Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
12,799
datasets available to search
ShareScore release 0.9.0
Dataset results
12,799 results for “immunity”
Data from: Telomere length declines with age, but relates to immune function independent of age in a wild passerine
<p><span>Telomere length (TL) shortens with age but telomere dynamics can relate to fitness components independent of age. Immune function often relates to such fitness components and can also interact with telomeres. Studying the link between TL and immune function may therefore help us understand telomere-fitness associations. We assessed the relationships between erythrocyte TL and four immune indices (haptoglobin, natural antibodies, complement activity, heterophil-lymphocyte ratio; n=477-589), from known-aged individuals of a wild passerine (<em>Malurus coronatus</em>). As expected, we find that TL significantly declined with age. To verify whether associations between TL and immune function were independent of parallel age-related changes (e.g. immunosenescence), we statistically controlled for sampling age, and used within-subject centring of TL to separate relationships within or between individuals. We found that TL positively predicted complement activity at the between-individual level (individuals with longer average TL had higher complement activity), but no other immune indices. In contrast, age predicted levels of natural antibodies and heterophil-lymphocyte ratio, allowing inference that respective associations between TL and age with immune indices are independent. Any links existing between TL and fitness are therefore unlikely to be strongly mediated by innate immune function, while TL and immune indices appear independent expressions of individual heterogeneity.</span></p>
Immune and genetic signature of HER2-driven breast carcinomas triggering anti-Yo paraneoplastic cerebellar degeneration
<ul> <li>Supplementary eTables from: Immune and genetic signature of HER2-driven breast carcinomas triggering anti-Yo paraneoplastic cerebellar degeneration: <ul> <li><strong>eTables 1</strong>: Results of DESeq2 on the differential gene expression analysis between Yo-PCD and control tumours for all genes and for differentially expressed genes.</li> <li><strong>eTables 2</strong>: Results of the Gene Ontology enrichment performed by clusterProfiler on genes over-expressed in Yo-PCD tumours</li> <li><strong>eTables 3</strong>: Results of the Gene Ontology enrichment performed by clusterProfiler on genes under-expressed in Yo-PCD tumours</li> </ul> </li> <li>Gene counts</li> <li>Gene TPMs</li> </ul>
Data and code for: No evidence of metabolic costs following adaptive immune activation or reactivation in house sparrows
<p>We examined the energetic costs of immune activation by measuring both basal (BMR) and exercise-induced maximal metabolic rates (MMR) in house sparrows before and after being injected with either saline (sham) or two novel antigens (keyhole limpet haemocyanin and sheep red blood cells; KLH and SRBC, respectively) after the primary and two subsequent vaccinations. We also examined the effect of experimentally-induced breeding levels of testosterone (T) on immune responses and their metabolic costs in both males and females. </p>
Evolutionary gain and loss of a pathological immune response to parasitism
<p><span>Parasites impose fitness costs on their hosts. Biologists often assume that natural selection favors infection-resistant hosts. Yet, when the immune response itself is costly, theory suggests selection may instead favor loss of resistance. Intraspecific variation in immune costs are rarely surveyed in a manner that tests evolutionary patterns, and there are few examples of adaptive loss of resistance. Here, we show that when marine threespine stickleback colonized freshwater lakes they gained resistance to the freshwater-associated tapeworm, <em>Schistocephalus solidus</em>. Extensive peritoneal fibrosis and inflammation is a commonly observed phenotype that contributes to suppression of cestode growth and viability, but also impose a substantial cost of reduced fecundity. Combining genetic mapping and population genomics, we find that opposing selection generates immune system differences between tolerant and resistant populations, consistent with divergent optimization.</span></p>
Multiplexed imaging mass cytometry reveals distinct tumor-immune microenvironments linked to immunotherapy responses in melanoma
