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SRP125001
Homo sapiens
60 Downloadable Samples
Illumina HiSeq 2000
Description
Chronic obstructive pulmonary disease (COPD) is a known risk factor for developing lung cancer suggesting that the COPD stroma contains factors supporting tumorigenesis. Since cancer initiation is complex we used a multi-omic approach to identify gene expression patterns that distinguish COPD stroma in patients with or without lung cancer. We obtained lung tissue from patients with COPD and lung cancer (tumor and adjacent non-malignant tissue) and those with COPD without lung cancer for proteomic and mRNA (cytoplasmic and polyribosomal) profiling. We used the joint and individual variation explained (JIVE) method to integrate and analysis across the three datasets. JIVE identified eight latent patterns that robustly distinguished and separated the three groups of tissue samples. Predictive variables that associated with the tumor, compared to adjacent stroma, were mainly represented in the transcriptomic data, whereas, predictive variables associated with adjacent tissue compared to controls was represented at the translatomic level. Kyoto Encyclopedia of Genes and Genome (KEGG) pathway analysis revealed extracellular matrix (ECM) and PI3K-Akt signaling pathways as important signals in the pre-malignant stroma. COPD stroma adjacent to lung cancer is unique and differs from non-malignant COPD tissue and is distinguished by the extracellular matrix and PI3K-Akt signaling pathways. Overall design: Polysome-profiling of lung tumor, adjacent non-cancerous lung stroma tissue samples from the same patient compared to patients without lung cancer across a range of forced expiratory volume in one second (FEV1)
Publication Title
Multi-omic molecular profiling of lung cancer in COPD.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 64 Downloadable Samples
- Illumina HiSeq 2000
Description
Chronic obstructive pulmonary disease (COPD) is an independent risk factor for lung cancer, but the underlying molecular mechanisms are unknown. We hypothesized that lung stromal cells activate pathological gene expression programs supporting oncogenesis. To identify molecular mechanisms operating in the lung stroma that support development of lung cancer. Study subjects included patients with- or without- lung cancer across a spectrum of lung function. We conducted multi-omics analysis of non-malignant lung tissue to quantify the transcriptome, translatome and proteome. Cancer-associated gene expression changes predominantly manifested as alterations in the efficiency of mRNA translation modulating protein levels in the absence of corresponding changes in mRNA levels. The molecular mechanisms driving these cancer-associated translation programs differed based on lung function. In subjects with normal to mildly impaired lung-function, the mammalian target of rapamycin (mTOR) pathway served as an upstream driver; whereas in severe airflow obstruction, pathways downstream of pathological extracellular matrix (ECM) emerged. Consistent with a role during cancer initiation, both the mTOR and ECM gene expression programs paralleled activation of previously identified pro-cancer secretomes. Furthermore, in situ examination of lung tissue documented that stromal fibroblasts express cancer-associated proteins from the two pro-cancer secretomes including IL6 in mild or no airflow obstruction and BMP1 in severe airflow obstruction. Two distinct stromal gene expression programs promoting cancer initiation are activated in lung cancer patients depending on lung function. Our work has implications both for screening strategies and personalized approaches to cancer treatment. Overall design: Polysome-profiling of non-cancerous lung stroma tissue samples from patients with or without lung cancer across a range of forced expiratory volume in one second (FEV1)
Publication Title
Distinct Cancer-Promoting Stromal Gene Expression Depending on Lung Function.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 474 Downloadable Samples
- Illumina HiSeq 2000, Illumina HiSeq 3000
Description
Single cell RNA-seq of neural stem cell and astrocytes from old mice Overall design: Single cell RNA-seq of neural stem cell and astrocytes from old mice
Publication Title
Quiescence Modulates Stem Cell Maintenance and Regenerative Capacity in the Aging Brain.
Sample Metadata Fields
Sex, Age, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
Illumina MouseRef-8 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Reprogramming mouse fibroblasts into engraftable myeloerythroid and lymphoid progenitors.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
Here we show that hematopoietic transcription factors Scl, Lmo2, Runx1 and Bmi1 can convert a developmentally-distant lineage (fibroblasts) into induced hematopoietic progenitors (iHPs). We analyzed transcriptomic data for cell undergoing the transdifferentiation process at several time-points of the process.
Publication Title
Reprogramming mouse fibroblasts into engraftable myeloerythroid and lymphoid progenitors.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 15 Downloadable Samples
- Illumina HumanRef-8 v3.0 expression beadchip
Description
The EMT program allows epithelial cells to become endowed with motility, invasiveness and stem cell traits. We investigated difference in signaling networks that are differentially utilized in EMTed and non-EMTed cells, thereby identifying therapeutic targets that are unique to EMT/cancer stem cells.
Publication Title
Protein kinase C α is a central signaling node and therapeutic target for breast cancer stem cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 120 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Whole-Genome and Epigenomic Landscapes of Etiologically Distinct Subtypes of Cholangiocarcinoma.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 72 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Analysis of gene expression in cholangiocarcinoma patients.
Publication Title
Whole-Genome and Epigenomic Landscapes of Etiologically Distinct Subtypes of Cholangiocarcinoma.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 48 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Analysis of gene expression in cholangiocarcinoma patients.
Publication Title
Whole-Genome and Epigenomic Landscapes of Etiologically Distinct Subtypes of Cholangiocarcinoma.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 53 Downloadable Samples
- IlluminaHiSeq2500
Description
Circulating tumor cells (CTCs) are the subject of several translational studies and clinical trials because their examination could offer an insight into tumor progression and clinical outcomes. Circulating tumor microemboli (CTM) are clusters of CTCs that have been described as malignant entities for over 50 years, although a comprehensive characterization of these cells is still lacking. Contrary to current consensus, we demonstrate that CTM isolated from colorectal cancer patients are not cancerous, but represent a discrete population of tumor-derived endothelial cells. CTM express epithelial and mesenchymal markers that are consistent with previous reports on circulating tumor cell phenotyping. However, they do not mirror the genetic variations of matching tumors. Transcriptome analysis of single-CTM reveals that these structures exhibit an endothelial phenotype, with further results supporting a tumor-derived endothelial lineage. CTM are widespread in blood sampled from preoperative cancer patients but not in healthy donors, suggesting CTM count as a potential biomarker of interest for colorectal cancer. CTM should not be confused with bona fide circulating epithelial tumor cells. The characterization of tumor derived endothelial cell clusters (TECCs) is likely of high diagnostic value, and may provide direct information about the underlying tumor vasculature at the time of diagnosis, during treatment and the course of the disease. Overall design: Profiling of 18 TECCs/CTM from 8 colorectal cancer patients. In addition profiling of matched 7 normal colonic mucosa, 9 primary colorectal tumor samples (of which three from the same patient), one colorectal cancer metastatis. Additionally, 14 laser-capture-dissected endothelia from the same patients and tissues, and 3 commercially available normal endothelial cell lines
Publication Title
Tumor-derived circulating endothelial cell clusters in colorectal cancer.
Sample Metadata Fields
No sample metadata fields
View Samples