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gen_ce72dcebc272d150014e00ac915d6e36 | Targeting TFEB transcription factor as a novel therapeutic approach for the treatment of Birt-Hogg-Dube’- associated kidney cancer | Worldwide Cancer Research | Telethon Institute Of Genetics And Medicine | HRCS22_16209 | Birt-Hogg-Dube’ is a hereditary cancer syndrome, due to loss of function mutations in the gene encoding Folliculin and characterized by benign skin tumors, lung and kidney cysts and renal cell carcinoma. Renal tumors represent the most severe manifestation of the disease and to date surgery is the only available therapeutic intervention. The design of effective targeted therapies depend on a better understanding of the primary cellular pathways in which folliculin serves as tumor suppressor. We recently found that depletion of TFEB in a kidney-specific mouse model of BHD syndrome fully rescued cystogenesis suggesting a key role of TFEB in Folliculin dependent pathologies. Encouraged by these findings, in this grant application we propose to understand the contribute of TFEB to the development of kidney tumors in Flcn heterozygous mice, which faithfully recapitulate kidney pathologies in BHD disease. In addition, we aimed at dissecting the TFEB downstream pathways responsible for tumor growth in BHD patients and functionally characterize a novel mechanism of regulation of TFEB localization, which could represent a novel therapeutic strategy for the treatment of BHD renal tumors. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_303c4bb32b2cfd131161892c09827889 | Pre-clinical evaluation of combination treatments for invasive lobular breast cancer | Worldwide Cancer Research | Royal College of Surgeons in Ireland | HRCS22_16210 | Invasive lobular carcinoma (ILC) is the second most common type of breast cancer (approximately 10-15% of all breast tumors). Women with ILC are usually older, used hormone replacement therapy and are more likely to have ER+ disease. Compared to other ER+ breast cancers, ILCs are more likely to metastasize to the peritoneum, gastrointestinal tract, and ovaries and are more frequently bilateral. Like other ER+ breast cancers, anti-estrogen resistance has emerged as a significant problem in the management of ILC, however, ILC is considered to be chemo-resistant and patients receive no additional benefit from chemotherapy. As such, there is a pressing need to develop tailored therapeutic options for endocrine-resistant ILC patients. As part of the FP7 RATHER project, we discovered that the BET protein Brd3 is a marker of poor prognosis in ILC but not in ER+ breast cancers as a whole. We subsequently validated this in an independent cohort from the METABRIC study. We also found that ILC cell lines that do not respond to anti-endocrine therapy are sensitive to BET inhibition (iBET), either as a single agent, or in combination with an FGFR inhibitor. Here we aim to progress our in vitro observations to anchor the therapeutic potential of iBET for endocrine-resistant ILC. To achieve this, we will capitalize on the recent discovery that ILC xenograft models can be readily established by mammary intraductal implantation. The efficacy of iBET either as a single agent or in combination with a FGFR inhibitor will be determined. One of our ILC cell models displays de novo resistance to iBET. ChIP-Seq, RNA-Seq and label-free quantitative mass spectrometry-based comparison of this model with our iBET sensitive ILC model will also allow us to dissect the transcriptional plasticity that underlies resistance to iBET and determine how best to overcome these in ILC patients. | 5.1 Pharmaceuticals | 6project_grants_public
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gen_462388c127e3278955c13cf742959e02 | Understanding spontaneous loss of heterozygosity | Worldwide Cancer Research | Institute Curie | HRCS22_16214 | Using a novel model established in my team of spontaneous stem cell genome instability in fruit flies, our proposed work will address several important currently open questions about a major pathway of tumor suppressor inactivation: loss of heterozygosity via mitotic recombination. How do genomic features contribute to initiation of mitotic recombination? What tissue-intrinsic and extrinsic factors contribute to LOH initiation and neoplastic growth? We will explore these questions using whole-genome sequencing approaches combined with sophisticated Drosophila genetics. Our findings will bring to light mechanisms that are at work in vivo in adult stem cells and have numerous implications both for basic science as well as potential future preventative measures for patients. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_9ab61cd6bc4a972e1cc2e12f9a8e12ff | Novel BBB penetrating peptide for the treatment of Parkinson’s disease | Cure Parkinson's | University of Helsinki | HRCS22_16255 | The prevalence of neurodegenerative diseases, such as Parkinson’s disease (PD), is growing rapidly due to an aging population. Current treatments for PD only relieve symptoms and cannot stop the progression of the disease, thus there is an urgent need for new therapies. Neurotrophic factors (NTFs) are secretory proteins that regulate the growth, survival, regeneration and plasticity of neurons. They have been explored as novel drugs for the treatment of Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS) and PD but their efficacy in clinical trials has been variable. Cerebral dopamine neurotrophic factor (CDNF), discovered in our lab, is an ER located protein that works completely differently from known NTFs, but protects and restores the function of dopamine (DA) neurons in rodent and rhesus monkey toxin models of PD more effectively than other NTFs. CDNF is currently in phase 1/2 clinical trials on PD patients in three medical centers. Despite the promising results in animal models of PD, NTF and CDNF-based treatments share a fundamental drawback: they require direct delivery to the brain through invasive surgery, since they cannot pass through the blood-brain barrier (BBB) and do not treat non-motor symptoms. Prof Saarma's group's recent discovery, however, may overcome this difficulty: they showed that a novel CDNF variant, the 61 amino acids (aa) long C-CDNF, enters DA neurons efficiently in culture. Furthermore, these data show that C-CDNF can cross through the BBB as measured by four different methods and has a neurorestorative effect in both 6-OHDA and MPTP toxin models of PD when administered subcutaneously. Although C-CDNF data are promising, they believe it is not yet the optimal CDNF-derived molecule for clinical trials. C-CDNF is 61 amino acids (aa) long and harbors three alpha-helical regions. The preliminary data suggest that deletion of helix 1 or helix 3 and the sequence after the helix 3 from C-CDNF does not affect the biological activity in vitro. Systemic administration of the shortest 33 aa long C-CDNF peptide (CDNF33) is even more effective in rat 6-OHDA model of PD and passes through the BBB more readily than the longer 61 aa long C-CDNF peptide (not shown). Thus, the goal of this project is to generate the smallest active C-CDNF polypeptides, using deletion and site-directed mutagenesis, and to optimize BBB penetration properties, stability, and activity to design the optimal C-CDNF polypeptide. Structural analysis will be followed by in vitro and in vivo testing in 6-OHDA and in alfa-synuclein (aSyn) aggregation models of PD in order to identify the best drug candidate for the disease. The innovative aspect of this proposal is a new groundbreaking concept of peripheral delivery of BBB-penetrating CDNF-derived polypeptides with trophic factor properties and their potential to simultaneously treat both the non-motor and motor symptoms of PD. The effect of C-CDNF variant on non-motor symptoms will also be tested and its mode of action studied. | 5.1 Pharmaceuticals | 6project_grants_public
