E-GEOD-16779
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA117533
PROVIDER: E-GEOD-16779 | ExpressionAtlas | 2014-11-25
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Analysis of undifferentiated pleomorphic sarcoma/malignant fibrous histiocytoma-like tumors from LSL-KrasG12D, p53Fl/Fl mouse model of soft tissue sarcoma. Murine soft tissue sarcomas (n = 17) were compared to normal muscle (n = 4). Tumors were isolated surgically from soft tissue sarcomas generated by conditional Kras and p53 alleles. Tumors were induced using an adenovirus expressing Cre recombinase. Normal muscle samples were isolated from mice of the same genotype without tumor induction.
2010-03-03 | E-GEOD-16779 | biostudies-arrayexpress
Project description:mRNA-seq for expression profiling of Myc and Yap1 activated mouse lung tumors and controls. 4 cohorts of lung tumors induced through nasal instillation of Cre/sgRNA(MS2)-encoding lentivirus in mice carrying conditional P53 loss (P53 F/F), oncogenic Kras (Kras LSL-G12D/+), and CRISPRa/SAM construct (Rosa26(LSL-SAM) or YFP reporter (Rosa26(LSL-YFP): 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-SAM) / lenti(CMV-Cre/U6-sgRNA(Myc) (PPKS/M); 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-SAM) / lenti(CMV-Cre/U6-sgRNA(Yap1) (PPKS/Y); 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-SAM) / lenti(CMV-Cre/U6-sgRNA(non-targeted) (PPKS/NT); 4 P53(L/L), Kras(LSL-G12D/+), Rosa26(LSL-YFP) / lenti(CMV-Cre/U6-sgRNA(non-targeted) (PPKY/NT)
2022-08-30 | E-MTAB-11122 | biostudies-arrayexpress
Project description:Microarray analysis of rhabdomyosarcomas generated using mice with conditional mutations in Kras and p53 using both in vivo and in vitro approaches to identify a cell of origin for rhabdomyosarcoma.
2011-01-30 | GSE25098 | GEO
Project description:Microarray analysis of rhabdomyosarcomas generated using mice with conditional mutations in Kras and p53 using both in vivo and in vitro approaches to identify a cell of origin for rhabdomyosarcoma. Contains rhabdomyosarcomas derived in vivo using Pax7-CreER mice and in vitro using sorted muscle progenitor cells, UPS derived from intramuscular Adeno-Cre injection, and normal muscle.
2011-01-30 | E-GEOD-25098 | biostudies-arrayexpress
Project description:Though p53 mutations are rare in Ewing sarcoma, there is a strong indication that p53-mutant tumors form a particularly bad prognosis group. As such, novel treatment strategies are warranted that would specifically target and eradicate tumor cells containing mutant-p53 in this subset of ES patients. PRIMA-1Met/APR-246 is a small organic molecule which has been shown to restore tumor suppressor function primarily to mutant p53 and to also induce cell death in various cancer cell types. We analyzed the apoptosis inducibility on Ewing sarcoma cells harbouring different p53 mutations upon exposure to APR-246. Gene expression profiles of three STA-ET-7 cell lines established from the same patient at different stages of the disease was assessed by microarray analysis as these cell lines responded variably to APR-246.
2013-11-12 | E-GEOD-49967 | biostudies-arrayexpress
Project description:A series of conditional mouse models of embryonal rhabdomyosarcoma, alveolar rhabdomyosarcoma and spindle cell sarcoma were generated and validated for relavence to corresponding human cancers. Conditional mouse models of embryonal rhabdomyosarcoma, alveolar rhabdomyosarcoma and spindle cell sarcoma were created by activation or deletion of Pax3:Fkhr, p53, Ptch1 or Rb1 genes.
2011-02-17 | E-GEOD-22520 | biostudies-arrayexpress
Project description:Mouse Models of Sarcoma Targeting KRas and p53
| PRJNA248466 | ENA
Project description:Cancer originates as the progressive accumulation of genetic mutations in proto-oncogenes and tumor suppressors. However, the early events underlying tumor initiation remain largely elusive, mostly due to the general lack of information regarding the cells-of-origin responsible for tumor formation as well as the precise impacts of genetic insults on tumor initiation in vivo. Here, we demonstrate that Sox2-positive (Sox2+) adult stem cells are responsible for epithelial squamous tumor formation. Conditional expression of oncogenic Kras (KrasG12D) and knockout of p53 (also known as Trp53) in Sox2+ cells quickly and specifically resulted in the formation of squamous tumors in the forestomach and esophagus. GFP-based lineage tracing experiments demonstrated that Sox2+ cells are the cells-of-origin of squamous tumors in the esophagus and forestomach. Of note, our data showed that p53 deletion alone did not suffice for tumor initiation. On the contrary, tumor initiation was observed upon KrasG12D activation whereas p53 deletion further contributed to the malignancy of the generated tumors, pointing out distinct roles for Kras activation and p53 deletion in squamous tumor formation and progression, to which a multihit carcinogenesis model can be applied. Global gene expression analysis revealed secreting factors upregulated in the generated tumors induced by oncogenic Kras, which contribute to tumor progression. Taken together, these results demonstrate that epithelial squamous tumors can specifically originate as a consequence of defined genetic mutations in a Sox2+ cell population and highlight the connections between proliferative stem cells and tumor development in vivo.
2017-01-01 | GSE66457 | GEO
Project description:Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are found in 30–40% of human colorectal cancers (CRC). However, specific therapeutics against KRAS-mutated CRC have not been established. We have previously reported mouse models for colon cancer with and without Kras mutations (CDX2P-G22Cre;Apcflox/flox; KrasG12D and CDX2P-G22Cre;Apcflox/flox mice, respectively). Herein, we aimed to identify candidate genes as novel therapeutic targets or biomarkers for KRAS-mutated CRC by comparing the gene expression profiles of these two mouse models.
2015-12-25 | GSE75435 | GEO
Project description:Profile gene expression from tumors that develop in mice bearing conditional activation of EWS-ATF1, compared to control mouse tissues from the chest wall as well as tumor samples from mouse models of synovial sarcoma and osteosarcoma achieved by conditional disruption of Rb1 and p53
2012-11-28 | GSE41293 | GEO