Non-small cell lung cancer (NSCLC) can be classified into the major subtypes adenocarcinoma (AC) and squamous cell carcinoma (SCC) subtypes. Although explicit molecular, histological and clinical characteristics have been reported for both subtypes, no specific therapy exists so far. However, the characterization of suitable molecular targets holds great promises to develop novel therapies in NSCLC. In the present study, global gene expression profiling of 58 human high grade NSCLC specimens revealed large transcriptomic differences between AC and SCC subtypes: More than 1.700 genes were found to be differentially expressed.
Global gene expression analysis reveals specific patterns of cell junctions in non-small cell lung cancer subtypes.
Disease, Disease stage
View SamplesDilated cardiomyopathy (DCM) is a common cause of heart failure and a leading cause of cardiac transplantation in western countries. The robust predictive expression profile of cardiomyopathic and NF hearts as well as the functional classification can help to identify promising candidates for DCM and may improve the early diagnosis of cardiomyopathy.
Identification of a common gene expression signature in dilated cardiomyopathy across independent microarray studies.
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Integrated cross-species transcriptional network analysis of metastatic susceptibility.
Specimen part
View SamplesMouse genetic crosses were established between the PyMT model of metastatic breast cancer and AKXD strain. Tumors were harvested from the animals for gene expression analysis to identify genes and network modules associated with progression to distant metastatic disease.
Integrated cross-species transcriptional network analysis of metastatic susceptibility.
Specimen part
View SamplesMouse genetic crosses were established between the PyMT model of metastatic breast cancer and NZB strain. Tumors were harvested from the animals for gene expression analysis to identify genes and network modules associated with progression to distant metastatic disease.
Integrated cross-species transcriptional network analysis of metastatic susceptibility.
Specimen part
View SamplesTranscriptomes of mesenchymal stromal cells from bone marrow (bmMSC) were compared to MSC from term placenta (pMSC).
Expression of Desmoglein 2, Desmocollin 3 and Plakophilin 2 in Placenta and Bone Marrow-Derived Mesenchymal Stromal Cells.
Specimen part
View SamplesUsing Drop-seq, we generated high-throughput single-cell expression data from wild-type and four mutant models with male infertility phenotype. Our study demonstrates the applicability of single-cell RNA-sequencing in study of male gonadal dysfunction and provides cell atlas resource for testis. Overall design: Drop-seq was performed on FACS sorted germ cell populations, wild-type whole testes and mutant whole testes. Different experimental batches for wild-type and mutant strains were generated.
Unified single-cell analysis of testis gene regulation and pathology in five mouse strains.
Sex, Specimen part, Subject
View SamplesThe estrogen-dependence of breast cancer has long been recognized, however, the role of 17-estradiol (E2) in cancer initiation was not known until we demonstrated that it induces complete neoplastic transformation of the human breast epithelial cells MCF-10F. E2-treatment of MCF-10F cells progressively induced high colony efficiency and loss of ductulogenesis in early transformed (trMCF) cells and invasiveness in Matrigel invasion chambers. The cells that
Epithelial to mesenchymal transition in human breast epithelial cells transformed by 17beta-estradiol.
No sample metadata fields
View SamplesPTEN loss or PI3K/AKT signaling pathway activation correlates with human prostate cancer progression and metastasis. However, in preclinical murine models, deletion of Pten alone fails to mimic the significant metastatic burden that frequently accompanies the end stage of human disease. To identify additional pathway alterations that cooperate with PTEN loss in prostate cancer progression, we surveyed human prostate cancer tissue microarrays and found that the RAS/MAPK pathway is significantly elevated both in primary and metastatic lesions. In an attempt to model this event, we crossed conditional activatable K-rasG12D/WT mice with the prostate conditional Pten deletion model we previously generated. Although RAS activation alone cannot initiate prostate cancer development, it significantly accelerated progression caused by PTEN loss, accompanied by epithelial-to-mesenchymal transition (EMT) and macrometastasis with 100% penitence. A novel stem/progenitor subpopulation with mesenchymal characteristics was isolated from the compound mutant prostates, which was highly metastatic upon orthotopic transplantation. Importantly, inhibition of RAS/MAPK signaling by PD325901, a MEK inhibitor, significantly reduced the metastatic progression initiated from transplanted stem/progenitor cells. Collectively, these data indicate that activation of RAS/MAPK signaling serves as a potentiating second hit to alteration of the PTEN/PI3K/AKT axis and co-targeting both pathways is highly effective in preventing the development of metastatic prostate cancers.
Pten loss and RAS/MAPK activation cooperate to promote EMT and metastasis initiated from prostate cancer stem/progenitor cells.
Specimen part
View SamplesTo amass candidate DIMM targets in addition to Phm (Park et al., 2008a), we used genome-wide microarray profiling by over-expressing DIMM throughout the embryonic nervous system. We compared profiles from experimental (elav>dimm) and control (elav-GAL4) embryos at 22-26 hr and 28-32 hr after egg laying (AEL). The design was intended to identify transcripts consistently up-regulated shortly after the induction of DIMM; in so doing, we could circumvent the lethality that ensues in late embryonic, and/ or by early larval stages, due to pan-neuronal DIMM expression.
Molecular organization of Drosophila neuroendocrine cells by Dimmed.
Specimen part
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