<p><strong>- melanoma_IMC_data.zip</strong></p> <p>The zip file contains the raw IMC images (in the raw_tiff folder) and corresponding single cell masks (in the mask folder) associated with the paper "Multiplexed imaging mass cytometry reveals distinct tumor-immune microenvironments linked to immunotherapy responses in melanoma". The MCD files by CyTOF IMC were exported to a multi-channel TIFF file including 41 channels, and the order of the channel was provided in the <strong>Melanoma_panel.csv</strong>. </p> <p><strong>- Melanoma_code_data.zip</strong></p> <p>The zip file contains the 4 folders described as follows: </p> <ul> <li>Folder ”data“: the processed data for the result shown in paper<br> - Folder "input": <br> - sc_data.csv: the single cell protein expression data;<br> - Folder "abundance": the cell type abundance files;<br> - Folder "clidata": the response and survival data for 4 melanoma datasets used in the paper; <br> - Folder "hc_result": TME archetypes annotation for each sample/ROI from hierarchical clustering;<br> - Folder "ICB": data for ICB analysis (presented in FigS3);<br> - Folder "meta": panel file for clustering;<br> - Folder "RNAseq_data": the RNAseq data for 4 melanoma datasets used in the paper;<br> - Folder "RNAseq_deconv": the result of cell type deconvolution from bulk RNAseq; <br> - Folder "spatial": data for neighbourhood analysis (presented in Fig3, FigS4).<br> - Folder "output": intermediate result for analysis.</li> <li>Folder "Rscript": R scripts for reproducing results in the paper.<br> - generate_Figs.Rmd: ploting figures presented in the paper;<br> - functions.R: functions used for analysis;<br> - Clustering.Rmd: determining cell types based on marker intensities;<br> - Spatial_analysis.Rmd: neighbourhood analysis to get significant interction/avoidance cell relationships.</li> <li>Folder "Figs": figures presented in paper.</li> <li>Folder "HE_figs": the H&E image and the ROIs distribution for each sample.</li> </ul>
Intratumoural heterogeneity and immune modulation in lung adenocarcinoma of female smokers and never smokers
<p>Count matrix and associated meta data for single nucleus transcriptomics of healthy and tumour lung tissue from lung adenocarcinoma patients. Cohort includes young and elderly, female and male, smokers and never smokers.</p>
BCL6 deletion in CD4 T cells reveals Th2 eff mediated immunity in the skin
<p>RNA-Seq datasets related to the study of Mouse Tfh cells.</p> <p>Recent studies propose that Group 2 T follicular helper (Tfh) cells have a higher degree of functional plasticity in addition to their well-defined roles in mediating IL-4-dependent switching of germinal centre B cells to the production of IgG1 and IgE antibodies. In particular Tfh cells have been proposed to be an essential stage in Th2 effector cell development that are able to contribute to innate Type 2 responses. We used CD4-cre targeted deletion of BCL6 to identify the contribution Tfh cells make to tissue Th2 effector responses in models of skin atopic disease and lung immunity to parasites. Ablation of Tfh cells did not impair the development or recruitment of Th2 effector subsets to the skin and did not alter the transcriptional expression profile or functional activities of the resulting tissue resident Th2 effector cells. However, the accumulation of Th2 effector cells in lung Th2 responses was partially affected by BCL6 deficiency. These data indicate that the development of Th2 effector cells does not require a BCL6 dependent step implying Tfh and Th2 effector populations follow separate developmental trajectories and Tfh cells do not contribute to Type 2 responses in the skin . This study reveals important findings that add to the growing literature around the plasticity and functional interconversion of T helper subsets. </p>
Data from: Differential gene expression during recall of behaviorally conditioned immune enhancement in rats: a pilot study
