Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Esophageal Squamous Cell Carcinoma tumors from Indian patients: nuclear-stabilized p53 (NS+) versus unstable p53 (NS-) protein

ABSTRACT: Esophageal Squamous Cell Carcinoma tumors from Indian patients: nuclear-stabilized p53 (NS+) versus unstable p53 (NS-) protein

PROVIDER: PRJNA902359 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Esophageal Squamous Cell Carcinoma tumors from Indian patients: nuclear-stabilized p53 (NS+) versus unstable p53 (NS-) protein

Project description:Transcriptional profiling of Esophageal Squamous Cell Carcinoma (ESCC) tumors comparing samples harbouring nuclear-stabilized p53 (NS+) versus unstable p53 (NS-) protein, determined through immunohistochemistry (IHC) staining of the tumor sections. The goal was to identify the genes that were differentially regulated between NS+ and NS- ESCC samples.

2024-03-29 | GSE218109 | GEO

Oral tongue cancer: p53 NS+ vs. p53 NS- tumor

Project description:Transcriptional profiling of squamous cell carcinoma of oral tongue, comparing p53 NS+ and p53 NS- tumors. Goal was to determine differentially expressed genes between them based on global gene expression.

2020-05-04 | GSE89146 | GEO

miR-309-dependent unstable maternal mRNAs are stabilized in smaug mutants

2009-04-23 | GSE13288 | GEO

miR-309-dependent unstable maternal mRNAs are stabilized in smaug mutants

Project description:The behavior of 410 miR-309-dependent maternal mRNAs (from Bushati et al., 2008) in embryos from wild type and smg-mutant females relative to wild-type stage 14 oocyte reference RNA. All are unstable in wild-type while almost 85% are stabilized in smg mutants mRNA was extracted from staged embryos as well as stage 14 oocytes as described previously (Tadros et al., 2007a). To assay mRNA quality, known stable (rpA1) and unstable (Hsp83) transcripts were probed on Northern blots. Total RNA was then reverse transcribed with random primers (Tadros et al., 2007a) and labeled asÃ?described in the Indirect Labeling of Total RNA for Microarray Hybridization protocol at http://www.flyarrays.com. The fluorescently labeled cDNA probes were hybridized to 14Kv1 microarrays obtained from the Canadian Drosophila Microarray Centre (http://www.flyarrays.com; GPL3603: http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GPL3603). Hybridization and scanning were performed using a PerkinElmer/GSI ScanArray 4000 scanner and the ScanArray software as previously described (Neal et al., 2003). The 16 bit TIFF image files were quantified using QuantArray Version 3 (PerkinElmer), using the adaptive quantification algorithm and analyzed using GeneTraffic Duo3.2 (Iobion Informatics/Stratagene). . The 14Kv1 arrays were normalized to a set of known stable transcripts: Rpl1, RpL32, Rps5a, Rps3, RpL22, mRpS30, mRpS22, CG6764, bonsai, RpS29, RpL11, mRpL1, CG6764, CG317, RpL37A, and RpL40.

2010-06-19 | E-GEOD-13288 | biostudies-arrayexpress

Differential gene expression in mACVR1 NS v wt-ACVR1 NS.

Project description:To study the effect of the ACVR1 G328V mutation in tumor neurospheres with a background of NRASV12 overexpression and p53 knockdown. The goal of this study was to identify differentially expressed genes between mACVR1 NS v wt-ACVR1 NS.

2020-04-16 | GSE148732 | GEO

Aberrant stabilized ETV4 expression cooperates with loss of p53 to promote invasive prostate carcinoma

Project description:Aberrant stabilized ETV4 expression cooperates with loss of p53 to promote invasive prostate carcinoma

| PRJNA535484 | ENA

Aberrant stabilized ETV4 expression cooperates with loss of p53 to promote invasive prostate carcinoma

Project description:Chromosomal translocations or upregulations involving ETS transcription factor are frequent events in prostate cancer pathogenesis and significantly co-occurrence with p53 or PTEN loss. Caused by the low stabilities of ETS proteins in cytosol, mouse models with aberrant expression of wild type ETS transcription factors had subtle phenotypes and only drive prostate cancer progression in the setting of Pten loss. Here we show that prostate specific aberrant expression of mutated ETV4 (V70P71D72-AAA, ETV4-AAA), which is resistence to COP1 mediated protein degradation, results in more stabilized ETV4 protein in mouse prostate. We found that ETV4-AAA mice develop marked prostatic intraepithelial neoplasia (mPin) and p53-dependent cell senescence within 2 weeks, but without tumor development when aged. Interestingly, ETV4-AAA positive cells reduce dramatically in a PTEN loss background, which means that there is no cooperation between ETV4-AAA and PTEN loss. Aberrant ETV4-AAA expression promotes progression of mPin to prostatic adenocarcinoma in a Tp53 deficiency or haploinsufficiency background. In contrast to PTEN loss induced mouse prostate cancers which loss NKX3.1 expression and resistant to castration therapy, these ETV4-AAA tumor cells well maintain AR and NKX3.1 expression and are sensitive to castration therapy.

2021-01-01 | GSE130311 | GEO

Analysis of Wild Type, H-NS KO and cover mutated H-NS Transcriptomes

Project description:The goals of this study are to compare the difference transcriptome of Wild Type, H-NS KO and cover mutated H-NS by RNA-seq

2021-03-25 | GSE169499 | GEO

Unstable Atherosclerotic Plaque Proteome

Project description:The rupture of unstable atherosclerotic plaques, leading to debilitating or fatal thrombotic events, is a major health burden worldwide. Limited understanding as to the molecular drivers of plaque instability and rupture hinders efforts in diagnosis and treatment prior to thrombotic events. Utilising an advanced pre-clinical mouse model (Tandem stenosis (TS) model), which presents human-like unstable atherosclerotic disease, we apply high-end omic methods to characterize the molecular signatures associated with plaque instability in atherosclerotic arteries. Through quantitative proteomic profiling, we depict unique proteome signatures of unstable plaques compared to stable plaques and healthy arteries. Coupled with single-cell RNA-sequencing of leukocytes, we describe the heterodimer complex S100a8/S100a9 as unique to unstable plaque, with neutrophils implicated as the transcriptional drivers of S100a8/a9 expression. We confirm S100a9 expression in human carotid atherosclerotic plaques and we further utilise the TS pre-clinical model to pharmacologically inhibit S100a8/S100a9, resulting in plaque stabilisation. Thus, we establish the TS model as a sophisticated translational tool for the profiling of unstable atherosclerotic plaques and demonstrate that unstable and stable atherosclerosis are highly different disease entities.

2023-05-10 | PXD030857 | Pride

Staphylococcus hominis strain:P1-NS | isolate:P1-NS

Project description:Staphylococcus hominis strain:P1-NS | isolate:P1-NS Genome sequencing

| PRJNA1175880 | ENA