Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Pancreatic cancer xenograft tumor RNA sequencing and pathologic differentiation of matched human tumors.

ABSTRACT: Epithelial to mesenchymal transition (EMT) in pancreatic cancer is believed to correlate with metastatic probability and aggressiveness. In the clinical setting, tumor staging and grading reflect tumor aggressiveness, tumor invasion, and gross metastasis and are used to guide treatment options. These data were analyzed to correlate commonly used laboratory RNA sequencing analysis with clinically defined differentiation status. This dataset provides evidence that mesenchymal genes are enriched in xenograft tumors from poorly differentiated human tumors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE252909 | GEO | 2024/01/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Determining Prostate Cancer Aggressiveness Utilizing a Novel DNA Methylation Approach

Project description:The clinical management of prostate cancer is challenging and currently relies primarily on staging, histological grading, and tumor size. In this study, we take advantage of the propensity of prostate cancer to be multifocal and categorize aggressiveness of individual prostate cancer foci based on DNA methylation patterns in primary and metastatic tumors.

2016-11-30 | GSE73549 | GEO

Glucose Metabolic Remodeling through Phosphoenolpyruvate Carboxykinase Isoform 2 Regulates Prostate Cancer Cell Tumorigenicity

Project description:Patients with aggressive prostate cancer generally present with poor outcomes. Identifying the factors regulating prostate cancer aggressiveness may open new avenues in therapy. Specifically, information from prostate cancer patient databases revealed that higher phosphoenolpyruvate carboxykinase isoform 2 (PCK2) levels correlate with more aggressive tumors and lower survival rates. Herein, we show that high tumorigenic prostate cancer cell clones express high levels of PCK2. We found that elevated levels of PCK2 are critical for the glucose metabolic remodeling and the maintenance of tumor-initiating cells (TICs) in aggressive prostate cancer. Our data suggest that PCK2 promotes tumorigenicity by lowering acetyl-CoA levels through reducing the mitochondrial tricarboxylic acid (TCA) cycle. Thus, PCK2 is a potential therapeutic target for aggressive prostate cancer. 2 subclones have been isolated from DU145 cells. The epithelial like (EL) clone has a high tumorigenicity ability and enriched tumor initiating cells than mesenchymal like (ML) clone. Genes with differential expression pattern between these two clones were detected by gene micorarray.

2016-01-04 | E-GEOD-76470 | biostudies-arrayexpress

Quantitative proteomic analysis of head and neck squamous cell carcinoma (HNSCC) based on pathological grading using FFPE blocks using high-resolution mass spectrometry

Project description:Oral squamous cell carcinoma is one of the most common cancers occurring worldwide associated with significant mortality and morbidity. Despite the early prognostic factors which such as histological tumor grading, staging, the extent of the tumor invasion, and involvement of regional lymph nodes, there is a demand for development of molecular markers which will help in unraveling molecular carcinogenesis associated with OSCC. In the current study, we carried out an in-depth proteomic analysis using high-resolution mass spectrometry to identify the differentially expressed proteins among the types of OSCC FFPE tissues. This resulted in the identification of 2,399 non-redundant proteins expressed differentially across histologically-classified well, moderate and poorly differentiated OSCC specimens.

2021-09-09 | PXD019456 | Pride

Differentially expressed genes after treatment with chemotherapy in breast cancer and their correlation with pathologic mid-response (Miller & Payne grade 3)

Project description:The aim of this study was to compare the gene expression profile changes breast tumors after the treatment with Anthracyclines and Taxanes. To this end, an oligonucleotide microarray was performed (Affymetrix’s HG-U133 Plus 2.0 array). This gene expression study was carried out on the biopsied tumor samples previous being treated with chemotherapy, and subsequently compared with themselves once treatment schedule ended. The post-chemotherapy biopsy was obtained from the surgical piece. The goal of this study was the finding of several genes related to apoptosis, proliferation, differentiation, survival and transformation-related genes and correlating their differences in expression with the degree of response to chemotherapy, determined by the Miller and Payne histological grading system.

2012-12-12 | GSE28583 | GEO

DNA Methylation Profiling Reveals Prognostically Significant Groups in Pediatric Adrenocortical Tumors: A Report From the International Pediatric Adrenocortical Tumor Registry

Project description:Pediatric adrenocortical carcinomas (ACCs) are aggressive; the overall survival of pediatric patients with ACCs is 40%-50%. Appropriate staging and histologic classification are crucial as children with incompletely resected tumors or metastatic disease have a dismal prognosis. The clinical course of pediatric adrenocortical tumors (ACTs) is difficult to predict using the current classification schemas, which rely heavily on subjective microscopic and gross macroscopic variables. Recent advances in adult ACT studies have revealed distinct DNA-methylation patterns with prognostic significance that have not been systematically interrogated in the pediatric population.