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gen_c09925a5fe2e427501ebed470e67ec22 | Combinatorial Engineering of Proteolytically Resistant APPI Variants that Selectively Inhibit Human Mesotrypsin for Cancer Therapy | Worldwide Cancer Research | Ben-Gurion University of the Negev | HRCS22_16274 | Mesotrypsin is a serine protease that is upregulated with tumor progression and associated with poor prognosis in many human cancers. In cancer models, mesotrypsin promotes tumor growth, invasion, and metastasis, making it an attractive target for therapeutic intervention. To date, no selective inhibitors against mesotrypsin, either natural or synthetic, have been reported. Developing selective inhibitors for mesotrypsin presents special challenges, as mesotrypsin shares high sequence homology and structural similarity with other serine proteases, and is resistant to inhibition by many polypeptide inhibitors. The human amyloid β-protein precursor Kunitz protease inhibitor domain (APPI) offers an attractive scaffold for engineering mesotrypsin inhibitors, but has the inherent disadvantage of rapid cleavage by the enzyme. In preliminary studies, we have used directed evolution to generate a novel prototype mesotrypsin inhibitor, based on the APPI scaffold, possessing picomolar affinity and improved proteolytic resistance to mesotrypsin. Herein, we propose to identify highly selective novel mesotrypsin inhibitors based on this prototype for clinical translation as imaging and therapeutic agents. We will use a yeast surface display platform and novel competitive screening strategy to identify selective mesotrypsin antagonists from inhibitor libraries. We will evaluate candidate inhibitors for mesotrypsin selectivity, proteolytic stability, and anticancer efficacy in cell culture models. Finally, we will begin preclinical evaluation of the best candidate as a targeting agent for tumor imaging and as a therapeutic. The proposed strategy is likely to produce mesotrypsin inhibitors of low toxicity and immunogenicity, with substantial translational potential as imaging agents and therapeutics. We further envision that our approach introduces a versatile platform that can be extended to target other serine proteases as well as other important target proteins, for the creation of new-generation therapeutics for cancer and other diseases. | 5.1 Pharmaceuticals | 6project_grants_public
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gen_7f843d36245720da689a8b3c93783a15 | Climate adaptation and sustainable rural health outcomes in Southern Africa | Wellcome Trust | Human Sciences Research Council | HRCS22_16275 | The proposed project seeks to assess the complex health impacts of some of the major climate adaptation actions in rural Southern Africa, using case studies of Zimbabwean communities located in the mid-Zambezi Valley area, in the north of the country, along the borders with Zambia and Mozambique. The specific focus will be on investigating nutritional and psychosocial health impacts of two of the main adaptation actions in the case study area. The project is expected to run for 30 months and will build on a previous longitudinal (2010-2016) academic research work on livelihoods and climate change adaptation in the area undertaken by the lead applicant. A blended methodology combining qualitative and quantitative data collection and analytical techniques will be used. A Theory of Change, setting out the links between processes, activities, outcomes and context and the changes that occur in the short, medium and long term, will anchor the impact evaluation. The project ultimately aims to generate an evidence-based framework for tracking and assessing the health impacts of climate adaptation actions in marginal rural Southern African communities, and to proffer means and ways of harnessing the positive impacts and addressing the negative outcomes for rural household and community resilience | No Research Activity assigned | 6project_grants_public
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gen_0fbae4f6d98a397d5fc3677fd553d520 | Identification of novel drug targets in the Notch pathway that are relevant to tumor formation | Worldwide Cancer Research | University of Milan | HRCS22_16294 | Recent work in Drosophila melanogaster has revealed a central role of the endo-lysosomal compartment in Notch signaling activation. However, endo-lysosomal Notch signaling is ill-understood in mammals and strategies to counteract it have not emerged yet, limiting our ability to act on tumors arising from Notch signaling alterations. We postulate that endo-lysosomal Notch signaling might play a yet unrecognized important role in Notch-dependent tumorigenesis that awaits experimental exploration. In Task 1, we aim to study 30+ new drug targets that we have identified in a recent screen for trafficking regulators of Notch in human cells. For this, we have established a pipeline for quantitative assessment Notch trafficking and activation. New genes that are found to act in the endo-lysosomal activation process will be modulated in specific Notch-dependent cancer cell lines, upon depletion or by pharmacologic treatment. In Task 2, the Drosophila homologs of the most promising ones will be analyzed to determine their effect on Notch-dependent tumorigenesis using genetic assays in vivo. For such effort, we will generate mutants by CRISPR/Cas9 gene editing and will study them using Notch and endocytic assays that recapitulate features of tumorigenesis in vivo. In task 3, based on the indications of task 2, we will use Drosophila as a host for tumor transplantation and drug testing. In summary, we will identify new regulators of endo-lysosomal Notch signaling, understand their role in tumorigenesis, and characterize their potential pharmacologic modulators. At a time in which clinical therapies based on targeting Notch signaling are still an unfulfilled promise, detailed understanding of Notch events associated to the endo-lysosomal system will be key to devise more effective and less toxic pharmacologic options. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_b15f8f0b58c1a4333cb2c1c3bbd8f905 | Adoptive immunotherapy of acute Leukemia with CD1c retargeted iNKT cells | Worldwide Cancer Research | Fondazione Centro San Raffaele | HRCS22_16304 | We have shown that a group of human T lymphocytes kills acute leukemia blasts by recognizing the leukemia-associated lipid antigen methyl-lysophosphatidic acid (mLPA) presented by the CD1c molecule, which is identical in all individuals, suggesting a donor-unrestricted adoptive immunotherapy approach. Indeed, we efficiently engineered total T lymphocytes from any donor with a selected mLPA-specific TCR to kill CD1c-expressing leukemia cell in vitro and in immunodeficient mouse xenografts. In this project, we aim at assessing whether the transfer of the mLPA-specific TCR into invariant Natural Killer T (iNKT) cells, a subset of lipid-specific lymphocytes expressing an invariant TCR restricted for CD1d molecules, may further improve efficacy and safety of this adoptive immunotherapy strategy. The advantages of using iNKT instead of T cells resides in their ability to: i. migrate into the bone marrow; ii. control graft versus host disease (GVHD) while promoting graft versus leukemia (GVL); iii. modulate/eliminate immunosuppressive cells in the tumor microenvironment (TME). We posit that iNKT cells may be harnessed to target, at the same time, leukemia cells with the mLPA-specific TCR, and therapeutically reprogram the TME with the endogenous one. The final aim of the project is to generate iNKT cells armed with a universal mLPA-specific TCR for off-the-shelf adoptive immunotherapy of human acute leukemia. | No Research Activity assigned | 6project_grants_public