<p><strong>Background:</strong> Behaviorally conditioned immune functions are suggested to be regulated by bidirectional interactions between CNS and peripheral immune system <em>via</em> the hypothalamic-pituitary-adrenal (HPA) axis, sympathetic nervous system (SNS), and the parasympathetic nervous system (PNS). Since the current knowledge about biochemical pathways triggering conditioned immune enhancement is limited, the aim of this pilot study was gaining more insights into that.</p> <p><strong>Methods: </strong>Rats were conditioned with camphor smell and poly I:C injection, mimicking a viral infection. Following stimulus re-exposure, animals were sacrificed at different time points, and neural tissues along the HPA axis was analyzed with a rat genome array together with plasma protein using Luminex analysis.</p> <p><strong>Results:</strong> In the hypothalamus, we observed a strong upregulation of genes related to Wnt/β-catenin signaling (Otx2, Spp1, Fzd6, Zic1), monoaminergic transporter Slc18a2 and opioid-inhibitory G-protein Gpr88 as well as downregulation of dopaminergic receptors, vasoactive intestinal peptide Vip, and pro-melanin-concentrating hormone Pmch. In the pituitary, we recognized mostly upregulation of steroid synthesis in combination with GABAergic, cholinergic and opioid related neurotransmission, in adrenal glands, altered genes showed a pattern of activated metabolism plus upregulation of adrenoceptors Adrb3 and Adra1a. Data obtained from spleen showed a strong upregulation of immunomodulatory genes, chemo-/cytokines and glutamatergic/cholinergic neurotransmission related genes, as also confirmed by increased chemokine and ACTH levels in plasma.</p> <p><strong>Conclusions:</strong> Our data indicate that in addition to the classic HPA axis, there could be additional pathways as e.g. the cholinergic anti-inflammatory pathway (CAIP), connecting brain and immune system, modulating and finetuning communication between brain and immune system.</p>
Can immune gene silencing via dsRNA feeding promote pathogenic viruses to control the globally invasive Argentine ant?
<p><span>Pest control methods that can target pest species with limited environmental impacts are a conservation and economic priority. Species-specific pest control using RNA interference is a challenging but promising avenue in developing the next generation of pest management. We investigate the feasibility of manipulating a biological invader's immune system using double-stranded RNA (dsRNA) in order to increase susceptibility to naturally occurring pathogens. We used the invasive Argentine ant as a model, targeting the immunity-associated genes <em>Spaetzle</em> and <em>Dicer-1</em> with dsRNA. We show that feeding of <em>Spaetzle</em> dsRNA can result in partial target gene silencing for up to 28 days in the laboratory and five days in the field. <em>Dicer-1</em> dsRNA only resulted in partial gene knockdown after two days in the laboratory. Double-stranded RNA treatments were associated with significant gene expression disruptions across immune pathways in the laboratory and to a lower extent in the field. We observed occasional changes in viral loads in dsRNA-treated groups. However, immune pathways disruption did not result in consistent increase in microbial infections, nor did they alter ant abundance in the field. Our study explores the feasibility of lowering a pest's immunity as a control tool. We demonstate that it is possible to alter immune gene expression of pest species and pathogen loads, though in our system the affected pathogens did not appear to influence pest abundance. We provide advice on future directions for dsRNA-mediated immune disruption in pest species, including potential avenues to improve dsRNA delivery as well as the importance of the biology of the pest system and its pathogens.</span></p>
Remote Immune Monitoring: Need, Opportunities and Challenges - Professor Kourosh Saeb-Parsy (University of Cambridge & Cambridge University Hospitals NHS Foundation Trust)
<p>This video is the seventh talk from our Future Blood Testing Network Plus Launch that took place on the 23/11/2021.</p> <p>Remote Immune Monitoring: Need, Opportunities and Challenges - Professor Kourosh Saeb-Parsy (University of Cambridge & Cambridge University Hospitals NHS Foundation Trust)</p> <p>Bio: Professor Kelvin Tsoi is an Epidemiologist specialized in Digital Health. His research interests focus on digital innovation in chronic disease management, including mobile and telecare application for hypertension management, technological implementation and social engagement for cognitive screening, artificial intelligent application on electronic health records. He also works as the traditional epidemiologist on evidence-based medicine and population cohort studies. He obtained his Bachler Degree from Department of Statistics and Doctor of