Similar studies for GEO DataSets (Select 200119654) - GEO DataSets

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Items: 20

Select item 2001196541.

Proline 152 mutation in p53 abolishes cognate DNA binding, induces gain of function tumorigenesis

(Submitter supplied) We have identified a relatively rare mutation in p53 in an Indian oral cancer patient sample at the fade end of its DNA binding domain [P152L]. Although P152L p53 DBD potentially binds to DNA, the full length protein is completely devoid of cognate site DNA binding ability. Also the mutant protein can efficiently tetramerize. Significantly, this mutant was found to induce cell mobility and proliferation with greater tumorigenic potential in nude mice, the mechanistic details of which is also investigated upon. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL11154
4 Samples

Download data: TXT

Series

Accession:: GSE119654

ID:: 200119654

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Select item 2001205342.

The lung-enriched p53 mutants V157F and R158L/P regulate a novel transcriptome in lung cancer

(Submitter supplied) Lung cancer is the leading cause of cancer-related deaths in the US, and alterations in the tumor suppressor gene TP53 are the most frequent somatic mutation among all histologic subtypes of lung cancer. Mutations in TP53 frequently result in a protein that exhibits not only loss of tumor suppressor capability but also gain of oncogenic function (GOF). The canonical p53 hotspot mutants R175H and R273H, for example, confer upon tumors a metastatic phenotype in murine models of mutant p53. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL18573
10 Samples

Download data: TXT

Series

Accession:: GSE120534

ID:: 200120534

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Select item 2001243493.

Change of gene expression of mutation of TP53 in LS174T cells

(Submitter supplied) Change of gene expression of mutation on TP53 exon3 or exon10 by CRISPR-Cas9 system in LS174T cells

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL20844
9 Samples

Download data: TXT

Series

Accession:: GSE124349

ID:: 200124349

Select item 2000891464.

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

(Submitter supplied) 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.

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL4133
40 Samples

Download data: TXT

Series

Accession:: GSE89146

ID:: 200089146

Select item 2001252625.

Apc, Kras, and Trp53 mutations

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL17400
27 Samples

Download data: CEL

Series

Accession:: GSE125262

ID:: 200125262

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Select item 2001252616.

Organoids derived from mouse normal colon and tumor samples with Apc, Kras, and Trp53 mutations in several combinations.

(Submitter supplied) For organoid preparation, we first treated the following 4 groups of 8-12 week old mice with tamoxifen: 1) CDX2P-CreERT2, Apc flox/+, Kras LSL-G12D/+, Trp53 flox/flox mice (n=2); 2) CDX2P-CreERT2, Apc flox/+, Kras LSL-G12D/+,Trp53 R270H/flox mice (n=3); 3) CDX2P-CreERT2, Apc flox/flox mice (n=3); 4) Wild-type control mice (n=4). The CDX2P-CreERT2 transgene expresses a tamoxifen (TAM)-regulated Cre protein (CreERT2) under control of human CDX2 regulatory sequences, allowing for TAM-inducible targeting of flox alleles in adult mouse terminal ileum, cecum, and colon epithelium. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL17400
12 Samples

Download data: CEL, XLSX

Series

Accession:: GSE125261

ID:: 200125261

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Select item 2001252607.

Mouse colon tumor samples with Apc, Kras, and Trp53 R270H or Tpr53 null mutations, and wild type controls.

(Submitter supplied) We treated the following 3 groups of 8-16 week old mice with tamoxifen: 1) CDX2P-CreERT2, Apc flox/+, Kras LSL-G12D/+, Trp53 flox/flox mice (n=6); 2) CDX2P-CreERT2, Apc flox/+, Kras LSL-G12D/+,Trp53 R270H/flox mice (n=6); 3) Wild-type control mice (n=3). The CDX2P-CreERT2 transgene expresses a tamoxifen (TAM)-regulated Cre protein (CreERT2) under control of human CDX2 regulatory sequences, allowing for TAM-inducible targeting of flox alleles in adult mouse terminal ileum, cecum, and colon epithelium. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL17400
15 Samples

Download data: CEL, XLSX

Series

Accession:: GSE125260

ID:: 200125260

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Select item 2001988028.

Differential gain-of-function activity of three p53 hotspot mutants in vivo

(Submitter supplied) To identify mutant p53 gain-of-function, primary murine osteosarcomas expressing p53 heterozygous mutants were compared to p53 heterozygous tumors. Transcriptomes regulated by different p53 hotspots were used to identify their mechanisms of action. Validation was done in cell line expressing mutant p53, to confirm its binding to transcription factors Stat3 and Egr1.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL21103
20 Samples

Download data: TXT

Series

Accession:: GSE198802

ID:: 200198802

PubMed Full text in PMC Similar studies

Select item 2000659679.