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gen_0c4a52adb1cd113f21f633a64604db20 | Innovative business models to advance access to next generation mAbs | Wellcome Trust | International AIDS Vaccine Initiative | HRCS22_16306 | The goal of this proposal is to convene a workshop that will help define novel business models bridging across innovators, biosimilar companies, product development partners, and other global stakeholders that place access at their core from the outset, for the next generation of mAbs. The aim of the proposed convening will be to harness expert insights to define approaches that promote timely, equitable, and sustainable access to mAbs in LMICs, with a focus on infectious disease mAbs in the pipeline. The workshop is co-convened by Unitaid, IAVI, and Medicines Patent Pool, with support from Wellcome. By convening key experts and stakeholders in a global dialogue around novel business models for mAbs access, we hope to advance several key outcomes: • Raising awareness and generating momentum around the need for alternative business models • Fostering collective dialogue and garnering expert advice in thinking through key aspects of business model innovation to inform partnership strategies and approaches • Cultivating strategic partnerships for novel business models for mAbs access | No Research Activity assigned | 3networking_collaborative
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gen_8fce168ff591389867faeccc09dbf0af | Translational Control of the Immune Response in the Tumor Microenvironment | Worldwide Cancer Research | University of Milan | HRCS22_16313 | No abstract available for this analysis. | No Research Activity assigned | 6project_grants_public
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gen_821844c9c3413023019c2fbde1cd63a9 | Role of the interferon system in DNA replication fork stability and chemo-resistance | Worldwide Cancer Research | University of Zurich | HRCS22_16321 | No abstract available for this analysis. | HRCS Research Uncodeable | 6project_grants_public
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gen_6354f90a7d1525287b7f259fc5ee5f92 | Chromatin organization and transcription factor targeting in the establishment of oncogene-induced senescence and cancer progression. | Worldwide Cancer Research | Fondazione Centro San Raffaele | HRCS22_16334 | Background. Oncogene-induced senescence (OIS) acts as a powerful tumor suppressive mechanism by inducing quasi-irreversible cell-cycle arrest when cells experience oncogenic stress. Senescent cells, however, can still overcome OIS leading to cancer onset. Senescence is caused by persistent DNA damage and it is characterized by massive chromatin reorganization and altered gene expression profiles, including the establishment of SASP, an inflammatory transcriptional program. Senescence can propagate to bystander cells, due to SASP-dependent paracrine and SASP-independent juxtacrine mechanisms. Key transcription factors (TFs) such as p53 and NF-kB mediate these processes but how chromatin impacts their activation and binding dynamics in OIS, in bystander senescence (BySen) and upon senescence overcome (SenOv) has been only marginally explored. Objective. We will test an uncharted hypothesis on early tumorigenesis: the massive chromatin reorganization observed upon OIS induction shape the search mechanism and the activity of the key TFs implicated in OIS, BySen and SenOv. To this end, we will integrate genomic technologies with unique microscopy approaches that we developed to probe TF activity at the single-cell and single-molecule level. Experimental Plan. We will model OIS – by oncogene induction - and SenOv – by histone demethylases overexpression - in human fibroblasts and melanocytes. We will analyze chromatin reorganization, TFs binding, and target gene expression in single cells using super-resolution and single-molecule microscopy to answer these questions: Does chromatin reorganization in OIS control the capability of TFs to find, bind and activate their targets? How does the further chromatin remodeling in BySen and SenOv affect TFs activity? How do paracrine signaling in modulate chromatin organization and TFs action? Significance. We will picture with single-cell resolution the interplay between chromatin architecture, TFs activity and paracrine signaling in a tumorigenesis model, leading to fundamental insights about early cancer progression that could be translated into the identification of novel druggable targets. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_6e35f5d88a6b6ea8bbb582d35c190f5b | Science-to-Policy; A Global Media Network Bridging North-South Divides | Wellcome Trust | Global Policy Reporting | HRCS22_16346 | Wellcome's strategic focus on four themes: infectious disease; climate; mental health; and discovery research covers many of the gravest challenges facing low- and middle-income countries. Translating new knowledge into policy, however, remains challenging. There remains little investment, particularly in LMICs, in independent global health media to air discoveries, channel debates, and hold policymakers accountable. Health Policy Watch provides a platform for LMIC journalists to develop and share their stories, echoing in both global North and South, and building capacity of LMIC media professionals. A 2020-21 Wellcome Grant led to a two-fold increase in Health Policy Watch readership, including in major LMIC 'hubs', e.g. South Africa, Kenya, Nigeria, India, Pakistan. This proposal aims at solidifying gains in a sustainable model focused on: 1. Reporting from Africa and Southeast Asia around Wellcome priorities - a) Tracking countries' action on health-relevant aspects of climate commitments and health co-benefits of sustainability in under-explored themes. b) LMIC challenges battling infectious diseases, including SARS-CoV2 in an equity & health systems lens; c) preventing new pandemics in a One-Health framework; d) African & Asian discovery research. 2. Sustainable media model - recruitment of other major donors; microfinance through targeted social media appeals, media collaborations and advertising. | 8.3 Policy, ethics and research governance | 3networking_collaborative
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gen_db1f6fe56b4301cd9b75b3350b31dc2d | Role of the RNA helicase DDX3X in Myc-induced lymphomagenesis | Worldwide Cancer Research | European Institute of Oncology | HRCS22_16355 | No abstract available for this analysis. | No Research Activity assigned | 6project_grants_public
