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3,514 results for “cell therapy”
RNA datasets to derive predictors for immune checkpoint inhibitor therapy of non-small cell lung cancer
<p>Nanostring nCounter datasets and corresponding clinical data of tumor samples of patients with advanced NSCLC who received anti-PD-1 immuntherapy. Prospectively divided into a discovery and a validation cohort.</p> <p>Please cite the corresponding publication in Annals of Oncology (10.1093/annonc/mdz049)</p>
Backpain exercise therapy remodels human epigenetic profiles in buccal and human peripheral blood mononuclear cells: An exploratory study in young male participants
<pre><strong>###### Files description #####</strong><br> <strong>Notes</strong>. 1) "BT" refers to before therapy and "AT" to after therapy. 2) 0 refers to FALSE and 1 to TRUE for binary variables. The provided files have tab-separated columns except the .RDS which is and R output of the mixOmics DIABLO integration analysis. <strong># Questionnaire</strong> > participants_categories.tsv: per participant (rows), output of the clustering with the participant ("ID") category ("category") per class<br> ("class") > questionnaire_agility_metrics.tsv: questionnaire and agility metrics per participant (rows) for the participants ("ID") with at least one paired AT+BT data in one type of biological sample (indicated in the columns "swab", "PBMC", and "plasma") <strong># PTMs</strong> Samples´ names are encoded as PBMC_AT_8_batch1, i.e. cells origin_time upon therapy_ID_batch (we removed _batch column suffix for the <br>processed files). NA indicates an undetected intensity. > raw_PBMC_light_labelled_intensities.tsv: raw intensity of light/endogenous peptides (row) by precursor per sample (column) from PBMC > raw_swab_light_labelled_intensities.tsv: idem from buccal cells > raw_PBMC_heavy_labelled_intensities.tsv: raw intensity of light/endogenous peptides (row) by precursor per sample (column) from PBMC > raw_swab_heavy_labelled_intensities.tsv: idem from buccal cells > raw_PBMC_heavynormalized_intensities.tsv: raw intensity of light peptides normalized by heavy peptides intensity (row) by precursor per <br>sample (column) > raw_swab_heavynormalized_labelled_intensities.tsv: idem from buccal cells > processed_cleaned_PBMC_log2intensities.tsv: processed (heavy normalized, imputed, batch-corrected) intensity of peptides aggregated by modification (PTM, row) by precursor per sample (column) after log2-transformation. The relative abundances are computed from this file. Rows without me/ac suffix represents the amount of unmodified peptide for the considered site. > processed_cleaned_swab_log2intensities.tsv: idem from buccal cells > rel_abundance_PTM_PBMC.tsv: relative abundance computed per precursor, e.g. for a given sample, the H3_K4+H3_K4me1+H3_K4me2+H3_K4me3 <br>relative abundance values must sum to 100, with the relative abundance of H3_K4 representing the absence of modified K4. > rel_abundance_PTM_swab.tsv: idem from buccal cells > tests_from_rel_abundance_PTM_swab_PBMC.tsv: per type of samples ("Sample.origin", i.e.swab of PBMC) and per PTM (rows, "PTM"), report <br>the output of classic (p-values, adjusted with Benjamini-Hochberg (BH), or Benjamini-Yekutieli procedure (BY), from raw and arcsin square <br>root transformed percentage) and PLS-DA tests (VIP - Variable Importance score - and its 95% confidence interval). The percentage of change<br>of each PTM after therapy relative tobefore therapy is reported in "perc_change.AT.over.BT" column. The "is_candidate" indicates if the PTM has been considered as a hit in the swab or PBMC. <strong># Plasma</strong> Samples´ names are encoded as PLASMA_AT_8_batch1, i.e. cells origin_time upon therapy_ID_batch. NA indicates an undetected intensity. > raw_plasma_maxquant_log2ibaq_intensities.tsv: raw data from protein group MaxQuant file. The iBAQ columns are used in later steps. > processed_cleaned_plasma_log2intensities.tsv: processed (imputed, batch-corrected) intensity of protein groups after log2-transformation. > tests_from_intens_plasma.tsv: per protein group ("Proteins.ID"), report the output of classic (p-values, adjusted Benjamini-Hochberg (BH),<br>or Benjamini-Yekutieli procedure (BY), from log2-transformed intensities) and PLS-DA tests (VIP and its 95% confidence interval). The log2 <br>fold change after therapy relative to before therapy is reported in "log2FC.AT.over.BT" column. The "is_candidate" indicates if the protein group has been considered as a hit. <strong># Integration</strong> > circos_input: output of DIABLO analysis with correlation threshold set to 0.7. Use the readRDS R function to open.</pre> <p> </p>
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>
Safety and Efficacy of Mesenchymal Stromal Cells Mitochondria Transplantation as a Cell-Free Therapy for Osteoarthritis
