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Gene expression profile of bone marrow from MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

ABSTRACT: We investigated, in a spontaneous mouse model of breast carcinogenesis (MMTV/NeuT), the modifications in the hematopoietic and stromal bone marrow (BM) compartments and their correlation with the pathological stage of the primary mammary lesions, following the idea that signs of the cross-talk between the BM and elements located in the tumor microenvironment, either neoplastic or stroma/immune cells, can be identified in the very early phases of cancer development, and lead to the instruction of a tumor-promoting hematopoiesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE116962 | GEO | 2019/12/03

REPOSITORIES: GEO

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Circulating miRNA profile of MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

Project description:We investigated, in a spontaneous mouse model of breast carcinogenesis (MMTV/NeuT), the modifications in the level of circulating miRNAs during different stages of disease, from early dysplastic stage to overt carcinoma, and their correlation with the pathological stage of the primary mammary lesions.

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Circulating miRNA profile of MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

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Gene expression profile of bone marrow from MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

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Gene expression profile of bone marrow and circulating miRNA profile from MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

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Role of endogenous type I Interferon in spontaneous, Her2/Neu oncogene-driven carcinogenesis

Project description:Type I Interferons (IFN-I) are anti-viral and immuno-modulating cytokines involved in many steps across tumor initiation and progression. IFN-I act directly on tumor cells inhibiting cell growth and indirectly by activating immune cells to mount antitumor response. To understand the role of endogenous IFN-I in spontaneous, oncogene-driven carcinogenesis, we characterized tumors arising in Her2/neu transgenic (neuT) mice carrying a non-functional mutation in the IFN-I receptor (IFNAR1), thus being unresponsive to this family of cytokines. Compared to parental neu+/-mice (neuT mice), IFNAR1-/- neu+/- mice (IFNAR-neuT mice) showed earlier onset and increased tumor multiplicity with marked vascularization. Of note, IFNAR-neuT tumors specifically exhibited deregulation of genes having adverse prognostic value in breast cancer patients, including breast cancer stem cells (BCSC) marker aldehyde dehydrogenase-1A1 (ALDH1A1). An increased amount of BCSC was observed in IFNAR-neuT tumors, as assessed by ALDH1A1 enzymatic activity, clonogenic assay and tumorigenic capacity. In vitro exposure of neuT+ mammospheres and cell lines to anti-IFN-I antibodies resulted in increased frequency of ALDH+ cells, suggesting that IFN-I control stemness in tumor cells. Altogether, these results reveal an essential role of IFN-I in NeuT-driven spontaneous carcinogenesis through intrinsic control of BCSC.

2018-05-22 | GSE110350 | GEO

Expression data from mesenchymal stem cells isolated from the bone marrow of tumor-bearing NeuT mice and relative BALB/c controls

Project description:We performed gene expression profiling of bone marrow-mesenchymal cells (BM-MSCs) isolated from BALB/c and NeuT mice at 12 and 24 weeks of age, representative of early and late stages of breast cancer tumorigenesis, respectively.

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DIMETHYLBENZANTHRACENE (DMBA) INDUCED MAMMARY CARCINOGENESIS IN MMTV-Neu and MMTV/p53 KO FEMALE MICE AND EFFECTS OF REXINOIDS

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.

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Widespread Non-Canonical Epigenetic Modifications in MMTV-NeuT Breast Cancer.

Project description:Breast tumors in (FVB × BALB-NeuT) F1 mice have characteristic loss of chromosome 4 and sporadic loss or gain of other chromosomes. We employed the Illumina GoldenGate genotyping platform to quantitate loss of heterozygosity (LOH) across the genome of primary tumors, revealing strong biases favoring chromosome 4 alleles from the FVB parent. While allelic bias was not observed on other chromosomes, many tumors showed concerted LOH (C-LOH) of all alleles of one or the other parent on sporadic chromosomes, a pattern consistent with cytogenetic observations. Surprisingly, comparison of LOH in tumor samples relative to normal unaffected tissues from these animals revealed significant variegated (stochastic) deviations from heterozygosity (V-LOH) in every tumor genome. Sequence analysis showed expected changes in the allelic frequency of single nucleotide polymorphisms (SNPs) in cases of C-LOH. However, no evidence of LOH due to mutations, small deletions, or gene conversion at the affected SNPs or surrounding DNA was found at loci with V-LOH. Postulating an epigenetic mechanism contributing to V-LOH, we tested whether methylation of template DNA impacts allele detection efficiency using synthetic oligonucleotide templates in an assay mimicking the GoldenGate genotyping format. Methylated templates were systematically over-scored, suggesting that the observed patterns of V-LOH may represent extensive epigenetic DNA modifications across the tumor genomes. As most of the SNPs queried do not contain standard (CpG) methylation targets, we propose that widespread, non-canonical DNA modifications occur during Her2/neuT-driven tumorigenesis.

| S-EPMC4415121 | biostudies-literature

Gene expression profile of bone marrow and circulating miRNA profile from MMTV-NeuT mouse model of spontaneous mammary carcinogenesis.

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-12-03 | GSE117071 | GEO

A hypoxic signature marks tumors formed by disseminated tumor cells in the Balb-neuT breast cancer model

Project description:Metastasis is considered to be the final and fatal stage of cancer progression. However, some evidence seems to indicate that tumor cell dissemination could occur early in the natural history of cancer progression. Early disseminated tumor cells (DTC) have been described in the bone marrow (BM) of patients suffering from diverse types of solid tumors as well as in experimental models. The presence of early DTC - which share many features of dormant tumor cells - was found to correlate with later development of metastasis in several cancer types. However, little is known about the tumorigenic features of DTC obtained at different time points along tumor progression. Here, we investigated the actual tumorigenic capacities of DTC. We found that early DTC obtained from BM of 15-17 week-old Her2-neu transgenic (BALB-neuT) mice were not tumorigenic in immunodeficient mice. In contrast, DTC-derived tumors were easily obtained (44 % frequency) when DTC from 19-22 week-old BALB-neuT mice (late DTC) were injected. Angiogenesis, which can contribute to regulate tumor dormancy in other systems, appeared dispensable to reactivate late DTC, although it accelerated growth of secondary DTC tumors. Gene expression profiling disclosed a distinctive transcriptional signature of late DTC tumors compared with that of mammary tumors, which was enriched for hypoxia-related transcripts and appeared to be maintained in cell culture ex-vivo. Immunohistochemical analysis confirmed high HIF-1α expression in DTC tumors, which was maintained in tumor-derived in vitro cultures. Altogether, these findings highlight a different tumorigenic potential of early and late DTC in the BALB-neuT model and describe a HIF-1α-related transcriptional signature in DTC tumors, which may render DTC angiogenesis-competent, when placed in a favourable environment.

2016-12-01 | GSE71251 | GEO

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