Philosophy from School of Public Health in the Chinese University of Hong Kong. He further received post-doctoral training in the Division of Gastroenterology and Hepatology, Department of Medicine and Therapeutics. He was also appointed as a Director of CUHK JC Bowel Cancer Education Centre to promote colorectal cancer screening. In 2011, he worked as a research scientist in Hospital Authority. He led projects covering a wide range of service areas on chronic diseases, such as service demand projection for schizophrenia and dementia. The experience of database management enhanced his understanding of the HA database structures. In 2013, he was invited to join the interdisciplinary team for Big Data research and worked closely with a team of engineers and data scientists. Currently, Professor Tsoi is an Associate Professor in JC School of Public Health and Primary Care, SH big Data Decision Analytics Research Centre and JC Institute of Ageing. I matriculated as a medical student at Fitzwilliam College in 1993. My interest in biomedical research was developed during my Part II year studying Anatomy A (neurosciences and developmental biology) and I subsequently enrolled on the MB-PhD programme. I completed my doctoral thesis in neurophysiology of circadian rhythms in 2000 and qualified as a medical doctor in 2001. While studying for my PhD, I pursued an active interest in teaching and started supervising undergraduates at Fitzwilliam (and other colleges) in 1998. I served as MCR President in 1999, became a Fellow in 2003 and Director of Studies in Clinical Medicine in 2004. I pursued a career in surgery after graduation and was appointed as a University Lecturer in Transplant Surgery in 2012.</p> <p>Further details on this event can be found at: https://futurebloodtesting.org/event/23-11-21-future-blood-testing-network-launch/</p> <p>This video is an output from the Future Blood Testing Network which is funded by EPSRC under Grant Number EP/W000652/1</p> <p>YouTube Link: https://youtu.be/ANZKGxj87E0</p>
Investigating the "two-hit hypothesis": effects of prenatal maternal immune activation and adolescent cannabis use on neurodevelopment in mice
<p>Prenatal exposure to maternal immune activation (MIA) and chronic adolescent cannabis use have both been identified as environmental risk factors for neuropsychiatric disorders. However, most individuals exposed to a single risk factor do not typically develop major mental illness, which suggests that multiple exposures may be required for illness onset. Here, we examine whether combined exposure to prenatal MIA and adolescent delta-9-tetrahydrocannabinol (THC), the main psychoactive component of cannabis, lead to enduring neuroanatomical and behavioural changes in adult offspring, potentially reflecting changes in humans indicative of mental illness. </p> <p>Mice were prenatally exposed to a viral mimetic, poly I:C (5mg/kg), or vehicle at gestational day (GD)9, and then postnatally exposed to chronic THC (5mg/kg) or vehicle by intraperitoneal injections during adolescent development (postnatal day [PND]28-45). Longitudinal in vivo whole-brain magnetic resonance imaging (MRI) was performed pre-treatment, PND25, post-treatment, PND50, and in adulthood, PND85, followed by a series of behavioural tests aimed at assessing anxiety-like and locomotor, social, and sensorimotor gating behaviour. Post-mortem assessment of cannabinoid (CB)1 and 2 receptor expressing cells was performed in developmentally altered regions identified by MRI (anterior cingulate and somatosensory cortices, striatum, and hippocampus). We hypothesized that there would be differential, but synergistic effects of each exposure.</p> <p>Briefly, we found subtle deviations in neurodevelopmental trajectory and subthreshold anxiety-like behaviours were observed in mice exposed to both risk factors. Sex-dependent effects were observed in patterns of shared brain-behaviour covariation, suggesting that exposure to MIA and THC may affect males and females in different ways. Density of CB1 and CB2 receptor positive cells was significantly decreased in all regions assessed for all mice exposed to either one or both risk factors, relative to controls.</p> <p>These findings suggest that there may be a cumulative effect of risk factor exposure on gross neuroanatomical and behavioural development, and that the endocannabinoid system may be sensitive to both prenatal MIA, adolescent THC, or the combination. For full details, see our publication: .