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296 results for “TP53”
Single-cell mouse and PC9 data for "TP53 loss with whole genome doubling mediates heterogeneous intra-patient therapy response through Chromosomal Instability"
<p>This repository includes the processed data (including copy number profiles and related analysis) for the E/EP mouse tumors and for the PC9 resistance cell lines for all the analyses of the manuscript "TP53 loss with whole genome doubling mediates heterogeneous intra-patient therapy response through Chromosomal Instability".</p><p>The code for the related analyses is available in GitHub at https://github.com/zaccaria-lab/TP53loss_WGD</p>
Data from: Genome-wide Screens Implicate Loss of Cullin Ring Ligase 3 in Persistent Proliferation and Genome Instability in TP53-Deficient Cells
<p>CSV files of whole-Genome Knockout Screens for Proliferation and Tumorigenic Growth. The data is retrieved from:</p> <p>Title: "Genome-wide Screens Implicate Loss of Cullin Ring Ligase 3 in Persistent Proliferation and Genome Instability in TP53-Deficient Cells"</p> <p>DOI: https://doi.org/10.1016/j.celrep.2020.03.029</p> <p>The excel sheet with data shown in figure 1B is converted to CSV files.</p>
USP8 and TP53 drivers are associated with CNV in a corticotroph adenoma cohort enriched for aggressive tumors
<p><b>Context:</b> Pituitary corticotroph adenomas are rare tumors that can be associated with excess adrenocorticotropic hormone (ACTH) and adrenal cortisol production, resulting in the clinically debilitating endocrine condition Cushing disease. A subset of corticotroph tumors behave aggressively, and genomic drivers behind the development of these tumors are largely unknown.</p> <p><b>Objective</b><strong>:</strong> To investigate genomic drivers of corticotroph tumors at risk for aggressive behavior.</p> <p><b>Design:</b> Whole-exome sequencing of patient-matched corticotroph tumor and normal DNA from a patient cohort enriched for tumors at risk for aggressive behavior.</p> <p><b>Setting:</b> Tertiary care center.</p> <p><b>Patients:</b> 27 corticotroph tumors from 22 patients analyzed. 12 tumors were macroadenomas, of which 6 were silent ACTH tumors, 2 were Crooke's cell tumors, and 1 was a corticotroph carcinoma.</p> <p><b>Intervention:</b> Whole-exome sequencing.</p> <p><b>Main outcome measure:</b> Somatic mutation genomic biomarkers.</p> <p><b>Results:</b> We found recurrent somatic mutations in USP8 and TP53 genes, both with higher allelic fractions than other somatic mutations. These mutations were mutually exclusive, with TP53 mutations occurring only in USP8-wildtype (WT) tumors, indicating they may be independent driver genes. USP8-WT tumors were characterized by extensive somatic copy number variation compared to USP8-mutated tumors. Independent of molecular driver status, we found an association between invasiveness, macroadenomas, and aneuploidy.</p> <p><b>Conclusions: </b>Our data suggest that corticotroph tumors may be categorized into a USP8-mutated, genome-stable subtype versus a USP8-WT, genome-disrupted subtype, the latter of which has a TP53-mutated subtype with high level of chromosome instability. These findings could help identify high risk corticotroph tumors, namely those with widespread CNV, that may need closer monitoring and more aggressive treatment.</p>
RAD54L2 counters TOP2-DNA adducts to promote genome stability (Etoposide treated RPE1 CRISPR screens in TP53 and RAD53L2 knock outs)
<p>The catalytic cycle of topoisomerase 2 (TOP2) enzymes proceeds via a transient DNA double-strand break (DSB) intermediate termed the TOP2 cleavage complex (TOP2cc), in which the TOP2 protein is covalently bound to DNA. Anti-cancer agents such as etoposide operate by stabilising TOP2ccs, ultimately generating genotoxic TOP2-DNA protein crosslinks that require processing and repair. Here, we identify RAD54-like 2 (RAD54L2) as a factor promoting TOP2cc resolution. We demonstrate that RAD54L2 acts through a novel mechanism together with zinc finger protein associated with TDP2 and TOP2 (ZATT/ZNF451) and independent of tyrosyl-DNA phosphodiesterase 2 (TDP2). Our work suggests a model wherein RAD54L2 recognises sumoylated-TOP2 and, using its ATPase activity, promotes TOP2cc resolution and prevents DSB exposure. These findings suggest RAD54L2-mediated TOP2cc resolution as a potential mechanism for cancer-therapy resistance and highlight RAD54L2 as an attractive candidate for drug discovery.</p>
BAM files of wild-type CP-A cells and the TP53 KO CP-A clones.
