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Mouse oral tumors induced by activation of Ras and p53 mutations

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: Carlos Caulin

PROVIDER: E-GEOD-28203 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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)

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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.

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Project description:The biologic basis for NSCLC metastasis is not well understood. Here we addressed this deficiency by transcriptionally profiling tumors from a genetic mouse model of human lung adenocarcinoma that develops metastatic disease owing to the expression of K-rasG12D and p53R172H. We identified 2,209 genes that were differentially expressed in distant metastases relative to matched lung tumors. Mining of publicly available data bases revealed this expression signature in a subset of NSCLC patients who had a poorer prognosis than those without the signature. Primary lung adenocarcinomas and metastases from p53R172H∆g/+ K-rasLA1/+ mice or syngeneic tumors were isolated, carefully dissected to remove the adjacent tissue, snap-frozen in liquid nitrogen and stored at -80° until use. Part of each dissected tumor was histologically evaluated by a board-certified pathologist. Synthesis of cRNA and hybridization to Mouse Expression Array 430A 2.0 chips were performed. Two-sided t-paired tests using log-transformed expression values determined significant differences between primary tumors and metastasis.

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

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

Project description: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

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Mutant-p53 stimulates Cxcl1 Expression from Distal Enhancers to Suppress Immune Response to Pancreatic Cancer [CUT&RUN]

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Mutant-p53 stimulates Cxcl1 Expression from Distal Enhancers to Suppress Immune Response to Pancreatic Cancer [EXOME-seq]

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Mutant p53 interactome study with IP-MS

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