Similar Datasets
Project description:Dynamics and transcriptomic driver landscape of metastatic osteosarcoma
| PRJNA588395 | ENA
Project description:Osteosarcoma (OS) is the most common primary bone tumour in children and young adults, and the second highest cause of cancer-related death in this age group. In spite of aggressive chemotherapy, disease-free survival has not improved significantly in the past 20 years, and 50% of patients subsequently develop fatal pulmonary metastasis. We have performed gene expression profiling of primary osteosarcoma biopsies (i) to identify prognostic markers, and (ii) to identify novel therapeutic targets. Keywords: Comaprison between disease status (metastatic vs non-metastatic) and normal Two-colour experiment. 7 samples for non-metastatic patients, 6 of which are analyzed in duplicate (dye-swaps); 11 samples for metastatic patients, 10 of which are analyzed in duplicate (dye-swaps); 5 samples of non-malignant bone analyzed individualy, no dye-swaps (i.e. 5 biological replicates).
2010-08-30 | E-GEOD-9508 | biostudies-arrayexpress
Project description:Osteosarcoma (OS) is the most common primary bone tumour in children and young adults, and the second highest cause of cancer-related death in this age group. In spite of aggressive chemotherapy, disease-free survival has not improved significantly in the past 20 years, and 50% of patients subsequently develop fatal pulmonary metastasis. We have performed gene expression profiling of primary osteosarcoma biopsies (i) to identify prognostic markers, and (ii) to identify novel therapeutic targets. Keywords: Comaprison between disease status (metastatic vs non-metastatic) and normal
2010-08-30 | GSE9508 | GEO
Project description:Osteosarcoma (OS) is the malignant bone tumor with a high tendency to metastasize to the lung, where the molecular mechanisms are unclear. The mouse OS cell line LM8 has been isolated originally from the Dunn OS cell line by in vivo selection as a subline with a high metastatic potential to the lung. We used gene chip-based global gene expression analysis of differential screening between parental Dunn and LM8 cells in order to reveal genes predominantly expressed in LM8 cells, which correlate with high metastatic potential. 2 cell lines
2011-03-04 | E-GEOD-26648 | biostudies-arrayexpress
Project description:Osteosarcoma (OS) is the malignant bone tumor with a high tendency to metastasize to the lung, where the molecular mechanisms are unclear. The mouse OS cell line LM8 has been isolated originally from the Dunn OS cell line by in vivo selection as a subline with a high metastatic potential to the lung. We used gene chip-based global gene expression analysis of differential screening between parental Dunn and LM8 cells in order to reveal genes predominantly expressed in LM8 cells, which correlate with high metastatic potential.
2011-03-04 | GSE26648 | GEO
Project description:Purpose: Lung metastasis is responsible for nearly all deaths caused by osteosarcoma, the most common pediatric bone tumor. How malignant bone cells coerce the lung microenvironment to support metastatic growth is unclear. This study delineates how osteosarcoma cells educate the lung microenvironment during metastatic progression. Experimental design: Using single-cell transcriptomics (scRNA-seq), we characterized genome- and tissue-wide molecular changes induced within lung tissues by disseminated osteosarcoma cells in both immunocompetent murine models of metastasis and patient samples. We confirmed transcriptomic findings at the protein level and determined spatial relationships with multi-parameter immunofluorescence. We evaluated the ability of nintedanib to impair metastatic colonization and prevent osteosarcoma-induced education of the lung microenvironment in both immunocompetent murine osteosarcoma and immunodeficient human xenograft models. Results: Osteosarcoma cells induced acute alveolar epithelial injury upon lung dissemination. scRNA-seq demonstrated that the surrounding lung stroma adopts a chronic, non-resolving wound-healing phenotype similar to that seen in other models of lung injury. Accordingly, metastasis-associated lung demonstrated marked fibrosis, likely due to the accumulation of pathogenic, pro-fibrotic, partially-differentiated epithelial intermediates. Inhibitionintermediates. Inhibition of fibrotic pathways with nintedanib prevented metastatic progression in multiple murine and human xenograft models. Conclusions: Our work demonstrates that osteosarcoma cells co-opt fibrosis to promote metastatic outgrowth. When harmonized with data from adult epithelial cancers, our results support a generalized model wherein aberrant mesenchymal-epithelial interactions are critical for promoting lung metastasis. Adult epithelial carcinomas induce fibrotic pathways in normal lung fibroblasts, whereas osteosarcoma, a pediatric mesenchymal tumor, exhibits fibrotic reprogramming in response to the aberrant wound-healing behaviors of an otherwise normal lung epithelium, which are induced by tumor cell interactions.
2024-06-19 | GSE270231 | GEO
Project description:Purpose: Lung metastasis is responsible for nearly all deaths caused by osteosarcoma, the most common pediatric bone tumor. How malignant bone cells coerce the lung microenvironment to support metastatic growth is unclear. This study delineates how osteosarcoma cells educate the lung microenvironment during metastatic progression. Experimental design: Using single-cell transcriptomics (scRNA-seq), we characterized genome- and tissue-wide molecular changes induced within lung tissues by disseminated osteosarcoma cells in both immunocompetent murine models of metastasis and patient samples. We confirmed transcriptomic findings at the protein level and determined spatial relationships with multi-parameter immunofluorescence. We evaluated the ability of nintedanib to impair metastatic colonization and prevent osteosarcoma-induced education of the lung microenvironment in both immunocompetent murine osteosarcoma and immunodeficient human xenograft models. Results: Osteosarcoma cells induced acute alveolar epithelial injury upon lung dissemination. scRNA-seq demonstrated that the surrounding lung stroma adopts a chronic, non-resolving wound-healing phenotype similar to that seen in other models of lung injury. Accordingly, metastasis-associated lung demonstrated marked fibrosis, likely due to the accumulation of pathogenic, pro-fibrotic, partially-differentiated epithelial intermediates. Inhibitionintermediates. Inhibition of fibrotic pathways with nintedanib prevented metastatic progression in multiple murine and human xenograft models. Conclusions: Our work demonstrates that osteosarcoma cells co-opt fibrosis to promote metastatic outgrowth. When harmonized with data from adult epithelial cancers, our results support a generalized model wherein aberrant mesenchymal-epithelial interactions are critical for promoting lung metastasis. Adult epithelial carcinomas induce fibrotic pathways in normal lung fibroblasts, whereas osteosarcoma, a pediatric mesenchymal tumor, exhibits fibrotic reprogramming in response to the aberrant wound-healing behaviors of an otherwise normal lung epithelium, which are induced by tumor cell interactions.
2024-05-09 | GSE252703 | GEO
Project description:Expression data of osteosarcoma 143B and metastatic variants
| PRJNA780937 | ENA
Project description:To investigate the molecular and cellular alterations occurring in the lung tissue during the pre-metastatic niche formation in osteosarcoma, we used two two experimental mouse models and a multi-omics approach.
2024-01-26 | PXD040814 | Pride
Project description:Landscape of the peritumoral TME of metastatic osteosarcoma and further underscore the translational relevance of the canine patient as a model of human disease.
2026-03-23 | GSE309676 | GEO