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296 results for “TP53”
Prediction of breast cancer prognosis by gene expression profile of TP53 status.
GEO Series GSE5546. Homo sapiens. 40 samples. Type: Expression profiling by array.
TP53 mutational status is a potential marker for risk stratification in Wilms tumour with diffuse anaplasia [expression]
GEO Series GSE60850. Homo sapiens. 36 samples. Type: Expression profiling by array.
Unscheduled HDAC4 repressive activity in human fibroblasts triggers TP53-dependent senescence and favours cell transformation
GEO Series GSE120040. Homo sapiens. 6 samples. Type: Expression profiling by array.
RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1
GEO Series GSE252264. Homo sapiens. 18 samples. Type: Expression profiling by high throughput sequencing.
Affymetrix OncoScan data for IDH and TP53 mutant gliomas
GEO Series GSE94652. Homo sapiens. 10 samples. Type: Genome variation profiling by SNP array.
Tet2 and Tp53 cooperate to promote leukemia and modulate response to inflammation [Bisulfite-Seq]
GEO Series GSE300000. Mus musculus. 7 samples. Type: Methylation profiling by high throughput sequencing.
The Ashkenazi-centric G334R variant of TP53 is severely impaired for transactivation but retains tumor suppressor function in a mouse model [ChIP-Seq]
GEO Series GSE277586. Homo sapiens. 44 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
TP53-mediated clonal hematopoiesis confers increased risk for incident peripheral artery disease
GEO Series GSE184420. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
TP53 mutational status is a potential marker for risk stratification in Wilms tumour with diffuse anaplasia
GEO Series GSE60940. Homo sapiens. 68 samples. Type: Expression profiling by array; Genome variation profiling by array.
Differences in syncytia formation by SARS-CoV-2 variants modify host chromatin accessibility and cellular senescence via TP53 [RNA-Seq]
GEO Series GSE241891. Homo sapiens; Chlorocebus sabaeus. 20 samples. Type: Expression profiling by high throughput sequencing.
Transcriptomic profile of TP53 wildtype or knockout cells after treated with mitomycin C or vehicle
GEO Series GSE132327. Homo sapiens. 4 samples. Type: Expression profiling by high throughput sequencing.
dataset related to article "Carcinomatosis under control by osimertinib in EGFR and TP53 mutated lung adenocarcinoma"
<p>Radiological images of the patient (case report)</p>
TP53 mutations are associated with improved survival in ovarian carcinoma patients receiving first-line chemotherapy plus bevacizumab: results from the MITO16A/MaNGO OV-2 study
<p><strong>PURPOSE</strong> Bevacizumab (BEV) is considered an effective treatment option for advanced ovarian carcinoma. However, to date, there are no biomarkers that define a BEV-responsive patient subpopulation.</p> <p><strong>METHODS</strong> In the context of the MITO16A/MaNGO OV-2 trial, a phase IV study of chemotherapy combined with BEV in first-line treatment of advanced ovarian carcinoma, we evaluated <em>TP53</em> mutations by next generation sequencing (NGS) and p53 protein expression by immunohistochemistry (IHC) on 202 and 311 cases, respectively. We further correlated NGS and IHC data with clinicopathological characteristics and survival of patients.</p> <p><strong>RESULTS</strong> <em>TP53</em> mutations of unknown function (named unclassified), mostly of the missense type, represented the majority of variants in our population (44.4%) and were associated with a significantly improved overall survival both in univariate (p=0.03, HR=0.43) and multivariate analysis (p=0.012, HR=0.39). Concordance between <em>TP53 </em>mutational analysis and protein expression was 91%. A trend toward improved OS was observed in patients with p53 IHC overexpression (HR=0.70, p=0.15) compared to p53 wild-type patients.</p> <p><strong>CONCLUSION </strong>Our results indicate that the presence of unclassified <em>TP53</em> mutations has favorable prognostic significance in patients with ovarian carcinoma receiving upfront BEV plus chemotherapy. In particular, unclassified missense <em>TP53</em> mutations characterize a subpopulation of patients with a significant survival advantage, independently of clinicopathological characteristics. Our findings warrant future investigations to confirm the prognostic impact of <em>TP53 </em>mutations in BEV-treated ovarian carcinoma patients and deserve to be assessed for their potential predictive role in future randomized clinical studies.</p>
TP53 mutational status is a potential marker for risk stratification in Wilms tumour with diffuse anaplasia [aCGH]
GEO Series GSE60852. Homo sapiens. 32 samples. Type: Genome variation profiling by array.
TP53 ALTERATIONS ASSOCIATE WITH POOR RESPONSE TO LENVATINIB IN PATIENTS WITH ADVANCED THYROID CANCER
<p>This set of raw data cannot be made publicly available as including sensitive information, but might be available to interested researchers upon reasonable requests. Please, forward you request to: l.fugazzola@auxologico.it</p>
Thyroid cancer harboring PTEN and TP53 mutations: A peculiar molecular and clinical case report
<p>To date, the molecular mechanisms that underline aggressiveness and resistance to tyrosine kinase inhibitors in some thyroid carcinomas (TCs) are not known yet. We report the case of a young patient with a metastatic poorly differentiated (PDTC) and follicular thyroid carcinoma (FTC) refractory to conventional therapies and to Sorafenib. The patient, despite an initial partial response, died of progressive disease 21 months after diagnosis. The genetic analysis performed on the primary tumor and on lymph nodes and distant metastases allowed to identify a frameshift mutation (p.P248Tfs*5) in the <em>PTEN</em> gene, never described in TC. This mutation was present in the primary tumor and, with a lower allelic frequency, in metastases diagnosed after treatment with Sorafenib. Mutations in <em>TP53</em> (p.C135Y and c.920-2A>G previously detected in anaplastic carcinomas and p.M133R never found in TC) were also detected in the primary tissue together with a mono-allelic expression of the p.C135Y mutant at RNA level. At metastatic sites level, we found only the <em>TP53</em> splicing mutation c.920-2A>G. The presence of defects in mismatch repair (MMR) proteins and genomic instability was also evaluated. The primary tumor showed a partial expression of MMR proteins together with a strong genomic instability. In conclusion, we demonstrated that the rare combination of somatic <em>PTEN</em> and <em>TP53</em> mutations in a patient with a metastatic FTC, together with the presence of tumor heterogeneity and genomic instability, might be associated with a high tumor aggressiveness and resistance to treatments.</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
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DANDI Archive for NWB datasets
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.