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2,435 results for “Metastasis”
Data set related to "Secretory and metabolic determinants of brain metastasis"
<p>This repository includes the data sets related to the publication titled "Secretory and metabolic determinants of brain metastasis"</p>
A cellular hierarchy in melanoma uncouples growth and metastasis
<p>Although melanoma is notorious for its high degree of heterogeneity and plasticity<sup>1,2</sup>, the origin and magnitude of cell state diversity remains poorly understood. Equally, it is not known whether melanoma growth and metastatic dissemination are supported by overlapping or distinct melanoma subpopulations. By combining mouse genetics, unbiased lineage tracing and quantitative modelling, single-cell and spatial transcriptomics, we provide evidence of a hierarchical model of tumour growth that mirrors the cellular and molecular logic underlying embryonic neural crest cell fate specification and differentiation. Our findings indicate that tumorigenic competence is associated with a spatially localized perivascular niche environment, a phenotype acquired through a NOTCH3-dependent intercellular communication pathway established by endothelial cells. Consistent with a model in which only a fraction of melanoma cells is fated to fuel growth, temporal single-cell tracing of a population of melanoma cells harbouring a mesenchymal-like state revealed that these cells do not contribute to primary tumour growth but, instead, constitutes a pool of metastatic-initiating cells that can switch cell identity while disseminating to secondary organs. Our data provide a spatially and temporally resolved map of the diversity and trajectories of cancer cell states within the evolving melanoma ecosystem and suggest that the ability to support growth and metastasis are limited to distinct pools of melanoma cells. The observation that these phenotypic competencies can be dynamically acquired upon exposure to specific niche signals warrant the development of therapeutic strategies that interfere with the cancer cell reprogramming activity of such microenvironmental cues.</p>
Dataset related to article "The soluble glycoprotein NMB (GPNMB) produced by macrophages induces cancer stemness and metastasis via CD44 and IL-33"
<p>This record contains data related to article “The soluble glycoprotein NMB (GPNMB) produced by macrophages induces cancer stemness and metastasis via CD44 and IL-33"</p> <p> </p> <p>Abstract</p> <p>In cancer, myeloid cells have tumor-supporting roles. We reported that the protein GPNMB (glycoprotein nonmetastatic B) was profoundly upregulated in macrophages interacting with tumor cells. Here, using mouse tumor models, we show that macrophage-derived soluble GPNMB increases tumor growth and metastasis in Gpnmb-mutant mice (DBA/2J). GPNMB triggers in the cancer cells the formation of self-renewing spheroids, which are characterized by the expression of cancer stem cell markers, prolonged cell survival and increased tumor-forming ability. Through the CD44 receptor, GPNMB mechanistically activates tumor cells to express the cytokine IL-33 and its receptor IL-1R1L. We also determined that recombinant IL-33 binding to IL-1R1L is sufficient to induce tumor spheroid formation with features of cancer stem cells. Overall, our results reveal a new paracrine axis, GPNMB and IL-33, which is activated during the cross talk of macrophages with tumor cells and eventually promotes cancer cell survival, the expansion of cancer stem cells and the acquisition of a metastatic phenotype.</p> <p> </p>
Identification of intratumoral bacteria that enhance breast tumor metastasis
<p>This file contains the supporting datasets for the manuscript entitled Identification of intratumoral bacteria that enhance breast tumor metastasis, by Gerbec et al. File includes 8 supporting datasets as well as a legend file with the description of each individual dataset.</p>
Supplementary Figures, Files and Datasets: Reduction of Metastasis via Epigenetic Modulation in a Murine Model of Metastatic Triple Negative Breast Cancer (TNBC)
