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Progression of KRas^G12D Rosa26-MYC tumours to invasive disease

ABSTRACT: Progression of KRas^G12D Rosa26-MYC tumours to invasive disease

PROVIDER: PRJEB24729 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2276410_1.fastq.gz	Fastqsanger.gz
	ERR2276410_2.fastq.gz	Fastqsanger.gz
	ERR2276411_1.fastq.gz	Fastqsanger.gz
	ERR2276411_2.fastq.gz	Fastqsanger.gz
	ERR2276412_1.fastq.gz	Fastqsanger.gz

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RNA-SEQ analysis of pancreatic ductal adenocarcinoma tumours in Pdx1-Cre;lsl-KRas[G12D] (KC), Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM] (KMC), Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM];c-Myc[fl/+] (KMC-Mycfl/+), and Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM];Zbtb17[fl/fl] mice (KMC-Miz1fl/fl)

Project description:Activation of endogenously expressed KRas[G12D] in the pancreas of mice gives rise primarily to early stage PanIN lesions, however such lesions can occasionally progress to end-stage ductal adenocarcinoma (PDAC). Progression of KRas[G12D]- initiated lesions to PDAC is accelerated by modest expression of MYC from the Rosa26 locus. Deletion of 1 copy of endogenous c-Myc or both copies of endogenous Zbtb17 (aka Miz1), slows progression to PDAC and extends healthful survival of Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM] (KMC) mice. Tumours were removed from mice with all 4 genotypes and validated by histological examination prior to RNA-SEQ analysis.

2020-03-16 | E-MTAB-8797 | biostudies-arrayexpress

Progression of KRas^G12D;Rosa26-MYC tumours to invasive disease

Project description:The aim of the study was to investigate gene expression tumour progression of KRas*/MYC driven lung tumours from adenocarcinoma in situ to invasive disease.

2018-06-01 | E-MTAB-6432 | biostudies-arrayexpress

Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach vs. Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach microarray

Project description:We wished to investigate the role of E-cadherin loss in our mouse parietal cell/pre-parietal cell E-cadherin knock-out, p53 knock-out, oncogenic Kras induced model of gastric cancer. As such, we isolated RNA from stomach tissue from our E-cadherin knock-out model (Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)) and our E-cadherin heterozygous model (Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)). We then performed a microarray on this stomach tissue from four independent mice of each genotype. Differentially expressed genes were identified and gene set overlap analysis was used to identify pathways enriched in one model over the other.

2018-05-01 | E-MTAB-5833 | biostudies-arrayexpress

Transcriptional profiling of mouse oesophageal tumours from AhcreERTR26flEYFP/wt LSL Kras+/G12D mice

Project description:To assess the transcriptional profile within tumours AhcreERTR26flEYFP/wt LSL Kras+/G12D animals were treated with diethylnitrosamine for 8 weeks prior to induction of the Kras allele with a single dose of Î²-naphthoflavone (20 mg/kg) and tamoxifen (0.25 mg). Subsequently, animals were treated with Sorafenib for 6 weeks. Gene expression array analysis was performed on 12 squamous cell carcinomas (SCCs) from 4 animals.

2016-07-08 | E-MTAB-4926 | biostudies-arrayexpress

RNA-SEQ analysis of pancreatic ductal adenocarcinoma tumours in Pdx1-Cre lsl-KRas[G12D] (KC), Pdx1-Cre lsl-KRas[G12D] Rosa26-lsl-MYC[DM] (KMC), Pdx1-Cre lsl-KRas[G12D] Rosa26-lsl-MYC[DM] c-Myc[fl/+] (KMC-Mycfl/+), and Pdx1-Cre lsl-KRas[G12D] Rosa26-lsl-MYC[DM] Zbtb17[fl/fl] mice (KMC-Miz1fl/fl)

Project description:RNA-SEQ analysis of pancreatic ductal adenocarcinoma tumours in Pdx1-Cre lsl-KRas[G12D] (KC), Pdx1-Cre lsl-KRas[G12D] Rosa26-lsl-MYC[DM] (KMC), Pdx1-Cre lsl-KRas[G12D] Rosa26-lsl-MYC[DM] c-Myc[fl/+] (KMC-Mycfl/+), and Pdx1-Cre lsl-KRas[G12D] Rosa26-lsl-MYC[DM] Zbtb17[fl/fl] mice (KMC-Miz1fl/fl)

| PRJEB36783 | ENA

Expression data comparing KRas(G12D/+);CreT, R26(H1047R/+);KRas(G12D/+);CreT, and MMTV-Neu mouse mammary tumors

Project description:Breast Cancer (BC) has been associated with alterations in signaling through a number of growth factor and hormone regulated pathways. Mouse models for metastatic BC have been developed using oncoproteins that activate PI3K, Stat3 and Ras signaling. To determine the role of each pathway, we analyzed mouse mammary tumor formation when they were activated singly or pairwise. We used microarrays to detect differentially expressed genes in the KRas(G12D/+);CreT and R26(H1047R/+);KRas(G12D/+);CreT tumors Total RNA was extracted from tumors developed by Qiagen RNAeasy kit and hybridized on Affymetrix microarrays.

2015-09-16 | E-GEOD-73073 | biostudies-arrayexpress

E-MTAB-6432

Project description:Progression of KRas^G12D;Rosa26-MYC tumours to invasive disease

2019-01-16 | E-MTAB-6432 | ExpressionAtlas

RNA sequencing of SW1990 KRAS-G12D or KRAS-G12D/K128R knockin cell lines

Project description:RNA sequencing of SW1990 KRAS-G12D or KRAS-G12D/K128R knockin cell lines

| PRJNA1089940 | ENA

Expression data comparing KRas(G12D/+);CreT, R26(H1047R/+);KRas(G12D/+);CreT, and MMTV-Neu mouse mammary tumors

2015-09-16 | GSE73073 | GEO

Mutation-specific and common phosphotyrosine signatures of KRAS G12D and G13D alleles

Project description:KRAS is one of the most frequently mutated genes across all cancer subtypes. Two of the most frequent oncogenic KRAS mutations observed in patients result in glycine to aspartic acid substitution at either codon 12 (G12D) or 13 (G13D). Although the biochemical differences between these two predominant mutations are not fully understood, distinct clinical features of the resulting tumors suggest involvement of disparate signaling mechanisms. When we compared the global and phosphotyrosine proteomic profiles of isogenic colorectal cancer cell lines bearing either G12D or G13D KRAS mutation, we observed both shared as well as unique signaling events induced by the two KRAS mutations.

2021-06-09 | PXD009843 | Pride

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