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Gene expression in MMTV-PyMT whole tumor, CD3+ lymphocytes or CD11b+ myeloid cells with and without Class IIa HDAC inhibitor treatment

ABSTRACT: Gene expression in MMTV-PyMT whole tumor, CD3+ lymphocytes or CD11b+ myeloid cells with and without Class IIa HDAC inhibitor treatment

PROVIDER: PRJNA343770 | ENA |

REPOSITORIES: ENA

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MMTV-PyMT whole tumor gene expression with and without Class IIa HDAC inhibitor treatment

Project description:The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in the CD3+ or CD11b+ cells residing in MMTV-PyMT tumors.

2017-03-08 | GSE87163 | GEO

Differential gene expression in either CD3+ lymphocytes or CD11b+ myeloid cells due to Class IIa HDAC inhibitor treatment

Project description:The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in the CD3+ or CD11b+ cells residing in MMTV-PyMT tumors.

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Expression data from MMTV-PyMT Induced Tumors

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.

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Effect of Spot14 Loss on Gene Expression Profile of MMTV-PyMT Mouse Tumors

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.

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Expression data of MMTV-PyMT mice mammary tumor with or without JAM-A

Project description:Junction Adhesion Molecule-A (JAM-A) is present on leukocytes and platelets where it promotes cell adhesion and motility. We are interested in an interaction between JAM-A and tumor progression/metastases. To address this point, we mated JAM-A-/- mice and mouse mammary tumor model MMTV-PyMT mice which, which express polyoma middle T antigen under the control of mouse mammary tumor virus. MMTV-PyMT mice show 100% penetration of mammary tumor and highly metastases to lung. MMTV-PyMT mice without JAM-A show less primary tumor progression, therefore JAM-A enhance primary tumor progression. Then we are addressing the molecular mechanism of this phenomenon by in vivo. Furthermore, we would like to examine JAM-A deficient MMTV tumor signature. Each 3 MMTV-PyMT JAm-A+/+ (JamA+) and 3 MMTV JAM-A-/- (JamA-) mammary tumor were resected at early stages of tumor development for RNA extraction and hybridization on Affymetrix microarrays.

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Single-cell RNA profiling of mammary gland tumours in MMTV-PyMT mouse model of breast cancer.

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Effect of Spot14 Loss on Gene Expression Profile of MMTV-PyMT Mouse Tumors

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Expression data of MMTV-PyMT mice mammary tumor with or without JAM-A

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