<p>*denotes authors contributed equally to this work</p> <p>FileS1_Figures_Proofread.pdf: (Updated) Supplementary Figures (Figure S1: RNA-sequencing experimental design; Figure S2: Experiments measuring proliferation between drug-treated and control conditions indicate no significant difference 6 hrs. after scratch; Figure S3: Effect of 4SC-202 treatment on 4T1 tumor volume in mice; Figure S4: Differential expression between 4SC-202- and Vorinostat-treated 4T1 tumors; Figure S5: Top underexpressed differentially expressed genes 4SC-202 vs Control; Figure S6: HDACi target genes are not differentially expressed in RNA-sequencing data from 4SC-202-treated mice relative to control mice; Figure S7: Differential expression and expression of genes implicated gene ontology biological processes of interest; Figure S8: IPA visualization of the Regulation of Epithelial Mesenchymal Transition By Growth Factors Pathway emphasizing influence of 4SC-202-induced consensus DEGs; Figure S9: 4SC-202 modulates gene networks related to Cancer, Endocrine System Disorders, and Organismal Injury and Abnormalities; Figure S10: 4SC-202 modulates gene networks related to Cancer, Cellular Movement, and Organismal Injury and Abnormalities; Figure S11: 4SC-202 modulates gene networks related to Cell-mediated Immune Response, Cellular Movement, and Hematological System Development and Function; Figure S12: 4SC-202 differentially modulates gene networks related to Cellular Movement, Hematological System Development and Function, and Immune Cell Trafficking relative to Vorinostat); File S2: DAVID 4SC vs. Control 70DEG results: DAVID Annotation 4SC-202 vs Control 70 DEGs: Full functional annotation clustering results from DAVID Bioinformatics Resource for the 4SC-202-induced, consensus differentially expressed genes.; File S3: DAVID 4SC vs. Vori 33 DEGs results: DAVID Annotation 4SC-202 vs Control 33 DEGs: Full functional annotation clustering results from DAVID Bioinformatics Resource for the 4SC-202 versus Vorinostat consensus differentially expressed genes.; File S4: IPA 70 All Results: IPA Canonical Pathways Enrichment 70 DEGs: Full Ingenuity Pathway Analysis (IPA) canonical pathways enrichment results for the 4SC-202-induced, consensus differentially expressed genes.; File S5: IPA 33 Summary: Ingenuity Pathway Analysis (IPA) summary of the enrichment results for the 4SC-202-induced, consensus differentially expressed genes against Vorinostat.; File S6: Experiment RIN Numbers: RNA extraction quality control step, one of the various steps of quality control within the RNA-sequencing workflow. These RNA Integrity numbers are from the Agilent 2100 Bioanalyzer that looks for RNA contamination and degradation.; File S7: 4SC vs. Control all DEGs: Workflow results including all DEGs for 4SC-202 vs Control: Full excel file that contains all of the DEGs from the results of all workflows for 4SC-202.</p>
Landscape of Bone Marrow Metastasis in Human Neuroblastoma Unraveled by Transcriptomics and Deep Multiplex Imaging
<p>MELC (Multi-epitope ligand cartography) multiplex imaging data of our neuroblastoma cohort supporting the publication " Landscape of Bone Marrow Metastasis in Human Neuroblastoma Unraveled by Transcriptomics and Deep Multiplex Imaging". The zip folders contain raw image data of one to four fields of view (FoV). The folder "RoI" contains the masks of user-selected regions. "marker_status.csv" is used for normalization with RESTORE. "MELC_single_cell_data.csv" contains the normalized single-cell data with cell type assignments.</p>
Data from: Identification of a minority population of LMO2+ breast cancer cells that integrate into the vasculature and initiate metastasis.
<p>Metastasis is responsible for the majority of breast cancer-related deaths, however, identifying the cellular determinants of metastasis has remained challenging. Here, we identified a minority population of immature THY1+/VEGFA+ tumor epithelial cells in human breast tumor biopsies that display angiogenic features and are marked by the expression of the oncogene, LMO2. Higher abundance of LMO2+ basal cells correlated with tumor endothelial content and predicted poor distant recurrence-free survival in patients. Using MMTV-PyMT/Lmo2CreERT2 mice, we demonstrated that Lmo2 lineage-traced cells integrate into the vasculature and have a higher propensity to metastasize. LMO2 knockdown in human breast tumors reduced lung metastasis by impairing intravasation, leading to a reduced frequency of circulating tumor cells. Mechanistically, we find that LMO2 binds to STAT3 and is required for STAT3 activation by TNFα and IL6. Collectively, our study identifies a population of metastasis-initiating cells with angiogenic features and establishes the LMO2-STAT3 signaling axis as a therapeutic target in breast cancer metastasis.</p>
