with biphasic histology of carcinomatous (C) and sarcomatous (S) elements. These tumors represent a unique model to study the genetic and phenotypic diversity of cancer cells and the link between cellular plasticity and resistance to therapy. The aim of ICGC GCS program is to genomically characterize C and S components of 20 tumors, from endometrium or ovary, through an integrative analysis of whole genome sequencing, RNA sequencing and methylome array.
| EGAS00001002271 | EGA
Project description:Ovarian carcinosarcoma (OCS) is an aggressive and rare tumour type with limited treatment options. OCS is hypothesised to develop via the combination theory, with a single progenitor resulting in carcinomatous and sarcomatous components, or alternatively via the conversion theory, with the sarcomatous component developing from the carcinomatous component through epithelial-to-mesenchymal transition (EMT). In this study, we analysed DNA variants from isolated carcinoma and sarcoma components to show that OCS from 18 women is monoclonal. RNA sequencing indicated the carcinoma components were more mesenchymal when compared with pure epithelial ovarian carcinomas, supporting the conversion theory and suggesting that EMT is important in the formation of these tumours.
| EGAS00001006555 | EGA
Project description:This dataset provides whole genome sequencing data of normal/tumors pairs from 4 patients with uterine or ovarian carcinosarcoma using the HiSeq 2000 sequencing system. It includes 10 samples (4 normals, 4 uterine tumors and 2 ovarian tumors). Through separate whole genome sequencing of carcinomatous and sarcomatoid components, we analyse and compare the genomic alterations of these components.
| EGAD00001003898 | EGA
Project description:This dataset provides whole genome sequencing data of normal/tumors pairs from 9 patients with uterine or ovarian carcinosarcoma using the HiSeq 2000 sequencing system. It includes 27 samples (9 normals, 16 uterine tumors and 2 ovarian tumors). Through separate whole genome sequencing of carcinomatous and sarcomatoid components, we analyse and compare the genomic alterations of these components.
| EGAD00001003755 | EGA
Project description:Müllerian adenosarcomas are malignant gynecologic neoplasms. Advanced disease stage and sarcomatous overgrowth predict aggressive clinical courses. We conducted this study to characterize the genomewide copy number variations (CNV) in adenosarcomas. Paraffin samples from 13 cases were subjected to CNV analysis using OncoScan® FFPE Assay Kit. CNVs were significantly higher in cases with sarcomatous overgrowth. Frequent amplifications of chromosomal segments in 12p12.3 and 12q13.3-23.3 were noted, involving established or potential oncogenes including PIK3C2G (5 cases), MDM2, CPM, YEATS4, CDK4, GLI1, DDIT3 (co-amplified in 4 cases), as well as HMGA2 in 3 cases. MDM2 and CDK4 amplification was verified by fluorescence in situ hybridization.
2016-12-31 | GSE67107 | GEO
Project description:Full title: comparison of the genomic (arrayCGH) profiles of endometrial cancer with and without prior prolonged tamoxifen treatment for primary breast cancer Purpose: Tamoxifen has been a very effective treatment for breast cancer for several decades, however, at the same time increases the risk of endometrial cancer, especially after prolonged exposure. In addition, tamoxifen has been associated with a higher proportion of unfavorable uterine tumor subtypes (carcinosarcomas and serous adenocarcinomas) with worse survival. We investigated whether endometrial tumors, which developed after prolonged tamoxifen treatment for breast cancer, are genetically different from endometrial tumors without preceding tamoxifen exposure. Experimental design: Array CGH was used on archival formalin-fixed paraffin embedded (FFPE) endometrial tumors to determine genomic aberrations. We compared the genomic profiles of 52 endometrial tumors from breast cancer patients after long-term (>=2 years) tamoxifen use (endometrioid adenocarcinomas n=26, carcinosarcomas n=14 and serous adenocarcinomas n=12) with endometrial tumors from unexposed breast cancer patients (n=45). Genomic profiles were correlated with tamoxifen exposure, tumor subtypes and histopathological characteristics of the endometrial tumors. Results: The common uterine corpus cancers of the endometrioid subtype show few genomic aberrations. Tumors with many genomic aberrations were in general ER-negative. In contrast, carcinosarcomas and serous adenocarcinomas showed many aberrations, however they were indistinguishable from each other. Tumors that developed after prolonged tamoxifen use did not show more or different aberrations than unexposed tumors. This was true for all tumor subtypes. Conclusion: Endometrial carcinomas that develop after prolonged tamoxifen use can not be distinguished from non-users on basis of their tumor genomic profile. 52 endometrial tumors from breast cancer patients after long-term (>=2 years) tamoxifen use (endometrioid adenocarcinomas n=26, carcinosarcomas n=14 and serous adenocarcinomas n=12) and 45 endometrial tumors from unexposed breast cancer patients
2010-06-17 | E-GEOD-16680 | biostudies-arrayexpress
Project description:Adult rats (male Lister hooded) were pre-exposed for 3 d for 10 min /d (24 hr interval) to two different novel contexts. On day 4 rats received a single unsignaled scrambled footshock (0.5 mA for 2 s) 2 min into a 3min exposure to one of the two contexts. Rats were either returned to the CS conditioned context (CS+, EXT group) or to the other (CS-, NOR group) context for 10 min, 48h after contextual fear conditioning. Rats were housed in the home cages at all times outside the conditioning and re-exposure components. The novel context chosen to be the conditioned context was counterbalanced across the experimental groups. Rats were killed by CO2 inhalation 2 hours after CS- or CS+ exposure. CA1-enriched dorsal hippocampus was immediately dissected on ice before rapid freezing and storage at -80oC. The CS+ group represents rats that underwent extinction of contextual fear memory.
2015-09-25 | GSE66151 | GEO
Project description:Uterine leiomyosarcoma (ULMS) is a poorly understood gynecologic cancer with few effective treatments. This study explores molecular events involved in ULMS with the goal of identifying strategies.
2012-04-27 | GSE36610 | GEO