Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bulk RNA-seq profiling of p53-deficient mammary tumors driven by Runx1 and/or Rb1 loss

ABSTRACT: This data set includes gene expression profiles of Runx1/p53-null, Rb1/p53-null, and p53/Runx1/Rb1-null mammary tumors developed in their respective female mouse models carrying the corresponding conditional knockout alleles (for Runx1, Rb1, and p53). The tumors were induced from luminal mammary epithelial cells after intraductal injection of adenovirus expressing Cre from the Keratin 8 promoter.

ORGANISM(S): Mus musculus

PROVIDER: GSE316271 | GEO | 2026/04/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Microarray expression profiling data for premalignant mammary epithelial cells with a K8+ luminal origin

Project description:This dataset contains gene expression profiles of premalignant mammary epithelial cells (MEC) with loss of either p53 alone, or loss of both p53 and RUNX1, or loss of both p53 and BRCA1. The premalignant MECs were generated in female mice carrying their corresponding conditional knockout alleles as well as a conditional YFP-reporter, upon intraductal injection of Cre-expressing adenovirus under the control of the Keratin 8 (K8) promoter (Ad-K8-Cre) to their mammary glands.

2026-04-06 | GSE316272 | GEO

Single cell RNA-Seq data for Trp53/Brca1-null premalignant mammary epithelial cells and tumor cells with a K8+ luminal origin

Project description:BRCA1 mutation-carriers are predisposed to develop Basal-like breast cancer (BLBC), and p53 mutations are present in the majority of human BLBC cases, suggesting loss of these two tumor suppressors play key roles in development of BLBC. Recent studies suggest that the majority of human breast cancers, including BLBC, may originate from mammary epithelial cells (MECs) in the luminal lineage. However, how loss of p53 and BRCA1 contributes to development of BLBC from luminal MECs remains largely elusive. We developed a novel genetic targeting and lineage tracing approach based on intraductal injection of Cre-expressing adenovirus under the control of the pan-luminal Keratin 8 (K8) promoter (Ad-K8-Cre). We performed intraductal injection of Ad-K8-Cre to female mice carrying conditional knockout alleles of Brca1 (Brca1L) and Trp53 (Trp53L). The injected females developed mammary tumors similar to human BLBC within 12 months after injection. Here we characterized MECs targeted by Ad-K8-Cre at different time points after the intraductal injection, as well as mammary tumors developed in this model, by single cell expression analysis.

2019-06-27 | GSE130453 | GEO

RNA-Seq data for Trp53/Brca1-null premalignant mammary epithelial cells with a K8+ luminal origin

2019-06-27 | GSE126761 | GEO

Microarray expression profiling data for Trp53/Brca1-null mammary tumors derived from K8+ luminal cells

Project description:BRCA1 mutation-carriers are predisposed to develop Basal-like breast cancer (BLBC), and p53 mutations are present in the majority of human BLBC cases, suggesting loss of these two tumor suppressors play key roles in development of BLBC. Recent studies suggest that the majority of human breast cancers, including BLBC, may originate from mammary epithelial cells (MECs) in the luminal lineage. However, how loss of p53 and BRCA1 contributes to development of BLBC from luminal MECs remains largely elusive. We developed a novel genetic targeting and lineage tracing approach based on intraductal injection of Cre-expressing adenovirus under the control of the pan-luminal Keratin 8 (K8) promoter (Ad-K8-Cre). We performed intraductal injection of Ad-K8-Cre to female mice carrying conditional knockout alleles of Brca1 and Trp53. The injected females developed mammary tumors within 12 months after injection. Microarray expression profiling of these tumors showed that they most closely resembled human BLBC.

2019-06-27 | GSE114787 | GEO

Bulk RNA-seq profiling of p53-deficient mammary tumors driven by Runx1 and/or Rb1 loss

Project description:Bulk RNA-seq profiling of p53-deficient mammary tumors driven by Runx1 and/or Rb1 loss

| PRJNA1402139 | ENA

RNAseq expression of p53-null and p53-null/PLK2-null mammary tumors

Project description:RNAseq expression of p53-null and p53-null/PLK2-null mammary tumors

| PRJNA731110 | ENA

Murine Prostate Tissue: Rb1 null vs. Rb1 E2F binding deficient mutant

Project description:Transcriptional profilling of 60 day old prostate tissue from Rb1F/F:Trp53F/F:PB-Cre4 or Rb1R654W/F:Trp53F/F:PB-cre4 mice versus wild type prostate tissue. Profiles used to compare deregulation of known E2F target genes in prostate tissue expressing a mutant Rb1 gene to tissue lacking Rb1 expression. Tissue from two Rb1F/F:Trp53F/F:PB-Cre4 (null) mice or two Rb1654/F:Trp53F/F:PB-cre4 (mutant) mice compared to a pool of tissue from 3 wild type mice using two color arrays.

2010-11-27 | E-GEOD-25615 | biostudies-arrayexpress

RB1 deletion in RB-pathway disrupted cells results in DNA damage and cancer progression

Project description:Proliferative control in cancer cells is frequently disrupted by mutations in the RB-pathway. Paradoxically, RB1 mutations can arise late in tumorigenesis in cancer cells whose RB-pathway is already compromised by another mutation. In this study, we present evidence for increased DNA damage in CDKN2A deleted cancer cells when RB1 mutations are induced. We created isogenic RB1 wild type, heterozygous, and null genotypes. Cells with even one mutant copy of RB1 have increased basal levels of DNA damage and increased mitotic errors. Elevated levels of reactive oxygen species as well as impaired homologous recombination repair underlie this DNA damage. When xenografted into immune compromised mice RB1 mutant cells exhibit an elevated propensity to seed new tumors in recipient lungs. This study offers evidence that late arising RB1 mutations can facilitate genome instability and cancer progression that are beyond the pre-existing proliferative control deficit.

2019-06-18 | GSE125379 | GEO

Gene expression profiling of mouse tumors arising from Keratin 6-positive mammary cells

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

Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells tumors

Project description:We used novel genetically engineered mouse models to investigate the role of HELLS during tumorigenesis. Loss of HELLS drastically decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Tumors from Rb1/p107 DKO and Rb1/p107/Hells TKO mice were analyzed for gene expression using RNA-seq.

2020-03-09 | GSE143732 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data