FALP Radiology Reports: Annotated corpus for distant metastasis detection
<p>A critical task in oncology is extracting information related to cancer metastasis from electronic health records. Metastasis-related information is crucial for planning treatment, evaluating patient prognoses, and conducting cancer research. Unfortunately, findings of distant metastasis are written in radiology reports, often unstructured, making it difficult to extract relevant information automatically. In this study, we created a manually annotated clinical corpus using radiology reports of prostate, colorectal, and breast cancer patients. We developed a named entity recognition model to capture entities of distant metastasis. The entities were subsequently employed in automatically classifying the reports according to the presence or absence of metastasis. The NER model detected distant metastasis mentions with a weighted average F1 score performance of 0.84. Whole reports were finally classified with an F1 score of 0.92 for documents without distant metastasis (M0) and 0.90 for documents with distant metastasis (M1). These results show the model's usefulness in detecting distant metastasis entities in three different types of cancer and the consequent classification of reports.</p> <p>The manually annotated corpus (FALP Radiology Reports Corpus) and annotation guidelines are freely released to the research community.</p> <p>We are releasing the dataset in 2 formats:</p> <ol> <li>conll_files.zip: Contains the annotated corpus in IOB2 format. This corpus is separated into train, text, and development subsets.</li> <li>text_ann_files.zip: Contains the raw text files for each document along with its annotation file in Standoff format</li> </ol> <p>Annotation guidelines can be found in:</p> <p>Ricardo Ahumada, Pablo Báez, Gisselle Caamaño, Jocelyn Garay, & Inti Paredes. (2023). Annotation Guidelines for FALP radiology reports annotated corpus for distant metastasis detection (1.1). Zenodo. https://doi.org/10.5281/zenodo.7623509</p> <p>This work is licensed under the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. To view a copy of this license, visit <a href="http://creativecommons.org/licenses/by-nc-sa/4.0/">http://creativecommons.org/licenses/by-nc-sa/4.0/</a>.</p>
Understanding and leveraging phenotypic plasticity during metastasis formation - Dataset
<p>This repo contains the dataset from the manuscript "Understanding and leveraging phenotypic plasticity during metastasis formation" by Shah et al. This repo contains `.npy`, `numpy.ndarray` files created by the Python software package NumPy. Please see the `README.md` in the code repository (https://doi.org/10.5281/zenodo.7989748) for installation and usage.</p>
Supporting data for "Dissecting the cellular architecture of neuroblastoma bone marrow metastasis using single-cell transcriptomics and epigenomics unravels the role of monocytes at the metastatic niche"
<p>This data repository contains several datasets supplementing the paper “Dissecting the cellular architecture of neuroblastoma bone marrow metastasis using single-cell transcriptomics and epigenomics unravels the role of monocytes at the metastatic niche” by Fetahu, Esser-Skala, Dnyansagar et al. (2023).</p> <ul> <li>HOMER_Results.zip: detailed results of the HOMER analysis</li> <li>nblast_scopen_gene_activity_normalized_motifs_added.rds: Seurat object with scATAC-seq data</li> <li>snp_array.tgz: SNP array data</li> <li>R_data_generated.tgz: Files generated by the scRNA-seq analysis scripts in the GitHub repository associated with the publication.</li> </ul>
MALDI-IMS files of 53 experiments over sections of nevus, primary melanoma and melanoma metastasis in imzml format
<p>MALDI-IMS files of 53 experiments over sections of nevus, primary melanoma and melanoma metastasis in imzml format. The experiments were recorded in negative-ion mode with a MALDI LTQ-orbitrap XL (ThermoFisher) at 25 um/pixel of spatial resolution. We also uploaded three .ppt with a comparison between the eosin-hematoxilin images, the IHC (MelanA and HMB45) and the segmentation images</p>
Data from: Identification of a minority population of LMO2+ breast cancer cells that integrate into the vasculature and initiate metastasis.
Open the record for dataset details and reuse information.
