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1,035 results for “cancer invasion”
RNA-seq and CUT&Tag-seq datasets for MDA-MB-231 and MCF-10A cells from: Sp1 mechanotransduction regulates breast cancer cell invasion in engineered viscoelastic extracellular matrices
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Data from: Novel methods to define invasive procedures at the end-of-life were developed to improve quality of end of life care research: A population-based cohort study in colorectal cancer
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All simulation results, figures and code regarding the manuscript: Calibrating models of cancer invasion: parameter estimation using Approximate Bayesian Computation and gradient matching
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Circulating myeloid-derived suppressor cells facilitate invasion of thyroid cancer cells by repressing miR-486-3p
<p>Background: Myeloid-derived suppressor cells (MDSCs) have become increasingly recognized as facilitators of tumor development. However, the role of MDSCs in papillary thyroid carcinoma (PTC) progression has not been clearly explored.</p> <p>Objective: We aimed to evaluate the levels and function of circulating MDSCs in PTC.</p> <p>Methods: The proportion of circulating polymorphonuclear (PMN)-MDSCs and mononuclearMDSCs from patients with PTC or benign thyroid nodules and healthy controls was measured using flow cytometry. For immunosuppressive activity analysis, sorted circulating MDSCs were cocultured with CD3/CD28-costimulated T lymphocytes and the proliferation of T cells was determined. PTC cell lines (TPC-1 and BC-PAP) were cocultured with PMN-MDSCs, and the effects on cell migration, invasion, proliferation, and apoptosis were evaluated. The differential expressed microribonucleic acids (RNAs) and messenger RNAs and their function were also explored in TPC-1 cells cocultured with or without PMN-MDSCs.</p> <p>Results: PMN-MDSCs were increased in peripheral blood mononuclear cells of patients with PTC. Circulating PMN-MDSCs displayed strong T cell suppressive activity. PTC cells demonstrated enhanced invasive capabilities in vitro and in vivo when cocultured with sorted PMN-MDSCs. PMN-MDSCs decreased expression of miR-486-3p and activated nuclear factor kappa B2 (NF-κB2), a direct target of miR-486-3p. Rescue of miR-486-3p diminished the cell migration and invasion induced by PMN-MDSCs.</p> <p>Conclusion: Collectively, our work indicates that circulating PMN-MDSCs promote PTC progression. By suppressing miR-486-3p, PMN-MDSCs promote the activity of the NF-κB2 signaling pathway, resulting in accelerated invasion of PTC cells, which may provide new therapeutic strategies for treatment of thyroid cancer. </p>
Data from: CRISPR-Cas9 mediated CD133 knockout inhibits colon cancer invasion through reduced epithelial-mesenchymal transition
We previously reported that CD133, as a putative cancer stem cell marker, plays an important role in cell proliferation and invasion in colon cancer. To understand the role of CD133 expression in colon cancer, we evaluated the inhibitory effect of CD133 in colon cancer cells. In this study, we generated CD133knockout colon cancer cells (LoVo) using the CRISPR-Cas9 gene editing system. CD133+ colon cancer cells (LoVo) were infected with the lentiviral vector carrying CD133 gRNA and purified cell by culturing single cell colonies. CD133knockout cells was validated by western blot and flow cytometry analysis. In functional study, we observed a significant reduction in cell proliferation and colony formation in CRISPR-Cas9 mediated CD133 knockout cells in compare with control (P < 0.001). We also found the anticancer effect of stattic was dependent on CD133 expression in colon cancer cells. Although CD133knockout cells could not completely block the tumorigenic property, they showed remarkable inhibitory effects on the ability of cell migration and invasion (P < 0.001). In addition, we examined the epithelial mesenchymal transition (EMT)-related protein expression by western blot. The result clearly showed a loss of vimentin expression in CD133knockout cells. Therefore, CRISPR-Cas9 mediated CD133knockout can be an effective treatment modality for CD133+ colon cancer through reducing the characteristics of cancer stem cells.
