This SuperSeries is composed of the SubSeries listed below.
A macrophage gene expression signature defines a field effect in the lung tumor microenvironment.
No sample metadata fields
View SamplesAJ mouse is susceptible to lung carcinogenesis from urethane treatment and is a good model for human adenocarcinoma. We completed a study using microarray analysis of bronchoalveolar lavage cells from control or urethane treated mice. A unique macrophage expression signature in the lung tumor microenvironment was able to correctly classify the lavage samples.
A macrophage gene expression signature defines a field effect in the lung tumor microenvironment.
No sample metadata fields
View SamplesWe sought to detect predictive markers related to a Src kinase inhibitor (saracatinib) sensitivity in ovarian cancer. Cell proliferation assays assigned 18 ovarian cancer cell lines to sensitive or resistant to this drug.
PTTG1 Levels Are Predictive of Saracatinib Sensitivity in Ovarian Cancer Cell Lines.
Specimen part
View SamplesLung tumors
Analysis of orthologous gene expression between human pulmonary adenocarcinoma and a carcinogen-induced murine model.
No sample metadata fields
View SamplesIn a prospective case-control study, we identified novel transcriptional classifiers for TB among US patients and systematically compared their accuracy to other classifiers in published studies.
Blood Transcriptional Biomarkers for Active Tuberculosis among Patients in the United States: a Case-Control Study with Systematic Cross-Classifier Evaluation.
Sex, Age, Specimen part, Race
View SamplesRhomboid family protein RHBDF2, an upstream regulator of the epidermal growth factor (EGF) receptor signaling, has been implicated in cutaneous wound healing. However, the underlying molecular mechanisms are still emerging. Using a gain-of-function mutation in the mouse Rhbdf2 gene (Rhbdf2cub/cub), which shows a regenerative phenotype, we sought to identify the underlying mechanism.
Early induction of NRF2 antioxidant pathway by RHBDF2 mediates rapid cutaneous wound healing.
Specimen part, Treatment, Time
View SamplesA QTL intercross was performed bewteen C57BL/6J and KK/HIL for albuminurea, asthma and cardiovascular related phenotypes. Several QTL were identified for most phenotypes. We performed microarray analysis from liver samples to identify genes differentially expressed between the parental strains. The results helped us narrow down the QTL and identify the candidate genes based on differential expression between the parental strains.
A major X-linked locus affects kidney function in mice.
Sex, Specimen part
View SamplesPapillomaviruses (PVs) are able to induce papillomas, premalignant lesions, and carcinomas in a wide variety of species. PVs are classified first based on their host and tissue tropism and then their genomic diversities. A laboratory mouse papillomavirus, MmuPV1 (formerly MusPV), naturally infects NMRI-Foxn1nu/Foxn1nu (nude; T cell deficient) mice. C57BL/6J wild-type mice were not susceptible to MmuPV1 infection; however, immunocompetent, alopecic, S/RV/Cri-ba/ba (bare) mice developed small papillomas at injection sites that regressed. NMRI-Foxn1nu and B6.Cg-Foxn1nu but not NU/J-Foxn1nu mice were susceptible to MmuPV1 infection. B6 congenic strains, but not other congenic strains carrying the same allelic mutations, that lack B- and T-cells, but not B-cells alone, were susceptible to infection, indicating that mouse strain and T-cell deficiency are critical to tumor formation. Although lesions initially observed were exophytic papillomas around the muzzle, exophytic papillomas on the tail and condylomas of the vaginal lining could be induced by experimental infections. On the dorsal skin, locally invasive, poorly differentiated tumors developed with features similar to human trichoblastomas. Transcriptome analysis revealed significant differences between the normal skin in these anatomic sites and in papillomas versus trichoblastomas. The primarily dysregulated genes involved molecular pathways associated with cancer, cellular development, cellular growth and proliferation, cell morphology, and connective tissue development and function. Surprisingly, few of the genes commonly associated with basal cell carcinoma or squamous cells carcinoma were dramatically dysregulated.
Immune status, strain background, and anatomic site of inoculation affect mouse papillomavirus (MmuPV1) induction of exophytic papillomas or endophytic trichoblastomas.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Deregulated sex chromosome gene expression with male germ cell-specific loss of Dicer1.
Sex, Specimen part
View SamplesMicroRNAs (miRNAs) are a class of endogenous, non-coding RNAs that mediate post-transcriptional gene silencing by inhibiting mRNA translation and promoting mRNA decay. DICER1, an RNAse III endonuclease encoded by Dicer1, is required for processing short 21-22 nucleotide miRNAs from longer double-stranded RNA precursors. Here, we investigate the loss of Dicer1 in mouse postnatal male germ cells to determine how disruptions in the miRNA biogenesis pathway may contribute to infertility. Reduced levels of Dicer1 transcripts and DICER1 were confirmed in germ cell knock-out (GCKO) testes by postnatal day 18 (P18). Compared to wild-type (WT) at 8 weeks, GCKO males had no change in body weight, yet showed significant reductions in testis mass and sperm number. Histology and fertility tests confirmed spermatogenic failure in GCKO males. Array analyses at P18 showed 96% of miRNA genes were down-regulated and 37% of protein-coding genes were differentially expressed in GCKO testes. Interestingly, we observed preferential overexpression of genes on the sex chromosomes in GCKO testes, with more than 80% of the genes overlapping those proposed to undergo meiotic sex chromosome inactivation (MSCI) in the germ cells. Compared to WT, GCKO mice showed higher percentages of cells at early meiotic stages (leptotene and zygotene) but lower percentages at later stages (pachytene, diplotene and metaphase I), providing evidence that deletion of Dicer1 leads to disruptions in meiotic progression. Furthermore, we observed fewer elongating spermatids with proper translational activation of transition protein 2 (Tnp2), protamine 1 and 2 (Prm1 and Prm2) in GCKO testes after step 12-14. Therefore, deleting Dicer1 in early postnatal germ cells causes misregulation of transcripts encoded by genes on the sex chromosomes, impairs meiotic progression and post-meiotic translational control and results in spermatogenic failure and infertility.
Deregulated sex chromosome gene expression with male germ cell-specific loss of Dicer1.
Sex, Specimen part
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