E-MTAB-6432
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-6432 | ExpressionAtlas | 2019-01-16
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Progression of KRas^G12D;Rosa26-MYC tumours to invasive disease
| PRJEB24729 | ENA
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
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
Project description:Transcriptional profiling of intestinal changes in Apc Kras tumours with MYC activation and/or drug combination treatment
2021-01-01 | GSE159432 | GEO
Project description:To predict the progression risk of non-invasive gland-forming gastric neoplasms to invasive carcinoma, we assessed lineage continuity or discontinuity between the non-invasive and invasive neoplasms by applying hierarchical clustering analysis to the gene copy-number profiles of individual tumours. array-based Comparative Genomic Hybridization. Samples are including of 7 tumours of Vienna category 3, 12 tumours of Vienna category 4, 8 intramucosal cancers (Vienna category 5), 16 intramucosal lesions and 16 invasive parts (Vienna category 5); 40 reference for control, 19 control replicates
2014-08-06 | E-GEOD-60116 | biostudies-arrayexpress
Project description:Pituitary tumors are generally considered as benign. However, many are invasive (45 to 55%) and some are described as aggressive with a high proliferation rate and short post-operative time to recurrence and 0.2% metastasize. The molecular events associated to the progression of the pituitary tumor toward an aggressive and malignant phenotype is still unresolved. To bring new hypothesis on signaling pathways associated to the tumor progression, we applied a wide genome analysis approach combining transcriptome analysis and CGH analysis on the same 13 prolactin tumours classified as non-invasive (n=5), invasive (n=2) and agressive-invasive tumors (n=6). In 5/6 agressive-invasive tumours a loss of a common region in the p arm of the chromosome 11 was detected. This region extending from position 14.9 to position 46.5 Mb harbours the cytobands 11p15.2, 11p15.1, 11p14.3, 11p14.2, 11p14.1, 11p13, 11p12 and 11p11.2. In 3 of these 5 tumours considered as carcinomas because of the presence of metastasis, an allelic loss is also observed in the 11q arm. The combination of data coming from genome structure exploration and transcriptomic analysis showed that allelic loss impact the expression of genes harbored in the imbalanced region. Data filtering strategy allowed us to highlight among the 139 genes harbored in the 11p region loss, 5 genes (DGKZ, CD44, TSG101, GTF2H1 and HTATIP2) that could be candidate gene for triggering the progression of prolactin tumour toward an aggressive and malignant phenotype. Finally, specific DNA alterations give one molecular argument more to consider agressive-invasive tumour and carcinomas as a distinct step in progression of the pituitary tumours. Copy number analysis of Affymetrix Genome-Wide Human SNP Array 6.0 was performed for 13 prolactin tumors, 6 aggressive-invasive, 2 invasive, 5 non-invasive. The same analysis was performed for one normal pituitary and one genomic DNA called "reference 103" from Affymetrix.
2011-03-16 | E-GEOD-22615 | biostudies-arrayexpress
Project description:To predict the progression risk of non-invasive gland-forming gastric neoplasms to invasive carcinoma, we assessed lineage continuity or discontinuity between the non-invasive and invasive neoplasms by applying hierarchical clustering analysis to the gene copy-number profiles of individual tumours.
2014-08-06 | GSE60116 | GEO
Project description:Purpose: Majority of pancreatic cancer (PDAC) patient deaths are associated to the metastatic progression of disease. To identify novel targeted-therapies, a complete understanding of transformation in genetic landscape in tumors during disease progression is needed. Widely in use, the artificially immortalized PDAC cell lines do not rightly represent the progression because of multiple donors and disparate genetic characteristics. To identify key genes underlying the progression of PDAC from localized disease to a metastatic form, we performed whole transcriptome RNA-Sequencing analysis of cell models representing localised to metaststic stage through paired-end deep sequencing Method: Mouse expressing a Cre-activated KrasG12D allele inserted into the endogenous Kras locus, and these mice were crossed with mice expressing Cre recombinase in pancreatic tissue by virtue of a PDX-1 promoter-driven transgene. Next a cross between K-rasG12D Pdx-Cre and p16-/- mice, transgenic K-rasG12D Pdx-Cre p16-/- mice were generated harboring tissue specific mutant Kras and p16 deletion resulting in an earlier appearance of PanIN lesions followed by rapid progression into highly invasive and metastatic pancreatic cancers. Results: Transgenic K-rasG12D Pdx-Cre p16-/- mice developed spontaneous- localized, invasive and metastatic pancreatic tumors and transcriptome of these cell models representing localized, invasive and metastatic pancreatic tumors were sequenced. Conclusions: Based on genetic analysis of a same-lineage genetic background cell models, this study identifies a novel molecular pathway underlying the progression of pancreatic cancer disease. This study shows that Intestine Specific Homeobox (ISX) gene is a novel biomarker unique to pancreatic cancer progression.
2019-06-20 | GSE116635 | GEO
Project description:The potent MYC oncoprotein is deregulated in many human cancers, including breast carcinoma, and is associated with aggressive disease. To understand the mechanisms and vulnerabilities of MYC-driven breast cancer, we have generated an in vivo model that mimics human disease in response to MYC deregulation. MCF10A cells ectopically expressing a common breast cancer mutation in the PI3 kinase pathway (PIK3CAH1047R) lead to the development of organized acinar structures in mice. However, expressing both PIK3CAH1047R and deregulated-MYC lead to the development of invasive ductal carcinoma, thus creating a model in which a MYC-dependent normal-to-tumour switch occurs in vivo. These MYC-driven tumours exhibit classic hallmarks of human breast cancer at both the pathological and molecular levels. Moreover, tumour growth is dependent upon sustained deregulated MYC expression, further demonstrating addiction to this potent oncogene and regulator of gene transcription. We therefore provide a MYC-dependent model of breast cancer which can be assayed for in vivo tumour initiation, proliferation, and transformation from normal breast acini into invasive breast carcinoma. Taken together, we anticipate that this novel MYC-driven transformation model will be a useful research tool to both better understand MYC’s oncogenic function and identify therapeutic vulnerabilities.
2019-07-25 | GSE130513 | GEO
Project description:Background: Although histology is the corner stone for decision analysis in bladder cancer, it still needs refinement and new tools to better identify tumours with the highest risk of progression or recurrence. Objective: We designed a prospective study to evaluate whether microarray analysis could find a molecular signature for pathologic staging and/or grading. Design, setting and participants: Prospective multicentric study conducted from September 2007 to May 2008 (108 bladder tumours (45 pTa, 35 pT1 and 28> pT1)). Microarray analysis was performed with Agilent Technologies Human Whole Genome 4 x 44K oligonucleotide microarrays and used a method of dual color type versus a reference consists of a pool of tumours. From the lists of genes provided by the BrB Class Comparison analyses, we validated the microarray results of 38 selected differentially expressed genes by RT-QPCR in another bladder tumour cohort (n = 95). Results: The cluster M-^Ssuperficial vs invasive stageM-^T properly classified 92.9% of invasive stages and 66.3% of superficial stages. Among the superficial tumours, the cluster analysis showed that pT1b tumours were closer to invasive stages than pT1a tumours. We also found molecular differences between low and high-grade superficial tumours. However these differences were less caricatural than the one observed for staging.Conclusions: We confirm that the histopathological classification into subgroups pTa, pT1a and pT1b may have a translation in a M-^Smolecular signatureM-^T with a continuous progression of deregulation (overexpression or repression of these genes) from superficial (pTa) to more invasive (pT1a then b stage).
2013-08-13 | E-MTAB-993 | biostudies-arrayexpress