Gene expression profiling of MDA-MB-468 cells following p53-R273H mutant knock-down

(Submitter supplied) A total of 58 genes were up-regulated (> 1.5 fold-change) while 117 genes were down-regulated

Organism:: Homo sapiens

Type:: Expression profiling by array

Platform:: GPL6244
4 Samples

Download data: CEL, CHP

Series

Accession:: GSE65967

ID:: 200065967

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Select item 20008144110.

Mutant p53 R270H induces invasion and metastasis of mouse intestinal tumor organoids through gain-of-function mechanism

(Submitter supplied) Apc(D716) mutant mice develop benign intestinal adenoma, while Apc(D716) and p53 R270H compound mutant mice develop invasive adenocarcinoma in the intestine. We examined expression profile of tumor-derived organoids using Apc(D716), Apc(D716) p53 Null, Apc(D716) p53 R270H mutant mice by RNA sequencing, and identified mutant p53-induced gene set.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL17021
6 Samples

Download data: TXT

Series

Accession:: GSE81441

ID:: 200081441

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20010198011.

Transcriptome analysis of TP53-R248L overexpressed 19NS patient-derived glioblastoma cells

(Submitter supplied) This study demonstrates the role of TP53 gain-of-function (GOF) mutation on glioblastoma progression. However, little is known about the transcriptional alteration upon TP53 GOF mutation. In this study, we found that TP53 GOF mutation (R248L mutation) promotes the enrichment of multiple gene signatures related to inflammation and chemotaxis. Particularly, through in vitro and in vivo approaches, we verified that TP53 GOF mutation enhances NFKB signaling which in turn up-regulates CCL2 and TNFA. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL23525
2 Samples

Download data: TXT

Series

Accession:: GSE101980

ID:: 200101980

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Select item 20011817312.

Transcriptome analysis of mesenchymal CSC-like cells harboring mutant p53

(Submitter supplied) We show that mesenchymal CSC-like cells express an embryonic stem cell signature that is mutant p53 dependent

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL17021
17 Samples

Download data: TXT

Series

Accession:: GSE118173

ID:: 200118173

PubMed Similar studies SRA Run Selector

Select item 20006835313.

Mutant p53R273H regulated microRNA profiling in presence and absence of DNA damage in H1299 cells

(Submitter supplied) In the present study, we used a high-throughput small RNA deep sequencing followed by a systematic computational analysis to identify genome wide mutant p53R273H regulated miRNAs in both DNA damage dependent and independent context. Several miRNA-mRNA regulatory networks have been predicted that might contribute to mutant p53 GOF properties. Differentially regulated miRNA signature profile has been validated in the lung cancer patients harboring wildtype and mutant p53. more...

Organism:: Homo sapiens

Type:: Non-coding RNA profiling by high throughput sequencing

Platform:: GPL17301
8 Samples

Download data: CSV

Series

Accession:: GSE68353

ID:: 200068353

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20014356114.

Germline and somatic genetic variants in the p53 pathway interact to affect cancer risk, progression, and drug response

(Submitter supplied) Insights into oncogenesis derived from cancer susceptibility loci (single nucleotide polymorphisms, SNP) hold the potential to facilitate better cancer management and treatment through precision oncology. However, therapeutic insights have thus far been limited by our current lack of understanding regarding both interactions of these loci with somatic cancer driver mutations and their influence on tumorigenesis. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL20301
18 Samples

Download data: TXT

Series

Accession:: GSE143561

ID:: 200143561

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Select item 20013159215.

Transcriptional consequences of wild-type and missense mutant p53 in isogenic human acute myeloid leukemia (AML) cell lines

(Submitter supplied) TP53, encoding for the tumor suppressor p53, is the most frequently mutated gene in human cancer. The selective pressures shaping its mutational spectrum, dominated by missense mutations, have remained enigmatic, and neomorphic gain-of-function (GOF) activities have been implicated. We generated isogenic human leukemia cell lines of the most common TP53 missense mutations using CRISPR/Cas9. Functional, DNA binding, and transcriptional analyses revealed loss-of-function (LOF) without GOF effects of missense mutations. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL18573
96 Samples

Download data: TAB

Series

Accession:: GSE131592

ID:: 200131592

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Select item 20013148416.

Genome-wide binding of wild-type and missense mutant p53 in isogenic human acute myeloid leukemia (AML) cell lines

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL18573
32 Samples

Download data: BEDGRAPH

Series

Accession:: GSE131484

ID:: 200131484

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20026295117.

The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability

(Submitter supplied) Background: TP53, the most frequently mutated gene in human cancers, orchestrates a complex transcriptional program crucial for cancer prevention. While certain TP53-dependent genes have been extensively studied, others, like the recently identified RNF144B, remained poorly understood. This E3 ubiquitin ligase has shown potent tumor suppressor activity in murine Eμ Myc-driven lymphoma, emphasizing its significance in the TP53 network. more...