<p>BAM files (alignment to hg38) of wild-type CP-A cells and the TP53 knock-out (KO) CP-A clones (2c8, 3d2, 5f4). Please refer to Figure 2. of <span>doi:</span> https://doi.org/10.1101/2024.01.24.576991.</p>
(SNP Array) Single-Cell Multi-Omics Identifies Chronic Inflammation as a Driver of TP53 mutant Leukaemic Evolution
<p>Single nucleotide polymorphism (SNP) array data files related our publication titled "Single-Cell Multi-Omics Identifies Chronic Inflammation as a Driver of <em>TP53 </em>mutant Leukaemic Evolution".</p>
TP53 synthetic genomics data for benchmarking variant callers
<p>This is a synthetic genomics dataset generated with <a href="https://github.com/ncsa/NEAT">NEAT </a> for the gene TP53 for the use case of benchmarking somatic variant callers. The reports for all bam files where created using <a href="https://github.com/genome/bam-readcount">bam-readcount</a>.</p> <p>To find out more about our pipeline please visit <a href="https://github.com/BiodataAnalysisGroup/synth4bench">the Biodata Analysis Group GitHub</a> and also our <a href="https://biodataanalysisgroup.github.io/">GitHub page</a> :)</p>
Study of Magrolimab in Combination With Azacitidine Versus Physician's Choice of Venetoclax in Combination With Azacitidine or Intensive Chemotherapy in Patients With TP53 Mutant Acute Myeloid Leukemi
ClinicalTrials.gov study NCT04778397. IPD Sharing: NO. Countries: 15. Publications: 2.
Exploiting Pathogenic Tp53 Mutation for Early Diagnosis of Ovarian Cancer by Mean of Papanicolau Test
ClinicalTrials.gov study NCT04812938. IPD Sharing: YES. Countries: 1. Publications: 18.
APR-246 in Combination With Venetoclax and Azacitidine in TP53-Mutant Myeloid Malignancies
ClinicalTrials.gov study NCT04214860. IPD Sharing: NO. Countries: 1. Publications: 1.
Berzosertib and Irinotecan in Treating Patients With Progressive, Metastatic, or Unresectable TP53 Mutant Gastric or Gastroesophageal Junction Cancer
ClinicalTrials.gov study NCT03641313. IPD Sharing: YES. Countries: 1. Publications: 1.
Li-Fraumeni & TP53 (LiFT UP): Understanding and Progress
ClinicalTrials.gov study NCT04541654. IPD Sharing: YES. Countries: 1. Publications: 1.
Phase 1b/2 Safety and Efficacy of APR-246 w/Azacitidine for tx of TP53 Mutant Myeloid Neoplasms
ClinicalTrials.gov study NCT03072043. IPD Sharing: Not stated. Countries: 1. Publications: 1.
APR-246 in Combination With Azacitidine for TP53 Mutated AML (Acute Myeloid Leukemia) or MDS (Myelodysplastic Syndromes) Following Allogeneic Stem Cell Transplant
ClinicalTrials.gov study NCT03931291. IPD Sharing: Not stated. Countries: 1. Publications: 1.