<p><strong><span>Abstract</span></strong></p> <p><strong><span>Objective</span></strong></p> <p><span>The inflammatory responses from synovial fibroblasts and macrophages</span><span> and the mitochondrial dysfunction in chondrocytes<span> leading to oxidative stress, disrupt extracellular matrix (ECM) homeostasis</span> and accelerate the deterioration process of articular cartilage<span> in osteoarthritis (OA).<span> </span>In the last years, it has been proposed that mesenchymal stromal cells (MSC) transfer their functional mitochondria to damaged cells in response to cellular stress, becoming one of the mechanisms underpinning their therapeutic effects. </span>Therefore, we hypothesize that a novel cell-free treatment for OA could involve direct mitochondria transplantation, leading to the restoration of both cellular and mitochondrial homeostasis.</span></p> <p><strong><span>Methods</span></strong></p> <p><span>Mitochondria<span> were isolated from Umbilical Cord (UC)-MSC (Mito-MSC) and characterized based on their morphology, phenotype, functions, and their ability to be </span>internalized by <span>different articular cells. Furthermore, </span>the transcriptional changes following mitochondrial uptake by chondrocytes were evaluated using an Affymetrix analysis, Lastly, <span>the dose dependance therapeutic efficacy, biodistribution and immunogenicity of Mito-MSC w</span>ere assessed<span> in vivo, </span>through an intra-articular injection <span>in male C57BL6 mice in a </span>collagenase-induced OA <span>(CIOA) </span>model.</span></p> <p><strong><span>Results</span></strong></p> <p><span>Our findings demonstrate the functional integrity of Mito-MSC and their ability to be efficiently <span>transferred into chondrocytes, synovial macrophages, and synovial fibroblasts. </span>Moreover, the transcriptomic analysis showed the upregulation of genes involved in stress such as DNA reparative machinery and<span> inflammatory antiviral responses</span>.<span> </span>Finally, <span>Mito-MSC transplantation </span>yielded significant reductions<span> in joint mineralization, </span>a hallmark of OA progression<span>, </span>as well as improvements in OA-related histological signs, with the lower dose exhibiting better therapeutic efficacy. <span><span> </span></span>Furthermore, Mito-MSC were detected within the knee joint for up to 24 hours post-injection without eliciting an inflammatory response in CIOA mice. </span></p> <p><strong><span>Conclusion</span></strong></p> <p><span><span> </span>Collectively, our results reveal that mitochondria derived from MSC are transferred to key articular cells and are retained in the joint without generating an inflammatory immune response mitigating articular cartilage degradation in OA, probably through a restorative effect trigger by the stress antiviral response within OA chondrocytes.</span></p>
Associated code and data for "Multi-level computational modeling of anti-cancer dendritic cell vaccination utilized to select molecular targets for therapy optimization (doi: 10.3389/fcell.2021.74635)"
<p>This deposit contains the data, code, and analysis to reproduce the results in the manuscript - Lai X, Keller C, Santos-Rosales G, Schaft N, Dörrie J, Vera J. Multi-level computational modeling of anti-cancer dendritic cell vaccination utilized to select molecular targets for therapy optimization. Frontiers in Cell and Developmental Biolology. 2022; 9:746359; <a href="https://www.researchgate.net/publication/358461035_Multi-Level_Computational_Modeling_of_Anti-Cancer_Dendritic_Cell_Vaccination_Utilized_to_Select_Molecular_Targets_for_Therapy_Optimization">doi:10.3389/fcell.2021.746359</a>.</p> <p>If you have used the code for your research, please cite the original publication. Thank you very much.</p> <p> </p>
Supplementary material - Non-invasive Multimodal Imaging Reveals Early Therapy-Induced Senescence in Human Cancer Cells
<p>The repository features .xls and .txt worksheets including all the data used through this work and reported in the manuscript figures and graphs. More precisely, we included the following: </p> <ul> <li>Figure 2. Raw pixel-wise signals detected in NLO images of TIS cells control cells that were used to perform the colocalization graphs and analyses reported. We describe the average colocalization of SRS and F-CARS signals, and TPEF and E-CARS signals, in both phenotypes.</li> <li>Figure 4. Raw data from image analyses of TPEF and SRS channels of multimodal NLO images, divided in 5 different time points over the therapy follow-up period. The data describe the early rearrangement of mitochondria (TPEF) and lipid vesicles (SRS) in TIS cells, with respect to control counterparts.</li> <li>Figure 6. Raw data from image analyses of QPI images, divided in 4 different time points over the therapy follow-up period. The data describe the early morphological modifications of TIS cells, with respect to control counterparts.</li> </ul>
A Study of Oral Ixazomib Maintenance Therapy in Participants With Newly Diagnosed Multiple Myeloma (NDMM) Not Treated With Stem Cell Transplantation (SCT)
ClinicalTrials.gov study NCT02312258. IPD Sharing: YES. Countries: 35. Publications: 2.
