The objective is to generate a robust and validated predictor profile for chemotherapy response in patients with mCRC using microarray gene expression profiles of primary colorectal cancer tissue.
Gene expression profile predictive of response to chemotherapy in metastatic colorectal cancer.
Disease, Disease stage
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Reprogramming mouse fibroblasts into engraftable myeloerythroid and lymphoid progenitors.
Specimen part
View SamplesHere 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.
Reprogramming mouse fibroblasts into engraftable myeloerythroid and lymphoid progenitors.
Specimen part
View SamplesThe 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.
Protein kinase C α is a central signaling node and therapeutic target for breast cancer stem cells.
No sample metadata fields
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Whole-Genome and Epigenomic Landscapes of Etiologically Distinct Subtypes of Cholangiocarcinoma.
Specimen part
View SamplesAnalysis of gene expression in cholangiocarcinoma patients.
Whole-Genome and Epigenomic Landscapes of Etiologically Distinct Subtypes of Cholangiocarcinoma.
Specimen part
View SamplesAnalysis of gene expression in cholangiocarcinoma patients.
Whole-Genome and Epigenomic Landscapes of Etiologically Distinct Subtypes of Cholangiocarcinoma.
Specimen part
View SamplesCirculating 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
Tumor-derived circulating endothelial cell clusters in colorectal cancer.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
ST3GAL1-Associated Transcriptomic Program in Glioblastoma Tumor Growth, Invasion, and Prognosis.
Disease stage
View SamplesCell surface sialylation confers many roles in cancer biology including cell proliferation, invasiveness, metastasis and angiogenesis. We show here that ST3Gal1 sialyltransferase marks a self-renewing cellular fraction. Depletion of ST3GAL1 abrogates glioma cell growth and tumorigenicity. In contrast, TGFb induces ST3GAL1 expression and correlates with the pattern of ST3Gal1 activation in patient tumors of the mesenchymal molecular subtype. To delineate the downstream events of ST3Gal1 signaling, we utilized a bioinformatical approach that leveraged on the greater statistical power of large patient databases, and subsequently verified our predictions in patient-derived glioma cells. We identify FoxM1, a major stem cell regulatory gene, as a downstream effector, and show that ST3Gal1 mediates the glioma phenotype through control of FoxM1 protein degradation
ST3GAL1-Associated Transcriptomic Program in Glioblastoma Tumor Growth, Invasion, and Prognosis.
Disease stage
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