A comparison of gene expression between control versus IPF human lung MPC using human Affy 1.0st chips.
Disruption of lineage specification in adult pulmonary mesenchymal progenitor cells promotes microvascular dysfunction.
Specimen part, Disease, Disease stage
View SamplesComparison between inducible pluripotent stem cells from healthy patients and patients with BMPR2 mutation, at different differentiation stages.
Identification of a common Wnt-associated genetic signature across multiple cell types in pulmonary arterial hypertension.
Specimen part
View SamplesTranscriptome of CDKN1C-siRNA-injected embryos were compared to sham-injected embryos using RNA-sequencing to determine the genes and pathways downstream of the silenced gene that may have been altered. Overall design: Transcriptome comparison between two pools of embryos (i.e. CDKN1C-siRNA-injected vs sham-injected embryos)
Knockdown of CDKN1C (p57(kip2)) and PHLDA2 results in developmental changes in bovine pre-implantation embryos.
Specimen part, Subject
View SamplesWe report the impact of heterozygous loss of either Pdx1 or Oc1 on the developing pancreas at e15.5 Overall design: mRNA of mouse pancreata at embryonic day 15.5 from control, Pdx1Lac/+, Oc1+/- and double heterozygous (Pdx1LacZ/+;Oc1+/-) embryos
Threshold-Dependent Cooperativity of Pdx1 and Oc1 in Pancreatic Progenitors Establishes Competency for Endocrine Differentiation and β-Cell Function.
Specimen part, Cell line, Subject
View SamplesBACKGROUND. Human prostate cancer LNCaP and PC-3 cell lines have been extensively used as prostate cancer cell models to study prostate cancer progression and to develop therapeutic agents. Although LNCaP and PC-3 cells are generally assumed to represent early and late stages of prostate cancer development, respectively, there is limited information regarding comprehensive gene expression patterns between these two cells lines and relating these cells to prostate cancer progression based on their gene expression.
Unique patterns of molecular profiling between human prostate cancer LNCaP and PC-3 cells.
No sample metadata fields
View SamplesWe measured changes in expression of 3,826 genes in MMTV-rtTA/tetO-HER2 mammary carcinoma tissue after treatment with control vehicle or abemaciclib Overall design: Examination of changes in gene expression in 23 tumors (11 control, 12 abemaciclib)
CDK4/6 inhibition triggers anti-tumour immunity.
Specimen part, Subject
View SamplesMicroarray analysis of 28 brain metastasis samples from lung adenocarcinoma patients.
Isolated metastasis of an EGFR-L858R-mutated NSCLC of the meninges: the potential impact of CXCL12/CXCR4 axis in EGFR<sub>mut</sub> NSCLC in diagnosis, follow-up and treatment.
No sample metadata fields
View SamplesTo gain insights into tumor heterogeneity in anti-cancer drug responses of patient-derived xenograft models of HER2+ breast cancer brain metastases, we performed transcriptome gene expression profiling by Ion AmpliSeqâ„¢ Transcriptome sequencing that targets more than 20,000 human genes. Our data found that all anti-cancer drugs responders have significantly higher expression levels of AKT-mTOR-dependent signature genes as compared to the non-responders, suggesting that most HER2+ breast cancer brain metastases are depend on the AKT-mTOR pathway Overall design: Gene expression profiles of five PDX samples were generated by Ion AmpliSeq Transcriptome sequencing, in duplcate, using Ion torrent Proton machine.
Combination inhibition of PI3K and mTORC1 yields durable remissions in mice bearing orthotopic patient-derived xenografts of HER2-positive breast cancer brain metastases.
Specimen part, Disease, Subject
View Samplesperipheral blood samples of two leukemia patients in remission were profiled by single cell RNA sequencing approximately 1 year after receiving WT1 specific transgenic T cell therapy, at a time when patients were in clinical remission Overall design: single cell RNA sequencing of peripheral blood mononuclear cells
T cell receptor gene therapy targeting WT1 prevents acute myeloid leukemia relapse post-transplant.
Specimen part, Disease, Subject
View SamplesTriple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. After engendering acquired resistance to BET inhibition in previously sensitive TNBCs, we utilized integrative approaches to identify a unique mechanism of epigenomic resistance to this epigenetic therapy. Resistant cells remain dependent on BRD4, confirmed by RNA interference. However, TNBC cells adapt to BET bromodomain inhibition by re-recruitment of unmutated BRD4 to super-enhancers, now in a bromodomain-independent manner. Proteomic studies of resistant TNBC identify hyper-phosphorylation of BRD4 and strong association with MED1. Together, these studies provide a rationale for BET inhibition in TNBC and argue for combination strategies to anticipate clinical drug resistance. Overall design: RNA-Seq in parental and JQ1 resistant triple negative breast cancer (TNBC) in response to DMSO or JQ1 treatment over time
Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer.
No sample metadata fields
View Samples