miR-145-5p mimic inhibits bone metastasis of prostate cancer via the regulation of epithelial mesenchymal transition
<p><strong>Background.</strong> The bone is the most common site of distant metastasis in prostate cancer. However, treatments for the bone metastasis of prostate cancer remain unsatisfactory. MicroRNAs (miRNAs) are small noncoding RNAs that play a variety of critical roles in tumor development and progression. Studies have confirmed that miRNA mimics could regulate the response to therapy in many cancers. <strong>Methods.</strong> In this study, a set of forty-four miRNAs were reduced in prostate cancer patients with bone metastases by high-throughput sequencing analysis. Wound healing and transwell assays and western blotting analysis were used to explore the role of miRNA mimic in prostate cancer bone metastasis.<strong> Results.</strong> These mimics of down-regulated miRNAs may be able to cure prostate cancer bone metastasis, including hsa-miR-221-3p, hsa-miR-222-3p, hsa-miR-133a-3p, hsa-miR-222-5p, hsa-miR-204-3p, hsa-miR-145-5p, hsa-miR-3681-5p, hsa-miR-184, hsa-miR-144-3p, hsa-miR-204-5p, and hsa-miR-221-5p. To further investigate the role of these miRNA mimics on prostate cancer bone metastasis, miR-145-5p was randomly selected for validation. Bioinformatics analysis showed that miR-145-5p target genes significantly affected TGF-beta signaling pathway. Wound healing and transwell assays and western blotting analysis revealed that miR-145-5p mimic inhibited proliferation, migration and invasion. Importantly, miR-145-5p mimic increased the expression of E-cadherin and reduced the expression of matrix metalloproteinase 2 and 9. These results revealed that miR-145-5p mimic mediated epithelial mesenchymal transition. Meanwhile, miR-145-5p mimic enhanced the level of caspase 9, which is an important promoter of apoptosis. These results indicate that miR-145-5p mimic could inhibit the progress of prostate cancer bone metastasis via regulation of epithelial mesenchymal transition. In addition, miR-145-5p mimic could induce the apoptosis of prostate cancer cells with bone metastases. In summary, the miR-145-5p mimic is expected to become a novel strategy for the treatment of tumor metastasis.</p>
Leptomeningeal metastasis from Adrenocortical carcinoma: a case report
<p>Adrenocortical carcinoma (ACC) is an uncommon endocrine malignancy with limited treatment options. While overall 5-year survival rate in patients with ACC is 35%, the disease is often rapidly progressive with long-term survival in only 5% of patients. Although tumor stage, grade and excess hormonal activity predict unfavorable prognosis, additional biomarkers are needed to identify patients with aggressive disease.</p> <p>A 23-year-old woman presented with rapidly progressing signs and symptoms of Cushing's syndrome, with associated abdominal pain and fullness. Evaluation revealed a large left adrenal mass which had developed over 8 months. En bloc surgical resection was performed by an endocrine surgeon, and pathology revealed adrenocortical carcinoma with Ki67 of 60%. Despite adjuvant treatment with mitotane and etoposide-doxorubicin-carboplatin chemotherapy, the patient had rapid disease progression with metastatic spread to liver, lung, bone, brain and leptomeningies and she died eleven months after the initial diagnosis. Subsequent analysis of patient's tumor revealed mutations in TP53 and MEN1. RNA sequencing was compared against the The Cancer Genome Atlas data set and clustered with the high steroid, proliferative subtype, associated with the worst prognosis. The tumor also demonstrated a low BUB1B/PINK1 ratio as well as G0S2 hypermethylation, both predictive of very aggressive ACC.</p> <p>This case represents a subset of ACC characterized by rapid and fatal progression. Clinically available predictors as well as recently reported molecular signatures and biomarkers correlated with this tumor's aggressiveness, suggesting that development and validation of combinations of biomarkers may be useful in guiding personalized approaches to patients with ACC.</p>
Aneuploid embryonic stem cells drive teratoma metastasis: source data
