Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA96521 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The objective of this study was to determine the effect of Thyroid Hormone Responsive Protein Spot14 (Spot14) loss on the gene expression profiles of tumors from MMTV-Polyomavirus middle-T antigen (PyMT) mice. MMTV-PyMT/S14-heterozygous mice were crossed with S14-heterozygous mice and 1 cm tumors from MMTV-PyMT control (wild-type S14) or MMTV-PyMT/S14-null offspring were profiled using Affymetrix gene arrays. Tumor latency was not different between groups; however, tumors lacking S14 grew significantly slower than control tumors. Loss of S14 also decreased the levels of de novo synthesized fatty acids in mammary tumors. In additional studies, performed on MMTV-Neu mice, we found that S14 overexpression was associated with increased tumor cell proliferation and elevated levels of tumor fatty acids. Gene expression profiling revealed that S14 loss and overexpression in mouse mammary tumors altered pathways associated with proliferation and metabolism. This study provides important information about the role of S14 in mammary tumorigenesis and tumor metabolism. Microarray analysis was performed on 4 mammary tumors from MMTV-PyMT mice and 4 tumors from MMTV-PyMT/S14-null mice.
2014-09-01 | E-GEOD-55886 | biostudies-arrayexpress
Project description:Transcriptional profiling of miRNA levels in mammary tumors from 18 [PyMT x AKXD]F1 sublines. The PyMT strain was FVB/N-TgN(MMTV-PyVT)634Mul.
2013-01-15 | GSE43486 | GEO
Project description:The objective of this study was to determine the effect of Thyroid Hormone Responsive Protein Spot14 (Spot14) loss on the gene expression profiles of tumors from MMTV-Polyomavirus middle-T antigen (PyMT) mice. MMTV-PyMT/S14-heterozygous mice were crossed with S14-heterozygous mice and 1 cm tumors from MMTV-PyMT control (wild-type S14) or MMTV-PyMT/S14-null offspring were profiled using Affymetrix gene arrays. Tumor latency was not different between groups; however, tumors lacking S14 grew significantly slower than control tumors. Loss of S14 also decreased the levels of de novo synthesized fatty acids in mammary tumors. In additional studies, performed on MMTV-Neu mice, we found that S14 overexpression was associated with increased tumor cell proliferation and elevated levels of tumor fatty acids. Gene expression profiling revealed that S14 loss and overexpression in mouse mammary tumors altered pathways associated with proliferation and metabolism. This study provides important information about the role of S14 in mammary tumorigenesis and tumor metabolism.
2014-09-01 | GSE55886 | GEO
Project description:The primary cause of mortality in breast cancer is metastasis, a process which is still poorly understood. To study the process of breast cancer metastasis, we isolated focal hyperplasias from the MMTV-PyMT transgenic breast cancer model and transplanted to syngeneic hosts. The transplants underwent stereotyped progression to adenoma, early carcinoma, and late carcinoma at 5, 8 and 18 weeks post-transplant, respectively. We compared the gene expression profiles of adenomas and late carcinomas by microarray. Analysis of the data revealed that the most differentially expressed gene family between adenomas and late carcinomas were luminal differentiation genes, among them GATA-3. Adenomas were uniformly immunopositive for GATA-3, whereas early carcinomas displayed partial loss of GATA-3. Disseminated tumour cells and 18-week late carcinomas were invariably GATA-3 negative. We found that re-introduction of GATA-3 in late carcinomas induced markers of luminal differentiation and inhibited tumour dissemination to distant sites. Keywords: spotted oligonucleotide Full length GATA-3 was cloned into the PMIG retroviral vector, which contains an IRES-GFP cassette. Primary cultures of non-fluorescent MMTV-PyMT carcinomas were infected with the GATA-3 and control retroviruses and transplanted back into the cleared mammary fat pads of wild-type mice. After six weeks of growths, tumors were isolated and total RNA harvested by the Trizol method. Total RNA from GATA-3 infected tumor outgrowths were compared to empty vector infected tumor outgrowths.
2010-07-01 | E-GEOD-5223 | biostudies-arrayexpress
Project description:Effect of Spot14 Loss on Gene Expression Profile of MMTV-PyMT Mouse Tumors
| PRJNA241245 | ENA
Project description:Loss of E2F transcription factos alters metastatic capacity of MMTV-PyMT tumors. We used microarrays to futher characterize the effects of E2F loss on mammary tumorigenesis in MMTV-PyMT mice.
2018-02-22 | GSE104397 | GEO
Project description:Conventional transgenic and knockout models do not allow selective introduction of oncogenic alterations into the progenitor population of mammary cells; thus, the role of progenitor cells in mammary tumorigenesis is yet unknown. By generating transgenic mice expressing tva – encoding the receptor for avian leukosis virus subgroup A (ALV/A) – from the Keratin 6a (K6) gene promoter, we found that K6+ mammary cells are bipotential progenitor cells, but not stem cells. These K6+ cells were readily induced to form tumors by intraductal injection of RCAS (an ALV/A-derived vector) carrying the gene encoding polyoma middle T antigen. Compared with tumors induced by the same oncogene-expressing virus in transgenic mice expressing tva from the commonly used MMTV LTR or other murine models of breast cancer, tumors in this K6-tva line were unique in that they resemble the normal breast-like subtype of human breast cancer. Consequently, these observations suggest that the cell of origin affects mammary tumor phenotypes. This K6-tva model may be useful for preclinical testing of targeted therapy for normal-like breast cancers in patients. Keywords: Three group comparison We carried out Affymetrix array analysis of five RCAS-PyMT-induced tumors each from K6-tva mice and MMTV-tva mice, as well as five mammary tumors from MMTV-PyMT transgenic mice.
2011-05-09 | E-GEOD-20614 | biostudies-arrayexpress
Project description:Expression data of breast tumors in MMTV-PyMT+ female mice treated with DPM or vehicle
| PRJNA187511 | ENA
Project description:S100A10 (p11) is a plasminogen receptor that regulatess cellular plasmin generation by cancer cells. In the current study we used the MMTV-PyMT mouse breast cancer model to investigate the role of p11 in oncogenesis. Genetic deletion of p11 resulted in significantly decreased tumor onset, growth rate and spontaneous pulmonary metastatic burden in the PyMT/p11-KO mice. This phenotype was accompanied by substantial reduction in Ki67 positivity, macrophage infiltration and decreased vascular density in the primary tumors, and appearance of invasive carcinoma and pulmonary metastasis. Surprisingly, immunohistochemical analysis of wild-type MMTV-PyMT mice failed to detect p11 expression in the tumors or metastatic tumor cells and loss of p11 did not decrease plasmin generation in the PyMT tumors and cells. Furthermore, tumor cells expressing p11 displayed dramatically reduced lung metastasis when injected into p11-depleted mice, further strengthening the stromal role of p11. Transcriptome analysis of the p11-depleted tumors showed marked reduction in genes involved in breast cancer development, progression, and inflammation such as AREG, MUC1 and S100A8. The PyMT/p11-KO tumors displayed remarkable increase in inflammatory cytokines such as IL-6, IL-10 and IFN-γ. Gene expression profiling and immunohistochemistry primary breast cancer samples showed that p11 mRNA and protein was significantly higher in tumors compared to normal mammary tissue. The mRNA expression was significantly associated with poor patient prognosis and significantly elevated in high grade, triple negative tumors and tumors with high proliferative index. We used microarray to detail the global programme of gene expression underlying reduced growth/establishment of P11-KO PyMT tumours.
2023-06-01 | GSE151579 | GEO