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gen_c82a4c643c1b2c1333b40f525b2c9534 | Effects of intra-uterine HIV exposure on antibody functionality and B cell development | Wellcome Trust | University of Cape Town | HRCS22_16390 | Approximately 30% of pregnant women in South Africa are HIV-infected resulting in over 300 000 infants exposed to HIV in utero every year. Rates of infectious mortality are reportedly higher among HIV-exposed uninfected infants (iHEU) compared to HIV-unexposed uninfected infants (iHUU). Studies evaluating the effects of maternal HIV infection on vaccine responses in their respective infants show that iHEU have similar antibody titres as those elicited in iHUU. These results imply efficacious vaccination in iHEU which contradicts the observed higher morbidity and mortality rates in iHEU. Therefore, I hypothesise that exposure to HIV in utero may impact the maturation of B cells leading to production of antibodies with poor Fc functions. Our preliminary analysis revealed altered B cell phenotypes across age in iHEU compared to iHUU. Therefore, in this study I aim to characterise B cell properties such as reduced somatic hypermutation for affinity maturation among iHEU using RNA-sequencing. Furthermore, I will analyse IgG Fc glycosylation that is associated with Fc-FcR affinity and Fc effector functions. Subsequently, I will develop in vitro models to measure antibody dependent cellular phagocytosis (ADCP) and cytotoxicity (ADCC) specific to early childhood vaccines. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_ad32ffeefe662f7e18d7cfd0d7cbc2fd | Ultra-Sensitive, Switchable MRI Reporters for Lung Metastases | Worldwide Cancer Research | German Cancer Research Center | HRCS22_16398 | Early cancer detection and visualisation of disease progression are highly relevant for succesful therapy. Imaging reporters for minimally invasive methods such as MRI are thus an indispensable component and visualising information of the biological complexity of tumour tissue beecomes increasingly important for choosing the right therapy. This is particularly relevant for metastatses detection which is a central aspect of diagnostic imaging. MRI provides excellent soft tissue contrast but suffers from low sensitivity, particularly in the lung which is low in tissue water density but is the most common organ targeted by metastases. MRI reporters with molecular spcificity for metastaes are therefore highly needed but cannot be implemented with conventional detection. Here we address this problem with an imaging method that includes a pre-targeting approach for LHRH receptor-carrying metastases and subsequent detection through-spin hyperpolarised xenon. The enhanced magnetization of this noble gas together with a saturation transfer technique from the molecular reporter onto the gas will enable ca. 10 million-fold enhanced sensitivity. We will design "smart" nanoparticles that selectively highlight the signal of xenon that has been in contact with these reporters that carry luteinizing hormone-releasing hormone (LHRH) for specific binding to cancer cells. This approach shall visualize pulmonary micrometastates from breast cancer cells. The method serves as an example for a molecular target from which a platform can be developped for different tumour markers. The combination of novel techniques from MRI physics and bioengineering will provide "switchable" MRI agents with a specific MR response frequency for xenon through the metastases-bound reporters and will bring diagnostic lung imaging to an uprecedented sensitivity level. A versatile design respects the need for easy adaptation to implement personalized diagnostics to interrogate the presence of various molecular targets. | 4.1 Discovery and preclinical testing of markers and technologies | 6project_grants_public
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gen_d4f0807b2be3a578a274a80b945fe521 | Determinants of EML4-ALK Driven Lung Cancer Growth and Therapeutic Responses | Worldwide Cancer Research | German Cancer Research Center | HRCS22_16421 | Lung adenocarcinomas (LUAD) in non-smokers often harbour specific genetic aberrations, such as gene fusions involving the Anaplastic Lymphoma Kinase (ALK) and the echinoderm microtubule-associated protein-like 4 (EML4). This oncogenic fusion has been reported to have 15 different variants, which harbour the same ALK sequence but differ in the EML4 breakpoint. Variant 1 and variant 3 differ greatly in the proportion of EML4 and are two most frequent oncogenic inversion in ALK-positive patients. Despite the development of second-and third-generation ALK inhibitors, patient responses are limited by drug resistance. In half of relapsed cases, resistance arises from secondary mutations in the TK domain; however, the mechanisms of resistance in patients lacking secondary mutations remain poorly characterized. Besides, the impact of concurrent genomic alterations in EML4-ALK driven tumours remains largely unknown. TP53 is mutated in 30% of ALK-rearranged LUAD and appears to be synergistic with variant 3, giving rise to more aggressive human disease. Despite the direct relevance to patient treatment, how these co-incident genomic alterations influence the robustness of therapeutic responses has never been investigated. Here we propose to employ state-of-the-art technologies and methodologies to model Eml4-Alk variants in vivo and study the tumour evolution and dynamics of the most aggressive variants (Aim1). In Aim 2, we will determine the impact of co-incident genomic alterations on EML4-ALK-driven lung cancer development, by inactivating putative tumour suppressor genes in a variant-specific manner. Finally, in Aim 3, we will determine the impact of different Eml4-Alk variants and concomitant genomic alterations on response to ALK inhibition. By combining multiplex genome editing with drug treatment, we will perform the equivalent of hundreds of genotype-directed clinical trials in parallel and therefore this project will have a direct impact on personalised treatment for patients with EML4-ALK lung tumours. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_a2b783270e9eebd6f811c01fd8d6514f | Oncogene discovery in esophageal cancer through interrogation of 3D regulatory landscapes | Worldwide Cancer Research | Max Planck Institute for Molecular Genetics | HRCS22_16429 | Esophageal cancer is one of the most common and lethal cancers worldwide, yet currently no targeted therapeutics exists for its treatment. A critical roadblock in the development of targeted therapeutics for esophageal cancer is the lack of knowledge of the key oncogenic drivers in this cancer and the regulatory landscape that controls the expression of those genes. For example, genome-sequencing efforts of esophageal adenocarcinoma (EAC), the most frequent subtype of esophageal cancer, have revealed few frequently mutated genes to date, and those mutations have limited prognostic benefit, which suggests that mutations in non-coding DNA may play critical roles in EAC development. Gene expression programs are implemented in the three dimensional context of 3D chromosome structures, and our previous work suggests that the boundary elements of such 3D chromosome neighborhoods are frequently mutated in EAC. In this work, we propose to generate maps of the 3D regulatory landscape for multiple esophageal adenocarcinoma cells for the discovery of new oncogenic drivers. We will combine the 3D regulatory maps with whole genome sequence information to create a compressive catalog of candidate EAC driver mutations that occur in non-coding DNA elements, including chromosome neighborhood boundaries, and will use the 3D regulatory landscapes to identify oncogenes dysregulated around the mutated neighborhoods. We will functionally validate the candidate driver mutations and the new candidate oncogenes in cell line- and organoid models and using clinical information. This work will generate a functionally validated set of EAC oncogenes whose genomic sequence is otherwise intact. Results of this work will provide insights into the clinical utility of mutations disrupting chromosome neighborhoods in EAC, and facilitate the development and application of new therapeutic approaches for this common and deadly cancer. