Methylation array data of thymic epithelial tumors (TC, NET, THYM)
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ABSTRACT:
PROVIDER: EGAD00010002355 | EGA |
REPOSITORIES: EGA
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Project description:The molecular landscape of malignant thymic epithelial tumors (TET) is largely unknown. To better understand and target these clinically challenging entities, we characterize 81 patients harboring 46 thymus carcinomas (TC), 8 neuroendocrine tumors of the thymus (NET) and 27 thymomas using WGS/WES, transcriptome and methylome analysis. TC harbor different molecular alterations compared to thymoma and NET and have higher tumor mutational burden than thymomas. 14/76 TET patients show (likely) pathogenic germline alterations. Composite biomarker analysis indicates homologous repair deficiency in a subset of patients. We identify immunologically hot and cold TC. Cold TC show significantly shorter overall survival. 71/81 patients receive molecularly-informed therapy recommendations, which are applied in 28/71 cases leading to a DCR of 60% and an ORR of 24% (both n=25). 8/23 patients reach PFS ratios > 1.3, seven of them having TC.
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Project description:The thymus shapes the T cell receptor repertoire, and is one of the first organs to rapidly age, with gross changes in cellularity and architecture. To resolve the nature of these changes we used SMART-Seq2 on FACS purified thymic epithelial cells (TEC) across the first year of mouse life. We sorted 4 TEC populations in each of 5 mice at each age (1 week, 4 weeks, 16 weeks, 32 weeks and 52 weeks old).
2020-09-14 | E-MTAB-8560 | biostudies-arrayexpress
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2018-02-25 | GSE98894 | GEO
Project description:Thymic epithelial tumors are a group of neoplasms with heterogeneous histological features and clinical behavior. The identification of markers useful to predict patient prognosis and molecular targets for therapies is limited by a very little understanding of the biology of these neoplasms. We evaluated the copy number (CN) aberrations of genes involved in normal thymus development in thymic epithelial tumors, following the intriguing idea that the ectopic deregulation of genes relevant for proliferation and differentiation of embryonic cells, can contribute to tumor growth. Frequent CN losses of FOXC1 were observed in more aggressive tumors and correlated with a reduced protein expression; tumors negative for FOXC1 expression were associated with a shorter time to progression. In addition, FOXC1 showed tumor suppressor activity in in-vitro models. Our data indicate that FOXC1 loss can identify a group of thymic epithelial tumors with poor prognosis, possibly because its tumor suppressor properties. Two color array CGH of a series of 59 thymic epithelial tumors plus evaluation of 2 thymic carcinoma cell lines and one thymoma B1 cell line.
2013-05-03 | E-GEOD-23540 | biostudies-arrayexpress
Project description:Thymoma and thymic carcinoma represent the two most characterized types of Thymic epithelial tumors (TET) which arise from epithelial cell of thymus. According to the different morphological features, lymphocytes and epithelial cells ratio and grade of malignancy, TET are divided in thymoma A, AB, B1, B2, and B3 and thymic carcinoma. We used microarrays to detail the global programme of gene expression distinguishing tumoral and normal thymic tissue, thus identifying networks of correlated mRNAs-lncRNAs.
2020-12-10 | GSE158997 | GEO
Project description:Over activation of the aryl hydrocarbon receptor (AhR) by TCDD results ampng other phenotypes in severe thymic atrophy accompanied by immunosuppression. The link between thymic atrophy, skewed thymocyte differntiation and immunosuppression is still not fully resolved. This study investigates the TCDD elicted exprssion changes in the ET, cortical thymus epithelial cell line. Keywords: TCDD, AhR, thymic epithelial cells, thymic involution, thymus atrophy
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Project description:Regenerative responses predispose tissues to tumor formation by largely unknown mechanisms. High-mobility group box 1 (HMGB1) is a danger-associated molecular pattern contributing to inflammatory pathologies. Here, we show that HMGB1 derived from keratinocytes, but not myeloid cells, delays cutaneous wound healing and drives skin tumor formation. In wounds of mice lacking HMGB1 selectively in keratinocytes, a marked reduction in neutrophil extracellular trap (NET) formation is observed. Pharmacological targeting of HMGB1 or NETs prevents skin tumorigenesis and accelerates wound regeneration. HMGB1-dependent NET formation and skin tumorigenesis is orchestrated by the cytokine TNF and requires RIPK1 kinase activity. NETs are present in the microenvironment of keratinocyte-derived tumors in mice and lesional and tumor skin of patients suffering from Recessive Dystrophic Epidermolysis Bullosa (RDEB), a disease in which skin blistering predisposes to tumorigenesis. We conclude that tumorigenicity of the wound microenvironment depends on epithelial-derived HMGB1 regulating NET formation, thereby establishing a mechanism linking reparative inflammation to tumor initiation.
2019-10-16 | GSE138918 | GEO
Project description:Thymic epithelial cells (TECs) support T cell development in the thymus. Cortical thymic epithelial cells (cTECs) facilitate positive selection of developing thymocytes whereas medullary thymic epithelial cells (mTECs) facilitate the deletion of self-reactive thymocytes in order to prevent autoimmunity. The mTEC compartment is highly dynamic with continuous maturation and turnover, but the genetic regulation of these processes remains poorly understood. MicroRNAs (miRNAs) are important regulators of TEC genetic programs since miRNA-deficient TECs are severely defective. However, the individual miRNAs important for TEC maintenance and function and their mechanisms of action remain unknown. Here, we demonstrate that miR-205 is highly and preferentially expressed in mTECs during both thymic ontogeny and in the postnatal thymus. This distinct expression is suggestive of functional importance for TEC biology. Genetic ablation of miR-205 in TECs, however, neither revealed a role for miR-205 in TEC function during homeostatic conditions nor during recovery from thymic stress conditions. Thus, despite its distinct expression, miR-205 on its own is largely dispensable for mTEC biology. In order to identify miRNAs differentially expressed in mTECs, we purified cortical thymic epithelial cells (cTECs), mTECs and CD45+ cells as three distinct populations and prepared RNA for microarray analysis. Thymic subsets were FACS-purified from 4-week old NOD wildtype mice. Thymi from 10-12 female mice were pooled together for stromal cell isolation for a total of 3 CD45+, 2 cTEC and 3 mTEC biologic replicates.
2015-07-28 | E-GEOD-68674 | biostudies-arrayexpress
Project description:Over activation of the aryl hydrocarbon receptor (AhR) by TCDD results ampng other phenotypes in severe thymic atrophy accompanied by immunosuppression. The link between thymic atrophy, skewed thymocyte differntiation and immunosuppression is still not fully resolved. This study investigates the TCDD elicted exprssion changes in the ET, cortical thymus epithelial cell line. Keywords: TCDD, AhR, thymic epithelial cells, thymic involution, thymus atrophy ET cells were grown to 80-90% confluence and treated with 5nM TCDD or solvent control (1,4-Dioxane, 0,05%V). 2h,4h and 6h after treatment, RNA was isolated using TRIzol and gene expression measured. All experiments wer done in biological duplicates.
2008-12-30 | E-GEOD-10168 | biostudies-arrayexpress