This SuperSeries is composed of the SubSeries listed below.
Effects of genistein supplementation on genome‑wide DNA methylation and gene expression in patients with localized prostate cancer.
Sex, Age
View SamplesTo identify molecular effects of genistein on mRNA levels in prostate cancer, we compared gene expression profiles of genistein-treated tumors with placebo-treated samples. There were 628 probes that reached nominally significant p-values. The genes that were differentially expressed between genistein and placebo samples were involved in angiogenesis, apoptosis, epithelial to mesenchymal transition, and tumor progression. Gene enrichment analysis suggested that PTEN and PDGF were activated, while MYC, beta-estradiol, glucocorticoid receptor NR3C1, and interferon-gamma were repressed in response to genistein treatment. These findings highlight the effects of genistein on global changes in gene expression in prostate cancer and its effects on molecular pathways involved in prostate tumorigenesis.
Effects of genistein supplementation on genome‑wide DNA methylation and gene expression in patients with localized prostate cancer.
Sex, Age
View SamplesDifferential gene expression profiles were observed in response to Hras in either wild-type or Ppar-beta null primary keratinocytes and differentail gene edxpression profiles by GW0742 were only found in wild-type keratinocytes.
Peroxisome proliferator-activated receptor β/δ cross talks with E2F and attenuates mitosis in HRAS-expressing cells.
Specimen part
View SamplesFindings suggest that PPARalpha plays a decisive role in the development of hypertrophy, affecting the functional outcome of the heart. Unfortunately, information on the nature of PPARalpha-dependent processes in cardiac hypertrophy is fragmentary and incomplete.
Transcriptomic analysis of PPARalpha-dependent alterations during cardiac hypertrophy.
No sample metadata fields
View SamplesThe generation of induced pluripotent stem (iPS) cells 1-4 has spawned unprecedented opportunities for investigating the molecular logic that underlies cellular pluripotency and reprogramming, as well as for obtaining patient-specific cells for future clinical applications. However, both prospects are hampered by the low efficiency of the reprogramming process. Here, we show that juvenile human primary keratinocytes can be efficiently reprogrammed to pluripotency by retroviral transduction with Oct4, Sox2, Klf4 and c-Myc. Keratinocyte-derived iPS (KiPS) cells appear indistinguishable from human embryonic stem (hES) cells in colony morphology, growth properties, expression of pluripotency-associated transcription factors and surface markers, as well as in vitro and in vivo differentiation potential. Notably, keratinocyte reprogramming to pluripotency is, at least, 100-fold more efficient and 2-fold faster than that of fibroblasts. This increase in reprogramming efficiency allowed us to expand the practicability of the technology and to generate KiPS cells from single plucked hairs from adult individuals.
Efficient and rapid generation of induced pluripotent stem cells from human keratinocytes.
No sample metadata fields
View SamplesCancer stem cell (CSC) identification relies on transplantation assays of cell sub-populations sorted from fresh tumor samples. Herein, we attempt to bypass limitations of abundant tumor source and predetermined immune selection by in-vivo propagating patient derived xenografts (PDX) from human malignant rhabdoid tumor (MRT), a rare and lethal pediatric neoplasm, to an advanced state in which most cells behave as CSCs. Stemness is then probed by comparative transcriptomics of serial PDXs generating a gene signature of EMT, invasion/motility, metastasis and self-renewal, pinpointing putative MRT CSC markers. The relevance of these putative CSC molecules is analyzed by sorting tumorigenic fractions from early-passaged PDX according to one such molecule, deciphering expression in archived primary tumors and testing the effects of CSC molecule inhibition on MRT growth. Using this platform, we identify ALDH1 and lysyl oxidase (LOX) as relevant targets and provide a larger framework for target and drug discovery in rare pediatric cancers. Overall design: Tumorigenic fractions from early-passaged PDX
In Vivo Expansion of Cancer Stemness Affords Novel Cancer Stem Cell Targets: Malignant Rhabdoid Tumor as an Example.
Subject
View SamplesWe compared the heart of 6-weeks-old mice (young) with 18-months-old mice (old)
MicroRNA-34a regulates cardiac ageing and function.
Age, Specimen part
View SamplesWe utilized the Barley1 Affymetrix GeneChip for comparative transcript analysis of Betzes barley, Chinese Spring wheat, and Chinese SpringBetzes ditelosomic chromosome addition lines to physically map barley genes to their respective chromosome arm locations. We mapped barley genes to chromosome arms (1HS, 2HS, 2HL, 3HS, 3HL, 4HS, 4HL, 5HS, 5HL, 7HS, and 7HL) based on their transcript levels in the ditelosomic addition lines. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Hatice Bilgic. The equivalent experiment is BB55 at PLEXdb.]
Mapping barley genes to chromosome arms by transcript profiling of wheat-barley ditelosomic chromosome addition lines.
Specimen part
View SamplesSTEAP4 is a plasma membrane metallo-reductase involved in the transport of iron and copper. Recently, STEAP4 was implicated in promoting insulin sensitivity by acting in white adipose tissue (WAT) to control the production of inflammatory cytokines such as IL-6. Indeed, the loss of STEAP4 expression in mice leads to increased production of inflammatory cytokines in visceral WAT and systemic insulin resistance. In this report, we demonstrate that in mouse liver STEAP4 is produced at significant levels and that STEAP4 transcription is induced by IL-6. We further demonstrate that the STEAP4 gene is a direct target of phosphorylated STAT3 in mouse liver. In addition, hepatic STEAP4 expression is regulated by feeding and fasting, and obesity leads to the induction of STEAP4 expression in the liver. Interestingly, the regulation of STEAP4 in both feeding and fasting and the obese state appears to require the transcription factor C/EBPalpha that may act in concert with STAT3 as they both bind to the proximal STEAP4 promoter in vivo. Taken together these data suggest the transcriptional regulation of hepatic STEAP4 may play a critical role in the response to nutritional and inflammatory stress and contribute to the protective effect of STEAP4 in vivo.
Regulation of hepatic six transmembrane epithelial antigen of prostate 4 (STEAP4) expression by STAT3 and CCAAT/enhancer-binding protein alpha.
Sex, Specimen part
View SamplesMesenchyme-derived cells in the human airway wall including airway smooth muscle cells, fibroblasts and myofibroblasts are known to play important roles in airway remodeling. The lack of specific phenotypic markers makes it difficult to define these cell populations in primary cultures. The objectives of this study were to evaluate reported markers and to identify novel markers to define these cell types.
Can lineage-specific markers be identified to characterize mesenchyme-derived cell populations in the human airways?
Specimen part
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