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_f03e5353734b98356503042328a9f123 | Mechanisms of resistance to anti-TGF-beta therapies in metastatic colorectal cancer | Worldwide Cancer Research | Institute for Research in Biomedicine | HRCS22_16434 | Most colorectal cancer (CRC) patients die as a result of metastasis. Neither conventional chemotherapy nor current targeted therapies offer significant benefits once the disease has spread to distant organs. Immune checkpoint inhibitors have shown efficacy in only a small subset of patients bearing hypermutated CRCs. Arguably, these failures result from the incomplete understanding of metastatic CRC, which is in part due to lack of mouse models that recapitulate the advanced stages of the disease. We permuted conditional alleles of the WNT, EGFR, TGF-beta and p53 pathways in intestinal stem cells of mice. Quadruple mutant mice developed metastatic human-like intestinal adenocarcinomas. These tumors display key hallmarks of aggressive CRCs including T cell exclusion and a TGF-beta activated stroma. From these genetic mouse models we derived mouse tumor organoids (MTOs), which upon transplantation in immunocompetent recipients recreated both the primary and metastatic disease. Analysis of metastasis generated by MTOs revealed that tumor cells build an immunoprivileged microenvironment during liver colonization, by promoting T-cell exclusion and blocking the acquisition of a Th1 effector phenotype. Inhibition of TGF-beta signaling reverts this process and unleashes a potent cytotoxic T-cell response against tumor cells, which is long lasting and protects mice from metastatic disease. In mice with progressed liver metastatic disease, blockade of TGF-beta signaling rendered tumors susceptible to anti-PD-1/PD-L1checkpoint therapy. As poor prognosis CRCs are characterized by high levels of TGF-beta and immune evasion, our findings suggest that TGF-beta signaling inhibitors may have broad applications to treat patients with advanced CRC. However, we have discovered that a subset of mouse CRCs develop resistance to TGF-beta-based therapies during metastatic outgrowth. Here we propose to investigate this process and identify the mechanism co-opted by resistant CRCs to evade the action of the adaptive immune system triggered by treatment with TGF-beta inhibitors. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_885d690711506c6d78ca8beb6599649b | International integrated analysis to identify markers of poor survival in high-risk neuroblastoma | Solving Kids' Cancer | Vall d'Hebron Hospital Universitari | HRCS22_16441 | The outcome for patients with high-risk neuroblastoma is currently inadequate despite intensive multimodal therapy and despite continued treatment intensification (such as the addition of immunotherapy or tandem high-dose chemotherapy). To date, most patients with high-risk are treated in a broadly similar manner. Many researchers have looked at biomarkers (biological characteristics) that could identify those patients with the poorest outcome right from the time of diagnosis, so that these patients could be offered novel therapies very early in their disease course. So far, despite hundreds of studies evaluating factors routinely used in the clinic (such as age or number of metastasis) or more advanced technologies including complex genomic analyses, none of these biomarkers has been validated nor is available for clinical-decision making. The novelty of our approach is that we aim to integrate all (or as many as possible) biomarkers that have been described to date, pull together all the data, and analyse and compare all biomarkers head to head in the same dataset. We will do this in three phases: First, we will look at all published literature about neuroblastoma biomarkers from 1995 onwards and conduct a thorough analysis (this is called a systematic review and meta-analysis) to select the best biomarkers reported to date. Second, we will gain access to patient databases for each of the biomarkers (at the moment, each biomarker has been evaluated in a separate study/dataset) and create an enlarged INRG database including as many datasets, variables and biomarkers as possible; to then conduct an analysis integrating all the data together, which is called multivariate analysis. Thirdly, in order to confirm which biomarker(s) found on the first two phases are definitely the best one(s), we will analyse the best performing biomarkers in a homogeneous cohort of patients treated within a contemporaneous clinical trial, i.e. repeating all biomarkers in the same patients (which has never been done), to confirm which one(s) perform better and is taken forward to make treatment decisions in real clinical practice. With this ambitious approach, our proposal aims to identify patients with high-risk neuroblastoma with the poorest outcome at the time of diagnosis, with the final aim of giving these patients access to early therapies upfront, without waiting for them to relapse or become refractory to treatment. | 4.1 Discovery and preclinical testing of markers and technologies | 6project_grants_public
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gen_62f9927e81b95dd91c2b860fce8bff0e | Targeting CPEB-mediated translational balance in Hepatocellular Carcinoma | Worldwide Cancer Research | Institute for Research in Biomedicine | HRCS22_16442 | No abstract available for this analysis. | HRCS Research Uncodeable | 6project_grants_public
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gen_d46680739a45054cad449254bbccacbe | Resolving the tumour suppressor function of the E3 ubiquitin ligase Parkin | Worldwide Cancer Research | Walter and Eliza Hall Institute of Medical Research | HRCS22_16445 | The E3 ubiquitin ligase Parkin is critical for maintaining mitochondrial quality control as it is the key effector in damage-induced mitophagy. As well as a have key role in early onset Parkinson’s disease, Parkin is emerging as an important tumour suppressor, with mounting evidence indicating that the gene encoding Parkin (PRKN/PARK2) is one of the most frequently deleted or mutated genes in a wide variety of cancers including glioblastoma, colorectal, breast cancer. We have also identified links between Parkin loss and neuroblastoma, a common childhood cancer with poor prognosis and limited treatment options. How Parkin limits the growth of such diverse tumours is unclear. We hypothesise that the ability of Parkin to limit inflammation promoted by damaged mitochondria underpins its tumour suppressor function. We will use complementary cell and new mouse models coupled with innovative proteomics analyses to resolve how the E3 ubiquitin ligase Parkin controls inflammation as well as critical processes including apoptosis, cell cycle regulation and metabolism to define how Parkin activity limits the development of neuroblastoma. This proposal will identify Parkin or its specific substrates as new targets to treat neuroblastoma and potentially other cancers. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_8f7aec31911494f31e59c727e2fc5756 | Harnessing immune circadian rhythms to advance anti-tumour immunotherapeutic strategies | Worldwide Cancer Research | Pompeu Fabra University | HRCS22_16446 | No abstract available for this analysis. | HRCS Research Uncodeable | 6project_grants_public