</p> <p>In this dataset, you will find a total of 243 preprocessed structural MRIs (in MINC format) acquired at postnatal day ~25, ~50, and ~85 in mice exposed to poly I:C or vehicle control (0.9% sterile saline) at GD9, and then postnatally treated with vehicle or THC from PND 28-45. These are T1-weighted structural images at 100 micron isotropic resolution acquired on a 7 Tesla Bruker Biospec 70/30; matrix size of 180 x 160 x 90; 14.5 minutes, 20 degrees and TE/TR of 4.5/20 ms (2 averages, ~14 minutes). Anesthesia was induced with 3% isoflurane in oxygen and a (0.075 mg/kg bolus) dexmedetomidine injection. Anesthesia was maintained during the scan between 1.5-0.5% isoflurane, and a constant infusion of dexmedetomidine (0.05mg/kg/h continuous mg/kg during scan). T1-weighted scans were preprocessed by stripping native coordinates, flipping left-right to maintain fidelity, denoising, correcting inhomogeneities in the bias field using the N4 algorithm, and registering in LSQ6 alignment (i.e. 6 degrees of freedom are allowed for imagine alignment: translations and rotations along x, y, and z dimensions). The demographics information for each animal is included in the demographics.csv file. </p> <p>Behavioural tests were performed following the postnatal day 85 scans in all animals with a 2 day rest period. These include: open field test, three chambered social approach, and prepulse inhibition. The data for all of these tests is presented in its own individual .csv spreadsheet.</p> <p>Included in this data set are the structural MRIs in MINC format, the behavioural .csv data, and a readme.txt file providing further detail on the data structure and content, and on how to interpret the data column titles. DICOMS are also available for the structural MRI data, as are the raw (not-preprocessed) MINC files, available upon request to the authors. </p> <p>Finally, the authors would like to acknowledge the funding bodies that supported the completion of this work including the Canadian Institute for Health Research, the Fonds de Recherche du Québec en Santé, and the Healthy Brains for Healthy Lives at McGill University.</p>
Supplementary Tables for "Immune cell-specific smoking-related expression characteristics are revealed by re-analysis of transcriptomes from the CEDAR cohort"
<p>Supplementary Tables from "Immune cell-specific smoking-related expression characteristics are revealed by re-analysis of transcriptomes from the CEDAR cohort".</p>
Scaling in the Immune System and Computational Immunology: Lecture Series
<p>How different is the immune system in a human from that of a mouse? Do pathogens replicate at the same rate in different species? Answers to these questions have impact on human health since multi-host pathogens that jump from animals to humans affect millions worldwide.</p> <p>It is not known how rates of immune response and viral dynamics vary from species to species and how they depend on species body size. Metabolic scaling theory predicts that intracellular processes will be slower in larger animals since cellular metabolic rates are slower. We test how rates of pathogenesis and immune system response rates depend on species body size.</p> <p>We hypothesize that immune response rates are invariant with body size. Our work suggests how the physical architecture of the immune system and chemical signals within it may lead to nearly scale-invariant immune search and response.</p> <p>We fit mathematical models to experimental West Nile Virus (WNV, a multi-host pathogen) infection data and investigate how model parameters characterizing the pathogen and the immune response change with respect to animal mass.</p> <p>Phylogeny also affects pathogenesis and immune response. We use a hierarchical Bayesian model, that incorporates phylogeny, to test hypotheses about the role of mass and phylogeny on pathogen replication and immune response. We observe that:</p> <p><br> 1. Hierarchical models (informed by phylogeny) make more accurate predictions of experimental data and more realistic estimates of biologically relevant parameters characterizing WNV infection.</p> <p>2. Rates of WNV production decline with species body mass, modified by a phylogenetic influence.</p> <p> </p> <p>Our work is the first to systematically explore the role of host body mass in pathogenesis using mathematical models and empirical data. We investigate the complex interplay between the physical structure of the immune system and host body mass in determining immune response. The modeling strategies and tools outlined here are likely to be applicable to modeling of other multi-host pathogens. This work could also be extended to understand how drug and vaccine efficacy in humans may systematically differ from that in model organisms like mice, in which most initial experimental studies are conducted.</p> <p> </p>
