FCHL is a common, complex genetic lipid disorder with a largely unknown aetiology. Altered adipose tissue metabolism has been implicated as contributing to FCHL.
CDKN2B expression in adipose tissue of familial combined hyperlipidemia patients.
No sample metadata fields
View SamplesRNA from etiolated seedlings, light-treated seedlings, leaves and flowers was hybridized to ATH1 and AGRONOMICS1 arrays.
AGRONOMICS1: a new resource for Arabidopsis transcriptome profiling.
Age, Specimen part
View SamplesThe present research is devoted to the identification of gene(s) severely affected by LMNA mutations, leading to striated muscle laminopathies and more specifically the skeletal phenotype of Emery-Freifuss Muscular Dystrophy.
The non-muscle ADF/cofilin-1 controls sarcomeric actin filament integrity and force production in striated muscle laminopathies.
Age, Specimen part
View SamplesThe adipocyte-derived hormone adiponectin potently inhibits osteoclast formation in vitro.
Evidence that contamination by lipopolysaccharide confounds in vitro studies of adiponectin activity in bone.
Specimen part
View SamplesA transcription factor Nkx2-1 (also known as TTF-1) regulates the expression of different sets of genes. Gene expression analysis was performed using mRNAs from Nkx2-1-induced A549 cells compared to that from the control A549 cells. We used microarrays to detail the global program of gene expression controlled by Nkx2-1 and identified distinct classes of up-regulated and down-regulated genes.
Kras(G12D) and Nkx2-1 haploinsufficiency induce mucinous adenocarcinoma of the lung.
Cell line
View SamplesTransgenic mice (Scgb1a1-rtTA/[tetO]-KRAS.G12D/Nkx2-1+/-) develop mucinous lung tumors. Gene expression analysis was performed using mRNAs from the whole lungs of the mice compared to that of the control mice.
Kras(G12D) and Nkx2-1 haploinsufficiency induce mucinous adenocarcinoma of the lung.
Specimen part
View SamplesThe purpose of the present study was to investigate the association of glutathione S-transferase P1 (GSTP1) expression with resistance to neoadjuvant paclitaxel followed by 5-fluorouracil/epirubicin/cyclophosphamide (P-FEC) in human breast cancers. The relationship of GSTP1 expression and GSTP1 promoter hypermethylation with intrinsic subtypes was also investigated. In this study, primary breast cancer patients (n = 123, stage II-III) treated with neoadjuvant P-FEC were analyzed. Tumor samples were obtained by vacuum-assisted core biopsy before P-FEC. GSTP1 expression was determined using immunohistochemistry, GSTP1 promoter methylation index (MI) using bisulfite methylation assay and intrinsic subtypes using DNA microarray. The pathological complete response (pCR) rate was significantly higher in GSTP1-negative tumors (80.0%) than GSTP1-positive tumors (30.6%) (P = 0.009) among estrogen receptor (ER)-negative tumors but not among ER-positive tumors (P = 0.267). Multivariate analysis showed that GSTP1 was the only predictive factor for pCR (P = 0.013) among ER-negative tumors. Luminal A, luminal B and HER2-enriched tumors showed a significantly lower GSTP1 positivity than basal-like tumors (P = 0.002, P < 0.001 and P = 0.009, respectively), while luminal A, luminal B and HER2-enriched tumors showed a higher GSTP1 MI than basal-like tumors (P = 0.076, P < 0.001 and P < 0.001, respectively). In conclusion, these results suggest the possibility that GSTP1 expression can predict pathological response to P-FEC in ER-negative tumors but not in ER-positive tumors. Additionally, GSTP1 promoter hypermethylation might be implicated more importantly in the pathogenesis of luminal A, luminal B and HER2-enriched tumors than basal-like tumors.
GSTP1 expression predicts poor pathological complete response to neoadjuvant chemotherapy in ER-negative breast cancer.
Age, Specimen part, Disease stage
View SamplesGene expression profiles of Cbfb-deficient and control Treg cells were compared.
Indispensable role of the Runx1-Cbfbeta transcription complex for in vivo-suppressive function of FoxP3+ regulatory T cells.
Sex, Age, Specimen part
View SamplesWe used microarrays to determine global gene expression in primary tumor tissues (ESCC) and matched normal tissues (adjacent normal esophageal mucosa)
Hypoxia activates the cyclooxygenase-2-prostaglandin E synthase axis.
Sex, Age, Specimen part
View SamplesTo delineate the role of hypoxia in esophageal epithelial biology, we carried out gene array experiments using a non-transformed immortalized diploid human esophageal cell line, EPC2-hTERT (Mol Cancer Res. 2003;1:729-38). Unlike cancer cell lines, EPC2-hTERT has no genetic alterations at early passages that may affect the cellular response to hypoxia.
Hypoxia activates the cyclooxygenase-2-prostaglandin E synthase axis.
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