ZFP281 ChIP-sequencing of MMTV-Neu early lesion (EL) and primary tumor (PT) spheres
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA694622 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cancer cells can disseminate from early-evolved primary lesions. It is thought that a state of early disseminated cancer cell (early DCC) dormancy would precede genetic maturation of DCCs and metastasis initiation. Here we reveal at single cell resolution a previously unrecognized role of mesenchymal- and pluripotency-like programs in coordinating early cancer cell spread and a long-lived dormancy program in early DCCs. We identify in early lesions and early DCCs, the transcription factor ZFP281 as an inducer of mesenchymal- and primed pluripotency-like programs, which is absent in advanced primary tumors and overt metastasis. ZFP281 not only controls the early spread of cancer cells but also locks early DCCs in a prolonged dormancy state by preventing the acquisition of an epithelial-like proliferative program. Thus, ZFP281-driven dormancy of early DCCs may be a rate-limiting step in metastatic progression functioning as a first barrier that DCCs must overcome to then undergo genetic maturation. This data set aims identify ZFP281 targets in MMTV-Neu early lesion (EL) and primary tumor (PT) cells
2021-01-26 | GSE165444 | GEO
Project description:RNA sequencing of MMTV-Neu early lesion (EL) and primary tumor (PT) spheres
| PRJNA694615 | ENA
Project description:Cancer cells can disseminate from early-evolved primary lesions. It is thought that a state of early disseminated cancer cell (early DCC) dormancy would precede genetic maturation of DCCs and metastasis initiation. Here we reveal at single cell resolution a previously unrecognized role of mesenchymal- and pluripotency-like programs in coordinating early cancer cell spread and a long-lived dormancy program in early DCCs. We identify in early lesions and early DCCs, the transcription factor ZFP281 as an inducer of mesenchymal- and primed pluripotency-like programs, which is absent in advanced primary tumors and overt metastasis. ZFP281 not only controls the early spread of cancer cells but also locks early DCCs in a prolonged dormancy state by preventing the acquisition of an epithelial-like proliferative program. Thus, ZFP281-driven dormancy of early DCCs may be a rate-limiting step in metastatic progression functioning as a first barrier that DCCs must overcome to then undergo genetic maturation.
2021-01-26 | GSE165431 | GEO
Project description:To identify early events of erbB2-induced mammary tumorigenesis, we compared datasets from 14 genechip experiments including MMTV-neu tumors, preneoplastic neu mammary gland (adjacent neu), and age-matched, wild-type control mammary glands Keywords = transgenic mouse Keywords = MMTV-neu Keywords = erbB2 Keywords = HER2 Keywords = mammary tumor Keywords: ordered
2005-05-03 | GSE2528 | GEO
Project description:Cancer cells can disseminate from early-evolved primary lesions. It is thought that a state of early disseminated cancer cell (early DCC) dormancy would precede genetic maturation of DCCs and metastasis initiation. Here we reveal at single cell resolution a previously unrecognized role of mesenchymal- and pluripotency-like programs in coordinating early cancer cell spread and a long-lived dormancy program in early DCCs. We identify in early lesions and early DCCs, the transcription factor ZFP281 as an inducer of mesenchymal- and primed pluripotency-like programs, which is absent in advanced primary tumors and overt metastasis. ZFP281 not only controls the early spread of cancer cells but also locks early DCCs in a prolonged dormancy state by preventing the acquisition of an epithelial-like proliferative program. Thus, ZFP281-driven dormancy of early DCCs may be a rate-limiting step in metastatic progression functioning as a first barrier that DCCs must overcome to then undergo genetic maturation. This data set aims to characterize MMTV-Neu early and late lung disseminated cancer cells (DCCs).
2021-01-26 | GSE165459 | GEO
Project description:Cancer cells can disseminate from early-evolved primary lesions. It is thought that a state of early disseminated cancer cell (early DCC) dormancy would precede genetic maturation of DCCs and metastasis initiation. Here we reveal at single cell resolution a previously unrecognized role of mesenchymal- and pluripotency-like programs in coordinating early cancer cell spread and a long-lived dormancy program in early DCCs. We identify in early lesions and early DCCs, the transcription factor ZFP281 as an inducer of mesenchymal- and primed pluripotency-like programs, which is absent in advanced primary tumors and overt metastasis. ZFP281 not only controls the early spread of cancer cells but also locks early DCCs in a prolonged dormancy state by preventing the acquisition of an epithelial-like proliferative program. Thus, ZFP281-driven dormancy of early DCCs may be a rate-limiting step in metastatic progression functioning as a first barrier that DCCs must overcome to then undergo genetic maturation. This data set aims for a general characterization of the MMTV-Neu mouse model (primary site and lung DCCs) in early and late stages of cancer progression.
2021-01-26 | GSE165456 | GEO
Project description:CDC25A is a critical target of checkpoint, and its overexpression is observed in various cancers. Here we demonstrate that in vivo levels of Cdc25A expression determine the efficiency of transformation and tumorigenesis. Transgenic expression of CDC25A in murine mammary glands cooperates with tumorigenesis induced by expression of ras or neu. CDC25A- overexpressing tumors display aggressiveness and genomic instability with changes in fragile chromosomal regions, including the region orthologous to human 1p32-36. Experiment Overall Design: Tumors from two mice from each of two conditions (MMTV-cdc25a;MMTV-neu and MMTV-neu) were analyzed in a dye swap experiment. A total of four hybridizations were performed.
2008-06-12 | E-GEOD-4114 | biostudies-arrayexpress
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:We use RNA-seq to measure gene expression from mammary tumors from untreated MMTV-Neu mice.
2020-04-11 | GSE148452 | GEO
Project description:CDC25A is a critical target of checkpoint, and its overexpression is observed in various cancers. Here we demonstrate that in vivo levels of Cdc25A expression determine the efficiency of transformation and tumorigenesis. Transgenic expression of CDC25A in murine mammary glands cooperates with tumorigenesis induced by expression of ras or neu. CDC25A- overexpressing tumors display aggressiveness and genomic instability with changes in fragile chromosomal regions, including the region orthologous to human 1p32-36. Keywords: genetic modification, aCGH
2006-11-13 | GSE4767 | GEO