Single-cell profiling reveals immune-based mechanisms underlying tumor radiosensitization by a novel Mn porphyrin clinical candidate, MnTnBuOE-2-PyP5+ (BMX-001)
<p>Manganese porphyrins reportedly exhibit synergic effects when combined with irradiation. However, an in-depth understanding of intratumoral heterogeneity and immune pathways, as affected by Mn porphyrins, remains limited. Here, we explored the mechanisms underlying immunomodulation of a clinical candidate, MnTnBuOE-2-PyP<sup>5+</sup> (BMX-001, MnBuOE), using single-cell analysis in murine carcinoma<em> </em>model. Mice bearing 4T1 tumors were divided into 4 groups: control, MnBuOE, radiotherapy (RT), combined MnBuOE, and radiotherapy (MnBuOE/RT). In epithelial cells, epithelial-mesenchymal transition, TNF-α signaling via NF-кB, angiogenesis, and hypoxia-related genes were significantly downregulated in the MnBuOE/RT compared to the RT. All subtypes of cancer-associated fibroblasts (CAFs) were reduced in MnBuOE and MnBuOE/RT. Inhibitory receptor-ligand interactions, in which epithelial cells and CAFs interacted with CD8+ T cells, were significantly lower in the MnBuOE/RT than in the RT. Trajectory analysis showed that DC maturation-associated markers were increased in MnBuOE/RT. M1 macrophages were significantly increased in the MnBuOE/RT compared to the RT, whereas myeloid-derived suppressor cells were decreased. CellChat analysis showed that the number of cell-cell communications was the lowest in the MnBuOE/RT. Our study is the first to provide evidence for the combined radiotherapy with a novel Mn porphyrin clinical candidate, BMX-001 from the perspective of each cell type within the tumor microenvironment.</p>
Genomic Data for "Structure of Anellovirus-like Particles Reveal a Mechanism for Immune EvasionAnellovirus-like Particles Reveal a Mechanism for Immune Evasion"
<p>All genomic data supporting the paper 'Structure of Anellovirus-like Particles Reveal a Mechanism for Immune EvasionAnellovirus-like Particles Reveal a Mechanism for Immune Evasion'. Include amino acid sequence alignment used to produce supplemental figure 6 in the manuscript.</p>
Data from: Pleiotropy alleviates the fitness costs associated with resource allocation trade-offs in immune signaling networks
<p>Many genes and signaling pathways within plant and animal taxa drive the expression of multiple organismal traits. This form of genetic pleiotropy instigates trade-offs among life-history traits if a mutation in the pleiotropic gene improves the fitness contribution of one trait at the expense of another. Whether or not pleiotropy gives rise to conflict among traits, however, likely depends on the resource costs and timing of trait deployment during organismal development. To investigate factors that could influence the evolutionary maintenance of pleiotropy in gene networks, we developed an agent-based model of co-evolution between parasites and hosts. Hosts comprise signaling networks that must faithfully complete a developmental program while also defending against parasites, and trait signaling networks could be independent or share a pleiotropic component as they evolved to improve host fitness. We found that hosts with independent developmental and immune networks were significantly more fit than hosts with pleiotropic networks when traits were deployed asynchronously during development. When host genotypes directly competed against each other, however, pleiotropic hosts were victorious regardless of trait synchrony because the pleiotropic networks were more robust to parasite manipulation, potentially explaining the abundance of pleiotropy in immune systems despite its contribution to life history trade-offs.</p>
A model of within-host interactions between host resources, macroparasite infection and immune response