tRNA-derived fragment tRF-Glu49 inhibits cell proliferation, migration and invasion in cervical cancer by targeting FGL1
<p>A transfer RNA (tRNA)-derived fragment was found to be a new possible biological marker and target in carcinoma therapy. However, the effect exerted by tRFs on cervical carcinoma is still unclear. We identify the potential tumor suppressor gene tRF-Glu49 in cervical carcinoma through tRF and ti-RNA microarray investigation. We then demonstrated that tRF-Glu49 showed downregulation within the cervical carcinoma tissue and was associated with less aggressive clinical features and a better prognosis. Phenotypic studies revealed that tRF-Glu49 inhibited cervical cell proliferation, migration, and invasion processes. Mechanistic investigation revealed that tRF-Glu49 directly regulated the oncogene, fibrinogen-like protein-1 (FGL1). In general, according to the result achieved in this study, tRF-Glu49 can modulate cervical cell proliferation, migration, and invasion processes through the target process for FGL1, and tRF-Glu49 is likely to be a possible prognostic biological marker in patients with cervical carcinoma.</p>
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>
Minimally Invasive Simple Hysterectomy in Low Risk Cervical Cancer
ClinicalTrials.gov study NCT06416748. IPD Sharing: Not stated. Countries: 1. Publications: 3.
HER-2 Pulsed DC Vaccine to Prevent Recurrence of Invasive Breast Cancer Post Neoadjuvant Chemotherapy
ClinicalTrials.gov study NCT02061423. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Digital Breast Tomosynthesis (DBT) to Improve Assessment of Resection Margins in Invasive Breast Cancer
ClinicalTrials.gov study NCT04478669. IPD Sharing: UNDECIDED. Countries: 1. Publications: 12.
Phase II Study of Oral Metformin for Intravesical Treatment of Non-muscle-invasive Bladder Cancer
ClinicalTrials.gov study NCT03379909. IPD Sharing: NO. Countries: 1. Publications: 1.
Efficacy of Durvalumab in Non-muscle-invasive Bladder Cancer
ClinicalTrials.gov study NCT03759496. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Preoperative Intravesical Electromotive Mitomycin-c for Primary Non-muscle Invasive Bladder Cancer
ClinicalTrials.gov study NCT01149174. IPD Sharing: Not stated. Countries: 1. Publications: 1.
S1602: Different Strains of BCG With or Without Vaccine in High Grade Non- Muscle Invasive Bladder Cancer
ClinicalTrials.gov study NCT03091660. IPD Sharing: YES. Countries: 1. Publications: 1.
A Study of Atezolizumab Versus Placebo as Adjuvant Therapy in Participants With High-risk Muscle-invasive Bladder Cancer (MIBC) Who Are ctDNA Positive Following Cystectomy
ClinicalTrials.gov study NCT04660344. IPD Sharing: YES. Countries: 24. Publications: 2.
Sensitivity of Multiparametric MRI in Differentiation Between Muscle Invasive and Non-muscle Invasive Urinary Bladder Cancer
ClinicalTrials.gov study NCT05324033. IPD Sharing: UNDECIDED. Countries: 1. Publications: 18.
Image-guided Minimally Invasive Robotic Surgery Using Preoperative CT Scan for Gastric Cancer Patients
ClinicalTrials.gov study NCT01338948. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Prediction of Upgrade to Invasive Cancer in Patients Diagnosed With Ductal Carcinoma in Situ by Percutaneous Core Needle Biopsy
ClinicalTrials.gov study NCT04498611. IPD Sharing: Not stated. Countries: 1. Publications: 6.
PLZ4-Coated Paclitaxel-Loaded Micelles for the Treatment of Patients With Recurrent or Refractory Non-Muscle Invasive Bladder Cancer
ClinicalTrials.gov study NCT06173349. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Hypofractionated vs. Conventional Regional Nodal Radiation Therapy for Patients With Invasive Breast Cancer
ClinicalTrials.gov study NCT02912312. IPD Sharing: Not stated. Countries: 1. Publications: 2.
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
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.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
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.