Whole exome sequencing of MPA/DMBA-induced mouse mammary tumors
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB29718 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2900260_1.fastq.gz | Fastqsanger.gz | |||
| ERR2900260_2.fastq.gz | Fastqsanger.gz | |||
| ERR2900270_1.fastq.gz | Fastqsanger.gz | |||
| ERR2900270_2.fastq.gz | Fastqsanger.gz | |||
| ERR2900280_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 64 |
Similar Datasets
Project description:Exploration of the transcriptome of DMBA/MPA induced mammary tumors including murine subtyping
2019-02-28 | E-MTAB-7507 | biostudies-arrayexpress
Project description:The purpose is to study DMBA-induced transcriptome in WT and in Cip2a-/- mouse mammary gland tissues. We identified differentially expressed genes in DMBA-induced mammary gland in WT vs. Cip2a-/- mouse mammary glands.
2021-04-28 | GSE173405 | GEO
Project description:Murine models of mammary cancers have proven to be highly informative on numerous fronts including individual gene causation, microenvironmental analyses, and chemoprevention studies. The MMTV-Neu transgenic model of mammary cancer has proven to be a useful model and has been employed in several prevention studies. However, there are certain practical drawbacks to its use including long tumor latencies and a tendency to develop mutations in the transmembrane domain of Neu (unlike human HER2/Neu overexpressing breast cancers). Here we report modifications that were made in an attempt to optimize this mouse model for chemopreventive screening. First, homozygous MMTV-Neu and homozygous P53 KO mice were crossed to create a MMTV-Neu/P53+/- strain (which more closely approximates the genetic make-up of most HER2+ human patients). Second, to overcome the drawback of long tumor latencies, the mice were treated with DMBA for eight weeks. DMBA treatment greatly decreased the latency of mammary carcinomas in the MMTV-Neu mice although the resulting tumors remained histopathologically similar to those from MMTV-Neu control mice. Next, we examined gene expression in tumors derived from MMTV-Neu, MMTV-Neu/p53+/-, and DMBA treated mice. It was found that the characteristic MMTV-Neu tumor-defined expression pattern was still the most prevalent feature of all the MMTV-Neu tumors despite their being crossed to the p53 null allele, treated with DMBA, or both. However, tumors from the DMBA treated animals exhibited many unique gene expression changes including the high expression of stress response, defense, and inflammation genes. Finally, we demonstrated that the RXR agonists UAB30 and Targretin, both inhibited mammary cancer formation in MMTV-Neu mice, including those treated with DMBA. These results demonstrate the potential utility of this murine model for additional chemoprevention studies.
2021-01-31 | GSE35188 | GEO
Project description:Microarrays were used to analyse global gene expression changes in tumors from wild-type mice treated with GW9662 RNA was isolated (RNeasy Mini Kit, Qiagen) from progestin/DMBA induced mammary tumors from wild-type mice treated with GW9662
2012-06-25 | E-GEOD-33762 | biostudies-arrayexpress
Project description:Introduction: Over the past several years, we have been interested in understanding the mechanisms by which hormone-dependent (HD) mammary carcinomas grow in the absence of the stimulatory hormone. We have hypothesized that the stromal compartment plays a pivotal role in the acquisition of the hormone-independent (HI) phenotype by providing stimulatory factors that replace the proliferative effects of the hormone. Methods: We used DNA microarrays to compare the gene expression profiles of tumors from the MPA mouse breast cancer model, one hormone-dependent (C4-HD) and one hormone-independent (C4-HI), using whole tumor samples or laser-captured purified stromal and epithelial cells obtained from the same tumors. The expression of selected genes was validated by immunohistochemistry and immunofluorescence assays. Results: We identified 413 genes that were expressed in tumor stroma but not in epithelial cells. Eighty-five percent of these genes were upregulated, whereas the remaining 15% were downregulated in C4-HI tumors relative to their expression in the C4-HD tumor stroma. Several matrix metallopeptidases, including Mmp13, Mmp3, Mmp10 and Mmp9, were overexpressed in the C4-HI tumor microenvironment. On the other hand, 1100 genes were specifically expressed in the tumor parenchyma. Among them, the 29% were upregulated, whereas the remaining 71% were downregulated, in C4-HI relative to C4-HD tumor epithelium. Steap, Pdgfc, Runx2, Cxcl9 and Sdf2 were among the genes with high expression in the C4-HI tumor parenchyma. Interestingly, we found that Fgf2 was one of the few genes upregulated by MPA in C4-HD tumors, confirming its pivotal role in regulating tumor growth in this model. Conclusions: We demonstrate a gene expression profile that distinguishes epithelial from stromal cells in mammary tumors with different hormone dependence. Our results support the hypothesis that the tumor-associated stroma may contribute to hormone-independent tumor growth. The fact that Fgf2 was one of these few stimulatory genes is worth investigating. reference X sample
2011-01-22 | E-GEOD-23214 | biostudies-arrayexpress