<h3>The dataset of "<strong>Aneuploid embryonic stem cells drive teratoma metastasis</strong>"</h3><p>1. Pathway enrichment of scRNA-seq.csv: a table containing the pathway enrichment results. (<strong>Supplementary fig10 d</strong>)</p><p>2. Bulk_RNA_processed.RDS: a Seurat object containing the results of bulk RNA-seq. (<strong>Supplementary fig11 h-l</strong>)</p><p>3. Relative cell abundance of ES captured by scRNA-seq.csv: A table containing the relative abundance of ES sub-populations in all ES cells for each sample. (<strong>fig5 c</strong>)</p><p>4. WES_out.RDS: an R object containing the results of WES processed by maftools. (<strong>fig2 b-g</strong>)</p><p>5. bulk_RNA_raw_matrix.RDS: an R object containing the raw count matrix of bulk RNA-seq samples. (<strong>Supplementary fig11 h-l</strong>)</p><p>6. scRNA-seq DEGs -- ES_stem vs. ES_Ori(WT).csv: a table containing the results of DEG analysis. (<strong>fig5 f</strong>)</p><p>7. scRNA-seq DEGs -- ES_stem vs. ES_Ori(AC).csv: a table containing the results of DEG analysis. (<strong>fig5 f</strong>)</p><p>8. pseudo time DEGs of scRNA-seq.csv: DEGs that change as ES differentiation. (<strong>fig5 e</strong>)</p><p>9. scRNA-seq_meta_info.tsv.gz: the meta information of scRNA-seq data. (<strong>fig5 and Supplementary fig10</strong>)</p><p>10. scRNA-seq_raw_matrix.mtx.gz: the raw count matrix of scRNA-seq data. (<strong>fig5 and Supplementary fig10</strong>)</p>
Inhibition of DKK-1 Limits Osteosarcoma Metastasis in a Clinically Relevant Mouse Model
<p>Single-cell RNA-seq data of untreated (F43N, F43R) and DKK-1 inhibitor treated (OSW3, OSW4, OSW5, OSW6) patient derived xenografts (PDXs). </p> <p>human_cells_scanpy_object.h5ad -- contains Scanpy analysis of human cells from untreated and DKK-1 inhibitor treated PDXs</p> <p>raw_counts_cellranger_output.zip -- contains the raw expression counts of untreated and DKK-1 inhibitor treated PDXs cells outputted by CellRanger. </p>
BAF155 Methylation Drives Metastasis By Hijacking Super-enhancers and Subverting Anti-tumor Immunity
<p>Subunits of the chromatin remodeler SWI/SNF are the most frequently disrupted genes in cancer. However, how post-translational modifications (PTM) of SWI/SNF subunits elicit epigenetic dysfunction remains unknown. Arginine-methylation of BAF155 by coactivator-associated arginine methyltransferase 1 (CARM1) promotes triple negative breast cancer (TNBC) metastasis. Herein, we discovered the dual roles of methylated-BAF155 (me-BAF155) in promoting tumor metastasis: activation of super-enhanceraddicted oncogenes by recruiting BRD4, and repression of interferon / pathway genes to suppress host immune response. Pharmacological inhibition of CARM1 and BAF155 methylation not only abrogated the expression of an array of oncogenes, but also boosted host immune responses by enhancing the activity and tumor infiltration of cytotoxic T cells. Moreover, strong me-BAF155 staining was detected in circulating tumor cells from metastatic cancer patients. Despite low cytotoxicity, CARM1 inhibitors strongly inhibited TNBC cell migration in vitro, and growth and metastasis in vivo. These findings illustrate a unique mechanism of arginine methylation of a SWI/SNF subunit that drives epigenetic dysregulation, and establishes me-BAF155 as a therapeutic target to enhance immunotherapy efficacy.</p>
Recurrence and metastasis detection of breast cancer
<p>This dataset includes 88 H&E stained whole slide images (WSI) of breast cancer downloaded from TCGA (<a href="https://portal.gdc.cancer.gov/repository/">https://portal.gdc.cancer.gov/repository/</a>) with the type of Formalin-Fixed Paraffin-Embedded (FFPE), of which 5 cases have recurrence or metastasis.</p>
H&E colorectal lymph node metastasis nuclei dataset
<p>H&E colorectal lymph node metastasis nuclei dataset (neoplastic/non-neoplastic, 224x224 pixels at 40x magnification)</p> <p>This description will be updated soon.</p>
Dataset of High-Resolution Micro-CT Imaging of Tumor Invasion and Metastasis in a Murine Esophageal Cancer PDX Model
<p>This dataset features high-resolution micro-CT imaging data capturing the progression of tumor invasion and metastasis in an orthotopic patient-derived xenograft (PDX) model of esophageal cancer. Using contrast-enhanced micro-CT, we visualized detailed patterns of tumor invasion, including budding, multicellular streaming, and expansive growth, across multiple abdominal organs such as the stomach, pancreas, liver, and spleen. The dataset includes two specimens, highlighting both the primary tumor site and extensive metastases throughout the abdominal cavity. Our imaging preserved the native tissue architecture, providing a unique three-dimensional view of tumor-host interactions. This collection offers valuable insights for researchers studying the dynamics of esophageal cancer invasion and metastasis. Detailed descriptions of the micro-CT scanning parameters, image analysis, and sample preparation are provided within the dataset archive.</p>
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.