This SuperSeries is composed of the SubSeries listed below.
The origins of breast cancer prognostic gene expression profiles.
No sample metadata fields
View SamplesMetastasis predictive gene signatures can result from either somatic mutation, inherited polyrmorphism or both. This experiment is designed to look at the gene expression differences due to differences in somatic mutations in the initiating oncogene, PyMT. Met1 is from a fully metastatic FVB mammary tumor cell line, DB7 contains a mutation that permits tumor formation, but suppresses metastatic ability.
The origins of breast cancer prognostic gene expression profiles.
No sample metadata fields
View SamplesF1 hybrids from (AKR/J x FVB/NJ) and (DBA/2J x FVB/NJ) outcrosses display a 20-fold difference in mammary tumor metastatic capacity, due to differences in inherited polymorphisms. Expression studies were performed to determine whether polymorphism-driven gene expression signatures predictive of outcome could be generated from normal tissues
The origins of breast cancer prognostic gene expression profiles.
No sample metadata fields
View SamplesF1 hybrids from (AKR/J x FVB/NJ) and (DBA/2J x FVB/NJ) outcrosses display a 20-fold difference in mammary tumor metastatic capacity, due to differences in inherited polymorphisms. Expression studies were performed to determine whether polymorphism-driven gene expression signatures predictive of outcome could be generated from mouse tumor tissues
The origins of breast cancer prognostic gene expression profiles.
No sample metadata fields
View SamplesF1 hybrids from (AKR/J x FVB/NJ) and (DBA/2J x FVB/NJ) outcrosses display a 20-fold difference in mammary tumor metastatic capacity, due to differences in inherited polymorphisms. Expression studies were performed to determine whether polymorphism-driven gene expression signatures predictive of outcome could be generated from normal tissues
The origins of breast cancer prognostic gene expression profiles.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Network analysis reveals centrally connected genes and pathways involved in CD8+ T cell exhaustion versus memory.
Specimen part
View SamplesDuring acute viral infections, nave CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become exhausted and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each.
Network analysis reveals centrally connected genes and pathways involved in CD8+ T cell exhaustion versus memory.
Specimen part
View SamplesWe hypothesize that germline variation influences susceptibility to aggressive prostate tumor
GNL3 and SKA3 are novel prostate cancer metastasis susceptibility genes.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Interactions of chromatin context, binding site sequence content, and sequence evolution in stress-induced p53 occupancy and transactivation.
Cell line, Time
View SamplesWe performed RNA-seq from 6 days post fertilization hnf4a-/- and hnf4a+/+ zebrafish larval digestive tracts raised in the absence (Germ Free, GF) or presence (Conventionalized, CV) of microbiota. We found that zebrafish hnf4a activates almost half of the microbiota-suppressed genes, indicating that the microbiota supress Hnf4a trans-activity. We also provide evidence suggesting that microbial suppression of Hnf4a may contribute to IBD pathogenesis. Overall design: Generation and analysis of RNA-seq from hnf4a-/- and hnf4a+/+ zebrafish larvae in the absence (Germ Free, GF) or presence (Conventionalized, CV) microbiota.
Microbiota regulate intestinal epithelial gene expression by suppressing the transcription factor Hepatocyte nuclear factor 4 alpha.
No sample metadata fields
View Samples