2020-05-16 | GSE131350 | GEO

Differentially expressed genes after treatment with chemotherapy in breast cancer and their correlation with pathologic bad response (Miller & Payne grades 1 and 2)

2012-12-12 | GSE28826 | GEO

Differentially expressed genes after treatment with chemotherapy in breast cancer and their correlation with pathologic good response (Miller & Payne grades 4 and 5)

2012-12-12 | GSE28694 | GEO

AKT dependent Notch3 activation drives tumor progression in a model of mesenchymal colorectal cancer subtype

Project description:Recently a consensus molecular subtype (CMS) classification of colorectal cancer (CRC) has been established that is based on the transcriptional rather than the genetic profile of an individual tumor and which may ultimately help to individualize CRC therapy. So far, however, the lack of appropriate animal models that faithfully recapitulate the different molecular subtypes impedes adequate preclinical testing of stratified therapeutic concepts. Here we demonstrate that constitutive AKT activation in intestinal epithelial cells markedly enhances colonic tumor invasion and metastasis in Trp53DIEC mice (Trp53ΔIECAktE17K) upon challenge with the carcinogen azoxymethane (AOM). Gene-expression profiling indicates that Trp53ΔIECAktE17K tumors closely resemble the human mesenchymal colorectal cancer subtype (CMS4), which is characterized by the poorest survival rate among the four consensus molecular subtypes of CRC. Trp53ΔIECAktE17K tumors are further characterized by a NOTCH pathway gene signature and a distinct cell autonomous upregulation of Notch3 in tumor epithelia while treatment of Trp53ΔIECAktE17K mice with a NOTCH3-inhibiting antibody reduces invasion and metastasis. Conversely, selective activation of NOTCH3 by overexpression of NOTCH3-IC in Akt wt tumor organoids strongly promotes development of metastasis in an orthotopic transplantation model. In CRC patients NOTCH3 expression correlates positively with tumor grading and the presence of lymph node as well as distant metastases and is specifically upregulated in CMS4 tumors. Therefore, we suggest NOTCH3 as a putative target for advanced CMS4 CRC patients.

2021-09-08 | PXD014778 | Pride

Transcriptomic analyses of Kras induced zebrafish liver cancer

Project description:The krasV12-induced tumor progression was conducted on 100 transgenic fishes maintained in water containing 2µM mifepristone. Gross morphological and histological analyses were weekly performed on 15 randomly selected fishes to monitor tumor development. These analyses showed robust development of hepatocellular adenoma within 4 weeks of induction. Observation of tumor development and staging of tumorigenesis was conducted as described. For tumor regression the group of 15 fishes with HCC was transferred to mifepristone-free water. Histological examination revealed tumor shrinkage showing extensive scarring at the peripheral and focal tumor regions. Notably, complete tumor regression with scarred fibrosis of the former tumor tissue was observed after 4 weeks of mifepristone withdrawal.

2017-01-24 | GSE93965 | GEO

Mutant p53 Increases Incidence and Promotes Progression of Mammary Carcinomas in Mice

Project description:In human breast cancer, mutations in the p53 gene are associated with poor prognosis, suggesting a mutant p53 “gain of function”. To study this phenomenon, we co-expressed mutant p53R270H in mice in which SV40 early proteins initiate the development of mammary adenocarcinomas in descendants of mammary epithelial cells that survived involution (WAPT-mice). This model allows the characterization of mammary carcinomas that developed in the absence or presence of mutant p53, while the endogenous wild-type p53 is functionallycompromised. Co-expression of mutant p53 significantly aggravated the phenotype of bitransgenic mice, as evidenced by a higher tumor incidence, a worse clinical staging and histological grading, as well as an enhanced invasiveness of the tumors, and more frequent pulmonary metastasis. Our data indicate that mutant p53 does not exert this effect by increasing genomic instability. On the contrary, lower grade tumors in WAP-T mice generally accumulated more amplifications of pro-survival genes than the corresponding tumors in bitransgenic animals, suggesting that mutant p53 can compensate for such genetic alterations by alternative mechanisms, possibly by its transcriptional activities, and thereby facilitate tumor formation. As a common feature and associated with their enhanced invasiveness, high grade tumors showed high level amplification of the Met-locus. Keywords: mutant p53, SV40 early proteins, tumor progression, tumor grade, tumor stage, mammary carcinoma, animal model, Met

2007-12-31 | GSE7135 | 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