Project description:Epithelioid Sarcoma (ES) is a rare neoplasm uniquely comprised of cells exhibiting both mesenchymal and epithelial features. Having propensity for local and distant recurrence, it can pose a diagnostic dilemma secondary to pathologic complexity. Patients have dismal prognosis due to lack of effective therapy. HDAC inhibitors exhibit marked anti-tumor effects in various malignancies. Our studies demonstrate that pan-HDAC inhibitors constitute potentially novel therapeutics versus ES. Human ES cells (VAESBJ, HS-ES, Epi544) were studied in vitro to evaluate the effects of HDACi. Gene array analysis was used to identify the impact of HDACi on ES gene expression in three cell lines.
Project description:Epithelioid Sarcoma (ES) is a rare neoplasm uniquely comprised of cells exhibiting both mesenchymal and epithelial features. Having propensity for local and distant recurrence, it can pose a diagnostic dilemma secondary to pathologic complexity. Patients have dismal prognosis due to lack of effective therapy. HDAC inhibitors exhibit marked anti-tumor effects in various malignancies. Our studies demonstrate that pan-HDAC inhibitors constitute potentially novel therapeutics versus ES. Human ES cells (VAESBJ, HS-ES, Epi544) were studied in vitro to evaluate the effects of HDACi.
Project description:Several human cancers contain a small subpopulation of cells called cancer stem-like cells (CSCs)/cancer initiating cells (CICs), which are defined by the ability of self- renewal, multi-differentiation potential, and tumorigenesis. In current study, we focused on epithelioid sarcoma, which is very rare caner, and isolated CSCs/CICs from epitheloid sarcoma cell line ESX based on ALDH activity using ALDEFLUOR assay towards identification of a new CIC/CSC marker. We performed gene profiling between ALDHhigh and ALDH low cells using cDNA microarray for the identification of good markers of CSCs/CICs of epithelioid sarcoma.
Project description:Epithelioid hemangioendothelioma (EHE) is a rare vascular sarcoma that is associated with a WWTR1-CAMTA1 fusion gene in greater than 90% of cases. Cell lines were generated from WWTR1-CAMTA1 positive murine EHE tumors which also harbor a loss of CDKN2A. RNA sequencing was performed on cell lines.
Project description:Epithelioid hemangioendothelioma (EHE) is a rare vascular sarcoma that is associated with a WWTR1-CAMTA1 fusion gene in greater than 90% of cases. We aimed to investigate the transcriptional pathways activated in EHE. Total RNA was isolated from EHE tumors from surgical resection or autopsy specimens (n=6) followed by RNA-Seq. The results of this study identified a unique transcriptional profile for EHE and helped to validate a novel murine model of EHE.
Project description:Microarray analysis revealed differential gene expression patterns of rhabdomyosarcoma (A-204), leiomyosarcoma (SK-LMS-1) and epithelioid cell sarcoma (VA-ES-BJ) cells treated with TRAIL and/or taurolidine. To explore new therapeutic options in the treatment of sarcomas, we tested the antibiotic taurolidine (TRD) on A-204, SK-LMS-1 and VA-ES-BJ carcinoma cell lines alone and in combination with rhTRAIL (TNF related apoptosis-inducing ligand). Gene expression was analysed by RNA microarray. Cell lines were treated with Taurolidine, Trail and a combination of both and compaired to untreated cells
Project description:Epithelioid hemangioendothelioma (EHE) is a rare vascular sarcoma that is associated with a TAZ-CAMTA1 fusion in greater than 90% of cases and loss of CDKN2A in human EHE tumors is associated with late stage disease. Murine EHE tumors were created by conditionally expressing TAZ-CAMTA1 and conditionally knocking out Cdkn2a within vascular endothelium. Resultant tumors were used for single cell RNA sequencing and compared against age matched wild type mice tissue.
Project description:Epithelioid hemangioendothelioma (EHE) is a rare vascular sarcoma that is associated with a WWTR1-CAMTA1 fusion gene in greater than 90% of cases. Using an adaptation of the FLEx system, we generated a genetically engineered mouse model of EHE whereby the endogenous Wwtr1 Locus is replaced with an Wwtr1-Camta1 locus. Tumors generated from this mouse model were dissociated and a 10X genomics library preparation was performed. The barcoded library was then deep sequenced.