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GSE106571
Homo sapiens
7 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Patients with the genetic skin blistering disease recessive dystrophic epidermolysis bullosa (RDEB) develop aggressive and metastatic cutaneous squamous cell carcinoma which is the principal cause of premature mortality in this patient group. We performed gene expression profiling of RDEB-SCC cells compared to RDEB keratinocytes in order to identify tumor-specific molecules that could potentially be exploited for detection, diagnosis, and therapy of this devastating disease.
Publication Title
Extracellular Vesicles as Biomarkers for the Detection of a Tumor Marker Gene in Epidermolysis Bullosa-Associated Squamous Cell Carcinoma.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 111 Downloadable Samples
- Affymetrix Human Genome U95A Array (hgu95a)
Description
We used high density oligonucleotide arrays to identify molecular correlates of genetically and clinically distinct subgroups of B-cell chronic lymphocytic leukemia (B-CLL). Gene expression profiling was used to profile the five most frequent genomic aberrations, namely deletions affecting chromosome bands 13q14, 11q22-q23, 17p13 and 6q21, and gains of genomic material affecting chromosome band 12q13. A strikingly high degree of correlation between loss or gain of genomic material and the amount of transcripts from the affected regions leads to the hypothesis of gene dosage as a significant pathogenic factor. Furthermore, the influence of the immunoglobulin variable heavy chain (VH) mutation status was determined. A clear distinction in the expression profiles of unmutated and mutated VH samples exists, which can be discovered using unsupervised learning methods. However, when samples were separated by gender, this separation could only be detected in samples from male patients.
Publication Title
Microarray gene expression profiling of B-cell chronic lymphocytic leukemia subgroups defined by genomic aberrations and VH mutation status.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The mitogen-activated protein kinase (MAPK) p38alpha controls inflammatory responses and cell proliferation. Using mice carrying conditional p38alpha alleles, we investigated its function in postnatal development and tumorigenesis. When p38alpha is specifically deleted in the mouse embryo, fetuses develop to term but die shortly after birth, likely due to lung dysfunction. Fetal hematopoietic cells and embryonic fibroblasts deficient in p38alpha display increased proliferation, resulting from sustained activation of the c-Jun N-terminal kinase (JNK)/c-Jun pathway. Importantly, in chemical-induced liver cancer development, mice with liver-specific deletion of p38alpha show enhanced hepatocyte proliferation and tumor development that also correlates with JNK/c-Jun upregulation. Furthermore, increased proliferation of p38alpha-deficient hepatocytes and tumor cells is suppressed by inactivation of JNK or c-Jun. These results reveal a novel mechanism whereby p38alpha negatively regulates cell proliferation through antagonizing the JNK/c-Jun pathway in multiple cell types and in liver cancer development.
Publication Title
p38alpha suppresses normal and cancer cell proliferation by antagonizing the JNK-c-Jun pathway.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The non-coding Xist RNA triggers silencing of one of the two female X chromosomes during X inactivation in mammals. Gene silencing by Xist is restricted to special developmental contexts found in cells of the early embryo and specific hematopoietic precursors. The absence of critical silencing factors might explain why Xist cannot silence outside these contexts. Here, we show that Xist can also initiate silencing in a lymphoma model. Using the tumor context we identify the special AT rich binding protein SATB1 as an essential silencing factor. We show that loss of SATB1 in tumor cells abrogates the silencing function of Xist. In normal female lymphocytes Xist localizes along SATB1 filaments and, importantly, forced Xist expression can relocalize SATB1 into the Xist cluster. This reciprocal influence on localization suggests a molecular interaction between Xist and SATB1. SATB1 and its close homologue SATB2 are expressed during the initiation window for X inactivation in embryonic stem cells and are recruited to surround the Xist cluster. Furthermore, ectopic expression SATB1 or SATB2 enables gene silencing by Xist in embryonic fibroblasts, which normally do not provide an initiation context. Thus, SATB1 functions as a crucial initiation factor and may act to organize genes for silencing by Xist during the initiation of X inactivation.
Publication Title
SATB1 defines the developmental context for gene silencing by Xist in lymphoma and embryonic cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 22 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Gene network of erythropoietic cells
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples