Molecular mechanisms of cell cycle exit are poorly understood. A group of genes required for cell cycle exit and maintenance of cell quiescence in human fibroblasts following serum deprivation has been recently identified. Studies on lymphocytes following growth factor deprivation-induced cell cycle exit have predominantly focused on the initiation of apoptosis. A set of genes involved in lymphocyte quiescence have also been identified among genes highly expressed in resting lymphocytes and down-regulated after cell activation. In our study, proliferating IL-2-dependent human T cells were forced to exit cell cycle by growth factor withdrawal, and their gene expression profiles were examined.
Molecular signature of cell cycle exit induced in human T lymphoblasts by IL-2 withdrawal.
No sample metadata fields
View SamplesRNAseq (3''DGE) profiles of osteoblasts from four lung cancer-bearing mice and three tumor-free mice. Overall design: Osteoblasts were FACS-sorted using the following markers: CD45-CD31-Terr119-GFP+ from lineage depleted bone and bone marrow tissue of lung tumor-bearing or tumor-free age-, sex- and litter-matched KrasLSL-G12D/WT;p53Flox/Flox (KP)-Ocn GFP mice. Total RNA was prepared using the Trizol method followed cDNA preparation, amplification, Illumina adapter ligation and 3''end sequencing by Illumina HiSeq 2500
Osteoblasts remotely supply lung tumors with cancer-promoting SiglecF<sup>high</sup> neutrophils.
Sex, Age, Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide transcriptome profiling of homologous recombination DNA repair.
Specimen part, Cell line
View SamplesHomologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information.
Genome-wide transcriptome profiling of homologous recombination DNA repair.
Specimen part, Cell line
View SamplesHomologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities. Here, we identified an HRD gene signature that robustly predicted HRD status. Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK. We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map. Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information.
Genome-wide transcriptome profiling of homologous recombination DNA repair.
Specimen part, Cell line
View SamplesHomologous recombination-mediated DNA repair deficiency (HRD) predisposes to cancer development, but also provides therapeutic opportunities Here, we identified an HRD gene signature that robustly predicted HRD status Unexpectedly, concurrent loss of PTEN in BRCA1-deficient cells might extensively rewire the HR repair network and confer resistance to PARP inhibitor, partially through over-expression of TTK We used the HRD gene signature as a drug discovery tool and found several PARP-inhibitor-synergizing agents through the connectivity map Thus gene expression profiling can be used to define the functional status of the HR repair network providing prognostic and therapeutic information
Genome-wide transcriptome profiling of homologous recombination DNA repair.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A module of negative feedback regulators defines growth factor signaling.
No sample metadata fields
View SamplesHELA cells derived from human cervical tumor were subjected to EGF stimulation for 0,20,40,60,120,240 and 480 minutes.
A module of negative feedback regulators defines growth factor signaling.
No sample metadata fields
View SamplesMCF10A cells derived from spontaneously immortalized normal human mammary epithel were subjected to EGF/SERUM stimulation for 0,20,40,60,120,240 and 480 minutes.
A module of negative feedback regulators defines growth factor signaling.
No sample metadata fields
View Samples