Project description:Introduction: Over the past several years, we have been interested in understanding the mechanisms by which hormone-dependent (HD) mammary carcinomas grow in the absence of the stimulatory hormone. We have hypothesized that the stromal compartment plays a pivotal role in the acquisition of the hormone-independent (HI) phenotype by providing stimulatory factors that replace the proliferative effects of the hormone. Methods: We used DNA microarrays to compare the gene expression profiles of tumors from the MPA mouse breast cancer model, one hormone-dependent (C4-HD) and one hormone-independent (C4-HI), using whole tumor samples or laser-captured purified stromal and epithelial cells obtained from the same tumors. The expression of selected genes was validated by immunohistochemistry and immunofluorescence assays. Results: We identified 413 genes that were expressed in tumor stroma but not in epithelial cells. Eighty-five percent of these genes were upregulated, whereas the remaining 15% were downregulated in C4-HI tumors relative to their expression in the C4-HD tumor stroma. Several matrix metallopeptidases, including Mmp13, Mmp3, Mmp10 and Mmp9, were overexpressed in the C4-HI tumor microenvironment. On the other hand, 1100 genes were specifically expressed in the tumor parenchyma. Among them, the 29% were upregulated, whereas the remaining 71% were downregulated, in C4-HI relative to C4-HD tumor epithelium. Steap, Pdgfc, Runx2, Cxcl9 and Sdf2 were among the genes with high expression in the C4-HI tumor parenchyma. Interestingly, we found that Fgf2 was one of the few genes upregulated by MPA in C4-HD tumors, confirming its pivotal role in regulating tumor growth in this model. Conclusions: We demonstrate a gene expression profile that distinguishes epithelial from stromal cells in mammary tumors with different hormone dependence. Our results support the hypothesis that the tumor-associated stroma may contribute to hormone-independent tumor growth. The fact that Fgf2 was one of these few stimulatory genes is worth investigating.
2011-01-22 | GSE23214 | GEO
Project description:Zinc deficiency during pregnancy and postnatal life can adversely affect the health and predispose to an increased risk of developing human diseases at adulthood. The present study was designed to evaluate whether dietary zinc deficiency or supplementation during the pregnancy, lactation and juvenile stages interferes with the development of mammary tumors induced by 7,12-dimethylbenzanthracene (DMBA) in female Sprague-Dawley (SD) rats. Pregnant females SD were allocated into three groups: dams received diets containing adequate (35 mg/Kg chow), deficient (3 mg/Kg chow) or supplemented (180 mg/Kg chow) zinc levels during gestational day 10 (GD 10) until the litters weaning. Female offspring were allocated into three groups and received the same diets as their dams until postnatal day (PND) 51. At PND 51, females SD (n=16 each group) received a single dose of DMBA (50 mg/kg, ig) for initiation of mammary carcinogenesis, adequate zinc diets and were euthanized at PND 180. Tumors samples were collected and processed for histological evaluation and microarray analysis. Dietary zinc deficiency induced a significant reduction in female offspring body weight evolution at parturition, weaning and pubertal phases. At late in life, the early in life dietary zinc deficiency or supplementation did not alter the latency, incidence, multiplicity and volume or histological types of mammary tumors in relation to the adequate zinc group, and changed the expression of a small amount of genes. The present findings indicate that early-in life dietary zinc deficiency or supplementation did not significantly modify the susceptibility to development of mammary tumors induced by DMBA.
2017-04-08 | GSE86270 | GEO
Project description:Whereas canines are susceptible to mammary cancer at a frequency similar to humans, equines are largely resistant to the disease. We treated mammary stem cells from both species with the chemical carcinogen, DMBA, and found that equine cells are significantly more susceptible to treatment. These RNA-seq results represent samples from three individuals of dogs and horses in order to reveal transcriptional differences in response to treatment that may explain the phenotypic differences we observed.
2018-08-31 | E-MTAB-7103 | biostudies-arrayexpress
Project description:Studies of naturally occurring cancers in dogs, which share many genetic and environmental factors with humans, provide valuable information as a comparative model for studying the mechanisms of human cancer pathogenesis. While individual and small-scale studies of canine cancers are underway, more generalized multi-omics studies have not been attempted due to the lack of large-scale and well-controlled genomic data. Here, we produced reliable whole-exome and whole-transcriptome sequencing data of 197 canine mammary cancers and their matched controls, annotated with rich clinical and biological features. Our dataset provides useful reference points for comparative analysis with human cancers and for developing novel diagnostic and therapeutic technologies for cancers in pet dogs.
| S-EPMC6694171 | biostudies-literature
Project description:To determine if RU-486 would be effective as a chemopreventive agent, microarrays were used to analyse global gene expression changes in wild-type vs. MMTV-PAX8PPARg mice to determine their differential response to RU486 RNA was isolated (RNeasy Mini Kit, Qiagen) from progestin/DMBA induced mammary tumors from wi transgenic and wild-type mice treated with placebo or 2.5mg RU486 60-day release pellets
2012-04-29 | E-GEOD-33753 | biostudies-arrayexpress