RAD54L2 counters TOP2-DNA adducts to promote genome stability (Etoposide treated RPE1 CRISPR screens in TP53 and RAD53L2 knock outs)
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Assessment of clinical outcomes with immune checkpoint inhibitor therapy in melanoma patients with CDKN2A and TP53 pathogenic mutations
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USP8 and TP53 drivers are associated with CNV in a corticotroph adenoma cohort enriched for aggressive tumors
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Bispecific antibodies and CAR T cells targeting a TP53 mutation-associated neoantigen show discordant affinity requirements
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Single-nucleus Transcriptomics of IDH1- and TP53-mutant Glioma Stem Cells Displays Diversified Commitment on Highly Invasive Cancer Progenitors
<p><strong>Fig. S1</strong>. <strong>Marker genes for Seurat clusters.</strong> (<strong>A</strong>) distribution of marker genes for cluster 0 on the 2D-UMAP space. (<strong>B</strong>) distribution of marker genes for cluster 1 on the 2D-UMAP space. (<strong>C</strong>) distribution of marker genes for cluster 2 on the 2D-UMAP space. (<strong>D</strong>) distribution of marker genes for cluster 3 on the 2D-UMAP space. (<strong>E</strong>) distribution of marker genes for cluster 4 on the 2D-UMAP space. (<strong>F</strong>) distribution of marker genes for cluster 5 on the 2D-UMAP space. (<strong>G</strong>) Stuck violin plot of marker gene expression for Seurat clusters (bottom panel) and their annotation (right side panel). The violin shape displays the number of the cells expressing a gene, the continuous color panel defines median expression value of a gene from the absence of expression (white) to high expression (dark blue).</p> <p><strong>Fig. S2</strong>. <strong>Expression of genes marking cell malignization.</strong> (<strong>A</strong>) expression of collagens in Surat clusters (bottom panel) (<strong>B</strong>) expression of genes linked to Migration and ECM in Surat clusters (bottom panel) (<strong>C</strong>) expression of genes classified as Proto-oncogenes in Surat clusters (bottom panel). The violin shape displays the number of the cells expressing a gene, the violin color defines the Seurat cluster. Gene expression displayed in log-transformed normalized expression values.</p> <p><strong>Fig. S3</strong>. <strong>Expression of genes involved in proliferation and survival of cancer cells.</strong> (<strong>A</strong>) Genes involved in Wnt-pathway in Surat clusters (bottom panel). (<strong>B</strong>) Genes involved in Akt-pathway in Surat clusters (bottom panel). (<strong>C</strong>) Genes inducing resistance to cancer therapeutics in Surat clusters (bottom panel). The violin shape displays the number of the cells expressing a gene, the violin color defines the Seurat cluster. Gene expression displayed in log-transformed normalized expression values.\</p> <p><strong>Fig. S4</strong>. <strong>Expression of genes marking CSC profile.</strong> (<strong>A</strong>) Ion channel genes in Surat clusters (bottom panel). (<strong>B</strong>) Antioncogenes in Surat clusters (bottom panel). <strong>C</strong>. Stem-cell genes in Surat clusters (bottom panel). (<strong>D</strong>) Antiapoptotic genes in Surat clusters (bottom panel). The violin shape displays the number of the cells expressing a gene, the violin color defines the Seurat cluster. Gene expression displayed in log-transformed normalized expression values.</p> <p><strong>Fig. S5</strong>. <strong>Genes differentially expressed between UMAP clusters</strong>. (<strong>A</strong>) Heatmap for wt-GSCs. (<strong>B</strong>) Heatmap for mt-GSCs. Upper colour panel in the heatmap designates Seurat clusters. Gene expression is indicated by continuous colour panel starting from the most downregulated (blue) to the most upregulated (red).</p> <p><strong>Fig. S6</strong>. <strong>Marker genes defying cell annotations</strong>. (<strong>A</strong>) Stack violin plot displays marker gene expression in wt-GSC clusters. (<strong>B</strong>) Stack violin plot displays marker gene expression in mt-GSC clusters. Genes grouped by cell annotations (side description) and UMAP clusters (down column bar). The violin shape displays the number of the cells expressing a gene, the continuous color panel defines median expression value of a gene from the absence of expression (white) to high expression (dark blue).</p> <p><strong>Fig. S7</strong>. <strong>Differentially expressed proliferation and adhesion pathways comparing mutant samples to wild type.</strong> (<strong>A</strong>) ERBB signalling pathway. (<strong>B</strong>) Wnt signalling pathway. (<strong>C</strong>) Genes linked to Focal adhesion. (<strong>D</strong>) Genes classified as Cell adhesion molecules. Red rectangles display upregulated genes (proteins), green rectangles define downregulated genes (proteins). Pictures obtained by KEGG pathview.</p> <p><strong>Table S1. Glioma genotyping primers</strong></p> <p><strong>Table S2. Smart-seq2 Primers</strong></p>
(Preprocessing) Single-Cell Multi-Omics Identifies Chronic Inflammation as a Driver of TP53 mutant Leukaemic Evolution
<p>Files and scripts for preprocessing of dataset related to our publication titled "Single-Cell Multi-Omics Identifies Chronic Inflammation as a Driver of <em>TP53 </em>mutant Leukaemic Evolution".</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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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.
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