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
Project description:MMTV-PyVT Mammary tumors were harvested from PyVT-wild-type (WT), PyVT-Nr4a1 knockout (KO) littermates on a congenic FVB/NJ background,minced and incubated with collagenase type I digestion solution .The digested Mammary tumor cells were collected and maintained in DMEM medium containing 10% FBS for 24 hour.
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.
Project description:Comparison the gene expression profiles of mouse mammary tumors derived from MMTV-PyMT transgenic in five different strains including FVB/NJ, I/LnJ F1, NZB/B1NJ F1, MOLF/Ei F1 and LP/J F1 and identification of signatures of tumor virulence. **NOTE: Migrated from caArray 1.x, identifier='gov.nih.nci.ncicb.caarray:Experiment:1015897560599049:1' green-00155 Assay Type: Gene Expression Provider: Affymetrix Array Designs: mg_u74av2 Organism: Mus musculus (ncbitax) Material Types: organism_part, synthetic_RNA, whole_organism, total_RNA Disease States: Mouse mammary tumor
Project description:MicroRNAs (miRNAs) are small noncoding RNAs that typically inhibit the translation and stability of messenger RNAs (mRNAs), controlling genes involved in a variety of cellular processes. miRNA dysregulation is recognized to play an essential role in the development and progression of cancer. MMTV-PyMT mice (Jax Strain: FVB/N-Tg(MMTV-PyVT)634Mul/J) are a well-characterized transgenic mouse model of breast cancer. Upon activation of the MMTV-PyVT transgene (mouse mammary tumor virus (MMTV) long terminal repeat upstream of a cDNA sequence encoding the Polyoma Virus middle T antigen (PyVT)) female carriers develop palpable mammary tumors as early as 5 weeks of age. We performed miRNA microarrays on samples from the MMTV-PyMT transgenic mouse model to investigate the differential expression of miRNAs during development of malignant disease in this model.
Project description:Comparison the gene expression profiles of mouse mammary tumors derived from MMTV-PyMT transgenic in five different strains including FVB/NJ, I/LnJ F1, NZB/B1NJ F1, MOLF/Ei F1 and LP/J F1 and identification of signatures of tumor virulence. **NOTE: Migrated from caArray 1.x, identifier='gov.nih.nci.ncicb.caarray:Experiment:1015897560599049:1'
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.
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.