<p>This project was designed to mathematically investigate the of different host parasite-mitigation strategies on host condition. The R code herein comprises:</p> <ul> <li>An ODE model of within-host interactions between a macroparasite (e.g. helminth) infection, host resource levels and host immune response, and the consequent effects on host condition. In brief, resources are ingested and utilised by the host, leading to inceased condition. The host is infected by a parasite, which matures and establishes within the host; both age stages cause harm to the host, decreasing host condition. The presence of the parasite stimulates an immune response, which can either target larval or adult parasites (a resistance strategy), or ameliorate the harm they cause (a tolerance strategy). The host can also reduce resource intake in order to also reduce ingestion of parasite infective stages (an avoidance strategy). Resistance responses have an associated immunopathology, in that the immune response also harms the host.</li> <li>Code to plot model trajectories over time.</li> <li>Code to plot multiple trajectories as a heat map, in which the x-axis is time and the y-axis is a parameter representing the host investment in its parasite-mitigation strategy.</li> <li>Code to calculate the optimum host investment for each strategy, over various sets of parameter values, as determined by maximising mean host condition over a given timeframe, and to plot the output.</li> <li>The same are also provided for an ODE model in which the total immune response is allocated between the two resistance responses and tolerance (a combined strategy). The optimisation code optimises both the total investment in immune repsonse, and how much is allocated to the three different individual strategies.</li> </ul> <p>The model and results are described in detail in the associated manuscript. We also provide here the simulated datasets in which the optimum host investments were calculated over a range of different parameter values, as these take several hours to run on a standard desktop computer..</p>
Human lung cancer harbors spatially-organized stem-immunity hubs that associate with response to immunotherapy
<p>Data associated with Chen, Nieman, Spurrell et al "Human lung cancer harbors spatially-organized stem-immunity hubs that associate with response to immunotherapy" Nature Immunology, 2024. </p> <p>(1) Multiplex RNA scope. Processed cell-level data from 3 datasets, separated into manually selected "Stem Immunity" regions and "Tumor" regions, in separate files. </p> <p>(2) GeoMx. Unprocessed GeoMex data, with standard fields provided by Nanostring software. </p> <p>(3) MERFISH. Transcript-level information, including CellPose and Baysor segmentation. </p> <p>(4) Co-registered multispectral RNA and protein images. Processed cell-level data from 46 patients. Patient-level meta data information is available in supplementary table 1, tab B_Patient_Metadata. Fluorophore channel information is Figure 1a. </p> <p>Paper: <a title="https://secure-web.cisco.com/1OQRHTBMPf1SngM0FLdNuKQOPPx7fLOR87kGiirhnF_e0M74duym9zratwJMs0WJXqHJPAlkZoWXBoHafhJ72n9s0edU76bj8nCUblNWpOnoK6c8KGEQgcNuk8OuBqXAooW9yoh6etJ0bq6VGDmoFd95MrgMob6is1GxcOWx-XK996d_j8QDVu1rptbeyI8n08UfqmHA3n0A0P37k_-DYUWMh7VFNSmbLGzVqGG2n-czoFN3vL5JrMDPRvo0LDGJs96rzB6zYiaLdk6UgYXXc6eUV6FI64MTxmuXCbEmVRqONrjLdyG6HJULOrJLmKURM/https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41590-024-01792-2" href="https://secure-web.cisco.com/1OQRHTBMPf1SngM0FLdNuKQOPPx7fLOR87kGiirhnF_e0M74duym9zratwJMs0WJXqHJPAlkZoWXBoHafhJ72n9s0edU76bj8nCUblNWpOnoK6c8KGEQgcNuk8OuBqXAooW9yoh6etJ0bq6VGDmoFd95MrgMob6is1GxcOWx-XK996d_j8QDVu1rptbeyI8n08UfqmHA3n0A0P37k_-DYUWMh7VFNSmbLGzVqGG2n-czoFN3vL5JrMDPRvo0LDGJs96rzB6zYiaLdk6UgYXXc6eUV6FI64MTxmuXCbEmVRqONrjLdyG6HJULOrJLmKURM/https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41590-024-01792-2">https://www.nature.com/articles/s41590-024-01792-2</a></p>
Real-world comprehensive genomic and immune profiling reveals distinct age- and sex-based genomic and immune landscapes in tumors of patients with non-small cell lung cancer