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gen_79d56275bdbb9eeaa8903942708b6eea | PRECISION - supplementary award | Cancer Research UK | Netherlands Cancer Institute | HRCS22_16455 | Background Ductal carcinoma in situ (DCIS) now represents 20-25% of all breast neoplasia. This is due to large-scale detection by widely adopted population-based breast cancer screening programs . As a result, thousands of women are confronted with DCIS each year: more than 8,000 in the UK, 2,300 in the Netherlands, and over 50,000 in the US. Conventional management includes surgery, supplemented by radiotherapy and/or endocrine therapy, but overtreats the majority of DCIS as ~1% recur annually and breast cancer mortality is ~3% at 20 years. Uncertainty as to which DCIS lesions will progress to invasive cancer or, after excision, which will return with recurrent DCIS or invasive breast cancer drives this overtreatment. Distinguishing DCIS that may progress to lethal disease from the majority of harmless DCIS is therefore an urgent need to save thousands of women with low risk DCIS the burden of radical treatment without any survival benefit. Aim We aim to reduce the burden of overtreatment of DCIS (surgery, radiation therapy, hormonal therapies) through the development of novel tests that promote informed and shared decision-making between patients and clinicians, without compromising the excellent outcomes for DCIS management presently achieved. Methods First, three large retrospective DCIS cohorts (and supplementary sources) will be collected enabling subsequent in depth molecular studies. Second, extensive genomic characterisation, immune profiling and imaging analysis will be performed. In vivo and in vitro modelling will be performed to study the biology of DCIS in detail. Finally, all clinical, immune, and molecular data will be incorporated into a clinical risk prediction model. This risk prediction model can be validated in three prospective DCIS trials. Specifically, in the current project we will a.) collect tissue and blood samples from these trials and b.) start validation of the biomarkers detected in the retrospective series. How the results of this research will be used The discoveries from our laboratory studies, including a risk stratification model, will be cross-validated in prospective trials of DCIS active surveillance versus conventional treatment (the LORIS, LORD and COMET trials). As such, the main result of this study will be that we can identify a group of women for which active surveillance for DCIS could be a safer alternative to intensive treatment. Ultimately, this may also contribute to a more reassuring perception of risk regarding non-life threatening precancerous lesions in general, reducing anxiety and preserving quality of life. | 2.6 Resources and infrastructure (aetiology) | 6project_grants_public
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gen_adcb7da91c067a15c348736677fb974a | How can we harness cancer mechanobiology to prevent tumour progression? | Worldwide Cancer Research | University of South Australia | HRCS22_16463 | Metastatic breast cancer is currently incurable and new methods to halt invasion and metastasis are an important unmet clinical need. Rho-ROCK signalling in tumour cells is a key arbiter of the paracrine program by which cancers shape their microenvironments. We have established using an in vivo model of mammary cancer, that two key proteins, Creld2 and Ptx3 secreted by progressive breast cancers of all subtypes, mediate the recruitment and polarisation of cancer-associated fibroblasts (CAFs) and tumour-associated macrophages (TAMs). Crucially, these genetically normal cells are brought into the tumour's influence to promote tumour progression. We hypothesise that specific effector pathways downstream of ROCK synergise with tumour mechanobiology to selectively mediate the production and secretion of these paracrine factors. Identifying crucial signalling nodes within these pathways may prove a fertile source of novel approaches to target cancer progression. These studies complement ongoing research to identify the receptors in CAFs and TAMs that mediate the functions of Creld2 and Ptx3. Here we plan to: 1. Employ an in vivo model of microenvironment education and multiplex immunolabelling approaches to characterise the molecular mechanisms underlying the production and secretion of Ptx3 2. Adapt ex vivo primary cell culture approaches and in vivo functional assays to assess the contributions of ECM stiffness and the tumour secretome to the production of tumour-promoting CAFs and TAMs 3. Employ an alginate-based ex vivo 3D culture system to establish the biological relevance of CRELD2 and PTX3 to the tumour microenvironment of human patient samples. We believe that this highly innovative approach to understanding the interplay between signalling and mechanobiology in the tumour microenvironment will allow us to identify novel vulnerabilities that permit the targeting of breast and other cancers. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_83e3dbf83ec6033207321f7963d0941e | Motorized Traffic and Risk of Childhood Leukaemia | Children with Cancer UK | University of Modena and Reggio Emilia | HRCS22_16494 | This research project aims to assess the association between exposure to chemicals emitted by motorized traffic and industry emissions and childhood leukaemia onset. Specifically, we plan to carry out measurements of motorized traffic contaminant exposure through laboratory analyses of these pollutants and their metabolites in blood, urine, and hair samples of children newly-diagnosed with leukaemia at the Paediatric Haematology/Oncology Clinics of the Parma, Modena and Catania University Hospitals (n=100) along with sex- and age-matched controls (n=100) in 2019-21. The overall metabolomics pattern potentially induced by these air pollutants will also be assessed. We will focus on contaminants that are established or suspected carcinogens, including benzene, 1,3-butadiene, and polycyclic aromatic hydrocarbons (PAHs) together with heavy metals and metalloids, to clarify the role of these substances, and their mixtures, in the aetiology of childhood leukaemia. We will eventually seek to confirm exposure to motorized traffic by direct measurements through the installation of benzene and PM sensoring systems within the vicinity of the subjects residential houses. Moreover, we will assess potential lifestyle risk factors (including diet, smoking habits and occupation) through the administration of questionnaires to the children and their parents. | 2.2 Factors relating to physical environment | 6project_grants_public
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gen_fc40e29d45bbda9de7c3a1ffc5772033 | Characterisation of gene-lifestyle interactions associated with obesity-related traits in African populations | Wellcome Trust | University of the Witwatersrand | HRCS22_16509 | Obesity is increasing in Africa and elsewhere, but little is known of how genetic and environmental factors interact.The proposed research has the following components: (i) discovery phase: heterogeneity of variance analysis (HEVA) to determine candidate gene-environment interacting (GEI) variants in the Human Hereditary and Health in Africa (H3Africa) cardiovascular (CVD) working group to replicate the top-ranking signals. Additional variants will be selected from the GWAS trans-ethnic meta-analysis of East Asians, Europeans and Africans based on exhibiting heterogenous effects across the ethnic groups. Gradient Boosted LD adjusted (GraBLD) machine learning algorithms will be used to compute highly predictive genetic risk scores; (ii) cross-sectional and longitudinal analysis phase: single candidate GEI variants and genetic risk scores (of candidate GEI variants and from GraBLD analysis) will be combined with lifestyle factors in generalised linear models (cross-sectional analysis) and linear mixed models (repeated measures analysis) to determine plausible variants responsible for gene-lifestyle interactions in obesity-related traits. Assessments of sensitivity and specificity will be used to determine the predictiveness of these gene-lifestyle interactions and genetic risk scores. The transferability of the identified GEIs across African and European populations will be evaluated. The proposed research may help elucidate relevant risk factors and/or identify obesity intervention targets. