Tumors have the capacity to trigger the formation of blood vessels allowing them to spread to other body parts. We examined here the stem cells that form arteries and veins within tumors and propose that their inhibition reduces metastatic spread. Overall design: Examination of dynamics and differentiation of tissue resident endothelial hierarchy in a melanoma setting
Endovascular progenitors infiltrate melanomas and differentiate towards a variety of vascular beds promoting tumor metastasis.
Specimen part, Subject
View SamplesWe report transcriptomes of whole skin from different anatomic regions, dorsum, ventrum, chin and ear pinna, as well as ear cartilage/muscle complex at different post-natal time points. Whole tissue was microdissected from wild type mice. Overall design: Examination of miscrodissected whole skin from dorsum, ventrum and chin at six consecutive time points of the hair cycle, and comparison of ear pinna telogen skin vs. ear cartilage/muscle complex vs. dorsal telogen skin. Sample definition: CCT Chin skin, Competent telogen CEA Chin skin, Early anagen CMA Chin skin, Mid-anagen CLA Chin skin, Late anagen CC Chin skin, Catagen CRT Chin skin, Refractory telogen VCT Ventral skin, Competent telogen VEA Ventral skin, Early anagen VMA Ventral skin, Mid-anagen VLA Ventral skin, Late anagen VC Ventral skin, Catagen VRT Ventral skin, Refractory telogen DCT Dorsal skin, Competent telogen DEA Dorsal skin, Early anagen DMA Dorsal skin, Mid-anagen DLA Dorsal skin, Late anagen DC Dorsal skin, Catagen DRT Dorsal skin, Refractory telogen ERST Ear skin, Telogen LC Ear cartilage/muscle complex
A multi-scale model for hair follicles reveals heterogeneous domains driving rapid spatiotemporal hair growth patterning.
Specimen part, Cell line, Subject
View SamplesSLE is characterized by the production of autoantibodies that arise from the B cell lineage. Therefore, we sought to assess the epigenetic and transcriptome profiles of distinct B cell subsets known to be expanded in SLE from healthy and SLE subjects. These data define the differentiation heirarchy of B cell subsets and the epigenetic and transcriptional consequences of SLE on human B cells. Overall design: Five distinct B cell subsets were FACS isolated from a cohort of SLE and HC subjects. For a subset of subjects, circulating Antibody Secreting Cells (ASC) were also isolated for comparisons. Cells were FACS sorted into lysis buffer and RNA purified and transcriptome profiles determined by RNA-seq.
Epigenetic programming underpins B cell dysfunction in human SLE.
Specimen part, Disease stage, Subject
View SamplesCD24 is a potential oncogene reported to be overexpressed in a large variety of human malignancies. We have shown that CD24 is overexpressed in 90% of colorectal tumors at a fairly early stage in the multistep process of carcinogenesis. Anti-CD24 monoclonal antibodies (mAb) induce a significant growth inhibition in colorectal and pancreatic cancer cell lines that express the protein. This study is designed to investigate further the effects of CD24 down-regulation using mAb or small interfering RNA in vitro and in vivo. Western blot analysis showed that anti-CD24 mAb induced CD24 protein down-regulation through lysosomal degradation. mAb augmented growth inhibition in combination with five classic chemotherapies. Xenograft models in vivo showed that tumor growth was significantly reduced in mAb-treated mice. Similarly, stable growth inhibition of cancer cell lines was achieved by down-regulation of CD24 expression using short hairpin RNA (shRNA). The produced clones proliferated more slowly, reached lower saturation densities, and showed impaired motility. Most importantly, down-regulation of CD24 retarded tumorigenicity of human cancer cell lines in nude mice. Microarray analysis revealed a similar pattern of gene expression alterations when cells were subjected to anti-CD24 mAb or shRNA. Genes in the Ras pathway, mitogenactivated protein kinase, or BCL-2 family and others of oncogenic association were frequently down-regulated. As a putative new oncogene that is overexpressed in gastrointestinal malignancies early in the carcinogenesis process, CD24 is a potential target for early intervention in the prevention and treatment of cancer.
Targeting CD24 for treatment of colorectal and pancreatic cancer by monoclonal antibodies or small interfering RNA.
Specimen part, Cell line
View SamplesEctopic expression of DNMT3L in Drosophila causes melanotic tumor in the transgenic flies from fifth generation onwards.
DNMT3L enables accumulation and inheritance of epimutations in transgenic Drosophila.
Specimen part
View SamplesA series contains a set of transcript intensity values measured by Affymetrix microarray.
Systems-level analysis of cell-specific AQP2 gene expression in renal collecting duct.
Sex, Specimen part
View SamplesThis series of microarray data contain transcript intensity of mpkCCD cells.
Systems-level analysis of cell-specific AQP2 gene expression in renal collecting duct.
No sample metadata fields
View SamplesFreshly isolated rat kidney proximal tubules were subjected for transcript profiling.
Systems-level analysis of cell-specific AQP2 gene expression in renal collecting duct.
Sex, Specimen part
View SamplesFreshly isolated rat kidney medullary thick ascending limbs were subjected for transcript profiling.
Systems-level analysis of cell-specific AQP2 gene expression in renal collecting duct.
Sex, Specimen part
View SamplesPurpose: Lithium salts, used for treatment of bipolar disorder, frequently induce nephrogenic diabetes insipidus (NDI), limiting therapeutic success. NDI is associated with loss of expression of the molecular water channel, aquaporin-2, in the renal collecting duct (CD). Here, we use the methods of systems biology in a well-established rat model of lithium-induced NDI to identify signaling pathways activated at the onset of polyuria. Methods: We carried out RNA-sequencing in cortical CDs microdissected from rats treated with lithium for 12-72 hours (vs. time controls). Administration of anti-inflammatory doses of dexamethasone to lithium-treated rats countered the loss of aquaporin-2 protein. Protein mass spectrometry in microdissected cortical CDs provided corroborative evidence, but also identified decreased abundance of several anti-oxidant proteins. Cortical thick ascending limbs of Henle were also microdissected for RNA-Seq at 72 hrs. We carried out RNA-Seq for 2-3 CCD sample per rat (1 lithium-treated rat versus 1 control at 12, 24, 36 hrs). Results and conclusion: Integration of new data with prior data about lithium effects at a molecular level leads to a signaling model in which lithium increases ERK activation leading to induction of NF-?B signaling and an inflammatory-like response that represses Aqp2 gene transcription. Overall design: We carried out RNA-sequencing and protein mass spectrometry in cortical CDs microdissected from rats treated with lithium. We identified signaling pathways that initiate Lithium-induced NDI using systems biology approaches.
RNA-Seq and protein mass spectrometry in microdissected kidney tubules reveal signaling processes initiating lithium-induced nephrogenic diabetes insipidus.
Sex, Specimen part, Cell line, Subject, Time
View Samples