<p>Wallen ZD, Ko H, Nesline MK, Hastings SB, Strickland KC, Previs RA, Zhang S, Pabla S, Conroy J, Jackson JB, Saini KS, Jensen TJ, Eisenberg M, Caveney B, Sathyan P, Severson EA, Ramkissoon SH. <strong>Real-world comprehensive genomic and immune profiling reveals distinct age- and sex-based genomic and immune landscapes in tumors of patients with non-small cell lung cancer.</strong> <em>Front Immunol.</em> 2024 Jun 21;15:1413956. doi: <a href="https://doi.org/10.3389/fimmu.2024.1413956">10.3389/fimmu.2024.1413956</a>. PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/38975340/">38975340</a>; PMCID: <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC11224431/">PMC11224431</a>.</p> <p><strong>ABSTRACT</strong></p> <p>Younger patients with non-small cell lung cancer (NSCLC) (<50 years) represent a significant patient population with distinct clinicopathological features and enriched targetable genomic alterations compared to older patients. However, previous studies of younger NSCLC suffer from inconsistent findings, few studies have incorporated sex into their analyses, and studies targeting age-related differences in the tumor immune microenvironment are lacking. We performed a retrospective analysis of 8,230 patients with NSCLC, comparing genomic alterations and immunogenic markers of younger and older patients while also considering differences between male and female patients. We defined older patients as those ≥65 years and used a 5-year sliding threshold from <45 to <65 years to define various groups of younger patients. Additionally, in an independent cohort of patients with NSCLC, we use our observations to inform testing of the combinatorial effect of age and sex on survival of patients given immunotherapy with or without chemotherapy. We observed distinct genomic and immune microenvironment profiles for tumors of younger patients compared to tumors of older patients. Younger patient tumors were enriched in clinically relevant genomic alterations and had gene expression patterns indicative of reduced immune system activation, which was most evident when analyzing male patients. Further, we found younger male patients treated with immunotherapy alone had significantly worse survival compared to male patients ≥65 years, while the addition of chemotherapy reduced this disparity. Contrarily, we found younger female patients had significantly better survival compared to female patients ≥65 years when treated with immunotherapy plus chemotherapy, while treatment with immunotherapy alone resulted in similar outcomes. These results show the value of comprehensive genomic and immune profiling (CGIP) for informing clinical treatment of younger patients with NSCLC and provides support for broader coverage of CGIP for younger patients with advanced NSCLC.</p> <p><strong>DATA AVAILABILITY: </strong></p> <p>De-identified, individual-level patient data, genomic variants, and individual immune gene expression data used in the manuscript can be found in this repository (https://zenodo.org/record/11396552). An R markdown file with R code used to perform the analyses and generate figures is also provided in the repository along with the data. All versions of software used are provided in the Methods section of the manuscript. Raw sequencing data were derived from routine clinical testing of real-world patients and cannot be shared publicly. Data for immune gene expression signatures are not publicly available due to a non‑provisional patent filing covering the methods used to generate and analyze these data but are available from the corresponding author on reasonable request.</p>
Conserved angio-immune subtypes of the cancer microenvironment predict response to immune checkpoint blockade therapy
<p>Immune checkpoint blockade (ICB) therapy has revolutionized cancer treatment. However, only a fraction of the patients respond to ICB therapy. Accurate prediction of patients to likely respond to ICB would maximize the efficacy of ICB therapy. The tumor microenvironment (TME) dictates tumor progression and therapy outcome. Here, we classify the TME by analyzing the transcriptome from 11,069 cancer patients based on angiogenesis and T-cell activity. We find three distinct angio-immune TME subtypes conserved across 30 non-hematological cancers. There is a clear inverse relationship between angiogenesis and anti-tumor immunity in TME. Remarkably, patients displaying TME with low angiogenesis with strong anti-tumor immunity show the most significant responses to ICB therapy in four cancers. Re-evaluation of the renal cell carcinoma clinical trials provides compelling evidence that the baseline angio-immune state is robustly predictive of ICB responses. This study offers a rationale for incorporating baseline angio-immune scores for future ICB treatment strategies.</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.