Tailoring Maintenance Therapy to Cluster of Differentiation 5 Positive (CD5+) Regulatory B Cell Recovery in ANCA Vasculitis
ClinicalTrials.gov study NCT03906227. IPD Sharing: YES. Countries: 1. Publications: 1.
Study to Assess Safety and Impact of SelG1 With or Without Hydroxyurea Therapy in Sickle Cell Disease Patients With Pain Crises
ClinicalTrials.gov study NCT01895361. IPD Sharing: YES. Countries: 3. Publications: 3.
A Study of Oral Ixazomib Citrate (MLN9708) Maintenance Therapy in Participants With Multiple Myeloma Following Autologous Stem Cell Transplant
ClinicalTrials.gov study NCT02181413. IPD Sharing: YES. Countries: 33. Publications: 4.
Phase III Study Evaluating Efficacy and Safety of Canakinumab in Combination With Docetaxel in Adult Subjects With Non-small Cell Lung Cancers as a Second or Third Line Therapy
ClinicalTrials.gov study NCT03626545. IPD Sharing: YES. Countries: 26. Publications: 1.
Safety and Efficacy of Ruxolitinib Versus Best Available Therapy in Patients With Corticosteroid-refractory Acute Graft vs. Host Disease After Allogeneic Stem Cell Transplantation
ClinicalTrials.gov study NCT02913261. IPD Sharing: YES. Countries: 22. Publications: 5.
Brief Title: Study of Efficacy and Safety of Canakinumab as Adjuvant Therapy in Adult Subjects With Stages AJCC/UICC v. 8 II-IIIA and IIIB (T>5cm N2) Completely Resected Non-small Cell Lung Cancer Acr
ClinicalTrials.gov study NCT03447769. IPD Sharing: YES. Countries: 41. Publications: 1.
Phase III Study of RAD001 Adjuvant Therapy in Poor Risk Patients With Diffuse Large B-Cell Lymphoma (DLBCL) of RAD001 Versus Matching Placebo After Patients Have Achieved Complete Response With First-
ClinicalTrials.gov study NCT00790036. IPD Sharing: UNDECIDED. Countries: 34. Publications: 1.
Computational simulations show proof-of-concept for optogenetic suppression of ectopic activity in cardiac stem cell therapy
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'CellTrajectory' for cellular automata modelling of leukaemic stem cell dynamics in acute myeloid leukaemia: insights into predictive outcomes and targeted therapies
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Enzyme-like nanoparticle engineered-mesenchymal stem cell secreting HGF promotes visualized therapy for idiopathic pulmonary fibrosis in vivo
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'Biosim' for cellular automata modelling of leukaemic stem cell dynamics in acute myeloid leukaemia: insights into predictive outcomes and targeted therapies
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Identification of clinically relevant T cell receptors for personalized T cell therapy using combinatorial algorithms
<p>Single-cell RNA (scRNA) and single-cell TCR (scTCR)-sequencing data data for patients number 11, 12 and 14 from the article " Identification of clinically relevant T-cell receptors for personlized T-cell therapy". </p> <p>Each compressed file contains two subfolders. One is for the scRNA-seq (GEX-sequencing) and the other for the scTCR-seq (VDJ-sequencing). </p> <p>In the original article, scRNA-seq and scTCR-seq were aligned to the GRCh38 reference genome using <em>cellranger count </em>(10X Genomics, version 3.0.1) and <em>vdj </em>(10X Genomics, version 3.1.0) respectively. The subsequent data processing was performed using Seurat library (V.4.3.0) on R Statistical Software (V.4.0.3).</p>
Replication Data for: Precision Oncology, Cell Signaling and Targeted Therapy: A Holistic Approach to Molecular Cancer Therapeutics
<p>In recent decades, there has been a deluge in the large-scale production of anticancer agents, primarily due to advances in genomic technologies enabling precise targeting of oncogenic pathways involved in disease progression. This initiated a paradigm shift in cancer research and therapeutics based on the ability to study molecular changes throughout the genome. It provided a unique opportunity in the field of translational cancer research and have led to the concept of precision medicine in cancer therapy, raising hopes of developing better diagnostic and therapeutic means for the management of cancer. The purpose of this article is to briefly review the tools and techniques involved in precision oncology research and their applications in the field of cancer treatment. </p>
ScienceDex guides
Understand access before you commit
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.