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_3e9bfd4a7fefbdfc12d1e75ad06bfc1f | Causes and consequences of mental health challenges in autistic individuals during the transition to adulthood | MQ Mental Health Research | Karolinska Institutet Innovations (Sweden) | HRCS22_16513 | Research Questions Autistic individuals1 face profound challenges across their lives, including high rates of mental health problems. Many of these mental health problems emerge during the transition to adulthood, as illustrated in Figure 1, highlighting the critical need to understand mental health problems faced by autistic individuals during this period. The purpose of this project is to investigate causes and consequences of educational, occupational, and health challenges mental health problems in autistic individuals during the transition to adulthood. As shown in Figure 2, I will: 1.Identify risk factors for mental health problems in transitional-aged autistic adults: a) genetics; b) comorbidity; c) trajectories of childhood autistic traits. 2.Assess sex-specific mental health problems 3.Investigate long-term impacts of mental health problems during the transition to adulthood. Methods Cohorts: I will leverage three richly phenotyped cohorts, with follow-up spanning childhood and adulthood. Their coverage is shown in Figure 2. Swedish registers record healthcare, education, and welfare for the entire Swedish population. I have identified 26,538 autistic individuals from these registers, born 1973-1998, followed-up to ages 18-43. The Child and Adolescent Twin Study in Sweden (CATSS) includes 18,250 participants (10,848 genotyped), followed-up from ages 9-24. The Twins Early Development Study (TEDS) includes 7,124 participants, followed from birth to age 21. Risk factors, mental health problems, and outcomes are all assessed using questionnaires and registry data. All data are collected and have ethical approval. Study Designs: I will define genetic factors linked with autism using polygenic scores, and test their association with mental health problems from ages 18-24 in CATSS. The utility of genetic factors in predicting these outcomes will be compared with more conventional indicators, such as symptoms (aim 1a). I will test whether the association between autism and mental health problems is mediated by comorbidity in CATSS and Swedish registers (aim 1b). I will compare mental health problems at ages 16-21 across trajectories of autistic traits in TEDS, identified using latent growth curve models (aim 1c). Sex-specific mental health problems at ages 18-24 in CATSS and Swedish registers will be assessed using a stratified cohort design (aim 2). I will compare long-term outcomes from ages 25-43 between autistic individuals showing different numbers of mental health problems during the transition to adulthood, utilizing the extended follow-up of Swedish registers (aim 3). Regression models will be the chief analytic approach in all aims, with models varying by outcome (linear, logistic, or time-to-event). Expected Outcomes This truly interdisciplinary project unites contemporary methods and concepts from epidemiology, behavioural genetics, and lifespan psychology to address three novel aims of crucial priority in autism research. This project will move the field beyond establishing that autistic adults face challenges, towards assessing why this is so. This will subsequently inform strategies to identify and support particularly vulnerable autistic adults in navigating adult life, with the goal of improving their mental health and wellbeing by lifting barriers to their participation in society. 1'Autistic individuals' is the preferred terminology of many stakeholders when referring to autism | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_6d17cd26acca2b5ae4e11085d917d909 | Making vital connections; exploring how desmoplasia gets on pancreatic cancer's nerves | Worldwide Cancer Research | Temple University Health System | HRCS22_16520 | Pancreatic ductal adenocarcinoma (PDAC) will soon become the second USA deadliest neoplasia. PDAC features a fibrous stroma, desmoplasia, with low blood/nutritional supply and extensive innervation (neoneurogenesis/axonogenesis) associated with poor prognosis, neuropathy and perineural invasion. The roles of cancer-associated fibroblasts (CAFs) and their self-derived desmoplastic extracellular matrix (D-ECM), in aiding nutritional-deprived tumor survival and neoneurogenesis, which affect PDAC’s onset/progression, are understudied. Using mRNA from patient’s D-ECM producing CAFs vs. matching normal stellate cells, we discovered a specific glutamatergic presynaptic protein. A simultaneous multiplex immunofluorescent approach validated its overexpression and that of its postsynaptic partner. Increased expression of these proteins is typical in neurological syndromes allied to increased cancer risk. Preliminary data indicated that: D-ECM and CAFs increase both neuron and tumor cell longevity; functional synapses between CAF and other cells are formed; and, CAF-secreted vesicles expressing presynaptic protein engage with PDAC cells, expressing the postsynaptic protein to promote tumor growth. Hypothesis: PDAC is locally enabled by D-ECM, CAFs, neurons and CAF secreted vesicles in a synapse-like mechanism. Aim1: Investigate if CAFs support neoneurogenesis and PDAC cells in a synapse-like manner. We will test the functional need for CAF and neural synaptic proteins, as well as downstream enzymes and other proteins, in maintaining high extracellular glutamate levels, posited to sustain neoneurogenesis and PDAC survival under nutritional stress. Our D-ECM system together with gain and loss of function approaches will be used to investigate the synaptic protein roles in these processes. Aim2: Assess requirement for and level of “pre- and post-synaptic” proteins linked to human PDAC. We will use our multiplex immunofluorescent approach in a well annotated human PDAC cohort to question neoneurogenesis levels associated with quantities and locations of the synaptic pair and question their association with patient outcomes. Vesicles, positive for the pre-synaptic protein, will be probed in matching liquid biopsies. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_400d5632ef2530d52502b27892b96f78 | Enhancing CAR-T cell therapies for gliomas | The Brain Tumour Charity | Harvard University | HRCS22_16527 | No abstract available for this analysis. | No Research Activity assigned | 6project_grants_public
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gen_fe07735477a82674108f8aa1b67877e9 | Understanding the immune cell dysfunction in pediatric lymphoma | Worldwide Cancer Research | Karolinska Institutet Innovations (Sweden) | HRCS22_16528 | Lymphoma is the third most common type of cancer among children and accounts for 10-15% of all childhood cancers. Lymphoma in children and adults are divided into three main groups; Hodgkin lymphoma, B- and T-cell lymphoma. Lymphoma stems from faulty activation of B cells and, less frequently, T cells. Upon an infection, B cells undergo affinity maturation in germinal centers. B cells in germinal centers mutate their antibody-coding genes in a process that induce DNA damage during rapid B cell proliferation. B cell transformation into lymphoma may occur because of faulty DNA repair, defects in cell division, and impaired migration and interaction with other cells during the process of mutating and selecting the best fit B cells for antibody production. Patients with inborn errors in the immune system, primary immunodeficiency diseases, are prone to develop pediatric and adolescent lymphoma of very poor prognosis. An unmet need is to understand the molecular and cellular pathophysiology to define better treatment for patients with pediatric lymphoma, both in the primary and relapse setting, and for poor prognosis lymphoma of primary immunodeficiency patients. The goal of this project is two-fold: 1) To gain molecular insight into pediatric lymphoma by analysis of single cells from lymphoma specimens and 2) To develop and use methods where specific alteration in gene expression can be examined functionally and for defining new personalized and generalized therapeutic approaches. