Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Unique Transcriptional Profiles Underlie Osteosarcomagenesis Driven by Different p53 Mutants (RNA-Seq)

ABSTRACT: To identify mutant p53 GOF, murine primary osteosarcomas expressing p53R172H or p53R245W over null and p53-null osteosarcomas were processed for bulk sequencing; DEGs were identified in p53R172H and p53R245W expressing tumors by comparing to p53-null tumors; DEGs were used to identify dysregulated pathways and mutant p53 GOF

ORGANISM(S): Mus musculus

PROVIDER: GSE231849 | GEO | 2023/05/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Unique Transcriptional Profiles Underlie Osteosarcomagenesis Driven by Different p53 Mutants (ChIP-Seq)

Project description:To identify mutant p53 GOF and analyze mutant p53 ChIP peaks ChIP-seq was performed on hESC-derived human osteoblasts expressing homozygous WT p53 or heterozygous expression of p53R248W. Processing for ChIP was performed on day 24 after confirmation of osteoblast differentiation

2023-05-12 | GSE231850 | GEO

Differential gain-of-function activity of three p53 hotspot mutants in vivo

Project description:To identify mutant p53 gain-of-function, primary murine osteosarcomas expressing p53 heterozygous mutants were compared to p53 heterozygous tumors. Transcriptomes regulated by different p53 hotspots were used to identify their mechanisms of action. Validation was done in cell line expressing mutant p53, to confirm its binding to transcription factors Stat3 and Egr1.

2022-03-23 | GSE198802 | GEO

Expression data from salivary tumor tissues derived from MMTV-ras transgenic mice with wild-type p53, no p53 or gain-of-function mutant p53

2014-08-15 | GSE59452 | GEO

Expression data from salivary tumor tissues derived from MMTV-ras transgenic mice with wild-type p53, no p53 or gain-of-function mutant p53

Project description:Salivary tumors isolated from MMTV-ras transgenic mice expressing wild-type p53, no p53 or p53R172H gain-of-funcion mutant were subjected to genome-wide gene expression profiling to assess the effect of the different p53 status on tumor gene expression. A total of 12 spontaneous salivary tumors from MMTV-ras/p53+/+, MMTV-ras/p53-/- or MMTV-ras/p53R172H/R172H mice (4 tumors per genotype) were analyzed using Affymetric GeneChip for gene expression profiling. The multi-class comparison function of Significance Analysis of Microarray (SAM) with an FDR of 1% was used to identify genes that are differentially regulated across the three genotypic groups.

2014-08-15 | E-GEOD-59452 | biostudies-arrayexpress

Mouse oral tumors induced by activation of Ras and p53 mutations

Project description:The p53 gain of function p53R172H promotes accelerated tumor growth and progression to carcinoma. To identify gene expression changes associated with the oncogenic function of mutant p53 we compared the expression profiles of oral tumors induced by activation of oncogenic K-ras and p53 gain- or loss-of-function mutations Oral tumors were induced by activation of endogenous oncogenic K-rasG12D and p53 loss- or gain-of-function mutations (p53R172H) Oral tumors from mice carrying the p53R172H mutation or deletion of p53 were collected for gene expression analysis

2012-03-30 | E-GEOD-28203 | biostudies-arrayexpress

A cancer associated fibroblast hierarchy driven by mutant p53 induces perlecan deposition in the pancreatic tumor stroma to permit metastasis and impairs response to chemotherapy

Project description:Heterogeneous sub-populations of cancer cells exist within pancreatic tumors and shape the local stroma. Recent studies have provided evidence that subtypes of cancer-associated fibroblasts (CAFs) also coexist within pancreatic cancer tissues and can both promote and restrain disease progression. Here, we interrogate how cancer cells harboring distinct alterations in p53 (loss or gain-of-function) manipulate CAFs using matched CAFs and cancer cells isolated from the low metastatic KPflC (p53 null) and highly metastatic KPC (gain-of-function p53 mutant) mouse models of pancreatic cancer. We reveal the existence of a p53-driven hierarchy, where cancer cells with a gain-of-function (GOF) mutant p53 educate a dominant population of CAFs that drive the establishment of a pro-metastatic environment for GOF and null p53 cancer cells alike. We also demonstrate that CAFs educated by null p53 cancer cells may be reprogrammed by either GOF mutant p53 cells or their CAFs. Using proteomic characterization of CAF secretomes combined with CRISPR-Cas9 based editing identified perlecan as a key component of this pro-metastatic and resistant environment. Lastly, using longitudinal intravital imaging with a CDK1 FRET reporter and titanium windows, we observe that these dominant CAFs delay cancer cell response to gemcitabine/Abraxane in both GOF and null p53 cancer cells. We also reveal that depletion of perlecan in the stroma combined with chemotherapy prolongs mouse survival, supporting it as a potential novel target for development of anti-stromal therapies in pancreatic cancer.

2019-06-06 | GSE123646 | GEO

Mouse oral tumors induced by activation of Ras and p53 mutations

2012-03-31 | GSE28203 | GEO

Transcriptional profile of WT, p53 -/- and p53R172H esophageal cells

Project description:We report different transcriptional profiles of WT, p53-/- and p53R172H cells derived from mouse esophagi. P53-/- and p53R172H expressing mice were treated with 4NQO to enhance tumor formation.

2020-04-01 | GSE120353 | GEO

Acute and long-term effects of mutant p53 in vivo [MEF]

Project description:The specific roles of mutant p53’s dominant-negative (DN) or gain-of-function (GOF) properties in regulating acute response and long-term tumorigenesis is unclear. Using “knock-in” mouse strains expressing varying R246S mutant levels, we show that DN effect on transactivation is universally observed after acute p53 activation whereas the effect on cellular outcome is cell-type specific. Reducing mutant p53 levels abrogated the DN effect. Mutant p53’s DN effect protected against radiation-induced death, but did not accentuate tumorigenesis. Furthermore, the R246S mutant did not promote tumorigenesis compared to p53-/- mice in various models, even in the absence of MDM2, unlike the R172H mutant. Together, these data demonstrate that mutant p53’s DN property only affects acute responses, whereas GOF is not universal, being mutation-type specific.

2012-12-31 | GSE40416 | GEO

Acute and long-term effects of mutant p53 in vivo [B cells]

2012-12-31 | GSE40415 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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