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_eeb08da993b2c367d522457ad46a5e84 | A computational approach to identifying trans-diagnostic predictors of antidepressant response | MQ Mental Health Research | Trinity College Dublin | HRCS22_16535 | We need to develop tools that can improve the precision with which we allocate treatments in psychiatry. Current psychiatric disease classifications (DSM-5, ICD-10) ensure reliable diagnoses across clinicians, but their diagnostic categories do not allow for individual treatment predictions – for example, most patients with major depression do not recover after their first antidepressant treatment. This project aims to remedy this by using machine learning to develop an algorithm that can quantify how likely an individual is to respond to a range of antidepressant medications. Large samples are required to train a robust predictive model. To achieve this, all data collection will be web-based and subjects will be recruited worldwide. Predictors will include cognitive tests, which are linked to specific brain circuits and neurotransmitter systems that relate to psychiatric disease and treatment action, clinical symptoms and treatment variables, and demographics. Once the algorithm has been trained and validated on an independent test set, we will test its generalizability in three local clinics. The long-term goal of this work is to develop a tool that can be used by clinicians to achieve individual treatment predictions, something that will ultimately be tested in a randomized controlled trial. | 4.1 Discovery and preclinical testing of markers and technologies | 6project_grants_public
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gen_cc56e0228e76e5c2e55b1e705687218e | Understanding oncogenic transcriptional processes in synovial sarcoma | Worldwide Cancer Research | Trinity College Dublin | HRCS22_16545 | Synovial sarcoma is an often aggressive malignancy primarily effecting children and young adults. Unfortunately, these tumours often do not respond well to conventional therapeutic interventions and overall survival rates remain poor. The disease is caused by a recurrent chromosomal translocation generating a characteristic fusion protein, SS18-SSX. In synovial sarcoma cells the fusion protein assembles into SWI/SNF complexes, which are essential chromatin regulators that alter chromatin structure to regulate gene expression. Incorporation of SS18-SSX into these complexes alters their function, resulting in significant oncogenic gene expression changes. Targeting the oncogenic function of SS18-SSX presents and attractive therapeutic option for the development of mechanistically anchored cancer treatments; however the fusion itself has proven intractable for direct targeting. Here, we are pursuing a research program aimed at better understanding the function of SS18-SSX containing complexes and exploring new opportunities to therapeutically target complexes containing the fusion protein. Using CRISPR/Cas9 based approaches in functional genomics screening we’ve identified the acetyltransferase enzyme p300 as functionally essential in synovial sarcoma cells. By combining these data with in depth proteomic analyses of SS18-SSX interacting proteins we further identified that p300 physically associates with SS18-SSX. In Aims 1 and 2 of this research program we are combining biochemical and genomics approaches to characterise the composition and function of SS18-SSX/p300 containing complexes in synovial sarcoma cells. In Aim 3 we are taking an ambitious approach combining CRISPR/Cas9 screening with single-cell genomics analysis platforms to characterise the molecular function of SS18-SSX containing complexes in cancer cells. Together, these aims will provide a mechanistic understanding and potential therapeutic rationale for targeting p300 function as a novel therapy in patients. In addition to providing unprecedented molecular understanding of disease biology, which will likely highlight more opportunities to explore and develop future approaches to more effectively treat synovial sarcoma patients. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_32f69f1719f5ab612e881cf48aeaacb6 | Hysteresis conveys the EMT spread to the neighborhood tumor cells and metastasis | Worldwide Cancer Research | CERCA Institution | HRCS22_16556 | Cancer metastasis is a complex process with multiple challenges that disseminated tumour cells need to overcome to form overt metastasis, yet many biological aspects of metastasis are poorly understood. One of the most studied tumour cell phenotypic changes during metastasis is the epithelial-to-mesenchymal transition (EMT). This is a reversible transdifferentiation into a mesenchymal phenotype that favours cancer cell dissemination and cell plasticity to adapt to new conditions. We have recently described the dynamics of EMT at single cell level, by a molecular feedback loop that governs a bistable switch among the epithelial and mesenchymal state, also called hysteresis. However, how the dynamics affects group-decision processes at the cell population level has not been yet well studied. Remarkably, our recent data in 2D cell cultures show that EMT-like cells can spatially spread the EMT induction to the neighbourhood when the recipient cells are wired to undergo EMT by hysteresis. In this proposal, we aim to study the collective effects of hysteretic-EMT that resonates into spreading the EMT across cancer cell populations and its epigenetic mediators. For this purpose, we will use unique models of hysteresis and non-hysteresis cancer cells that we have previously generated, and inducible EMT systems with precise space and time control in 3D cultures in vitro, as well as in vivo breast cancer models. Advanced microscopy imaging, flow-cytometry analysis, ATAC-sequencing, and genome-wide DNA methylation will be used to model and unveil the mechanisms involved in the EMT spreading effect. Overall, this proposal will characterize the ability of cancer cells to amplify the EMT signal received by tumour cells, and the epigenetic mechanisms underlying it. This can lead to specific treatments to disrupt the spreading effect in order to halt cancer metastasis. | 2.1 Biological and endogenous factors | 6project_grants_public
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gen_2f1105a4f7a7f4b610ef9810946661a3 | Chlomipramine derivatives to target the ubiquitin ligase NEDD4 in lung cancer | Worldwide Cancer Research | FIRC Institute of Molecular Oncology | HRCS22_16567 | No abstract available for this analysis. | No Research Activity assigned | 6project_grants_public
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gen_a4e6bbd72f5f428aa0f7f087c4437891 | Strengthening Joint Scientific & Political Actions for Global Health | Wellcome Trust | World Health Summit | HRCS22_16601 | The most pressing global health challenges of our time require strong partnerships for multi-stakeholder exchange and appropriate policy responses. Against this background, the World Health Summit would like to strengthen its collaboration with expert organizations such as Wellcome Trust, to make a greater contribution to policy-making in the field of global health research and strengthen scientific and political activity in Berlin and beyond in the spirit of the sustainable development goals. | No Research Activity assigned | 3networking_collaborative
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gen_59cd4621431152ba23b329d5aaf43f5b | Alzheimer’s Research UK Drug Discovery Institute 2020: University College London | Alzheimer's Research UK | University College London | HRCS22_20352 | No abstract available for this analysis. | Infrastructure | 7research_infrastructure
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gen_3056ce2f195498fd0cb390ad79c4b320 | Kennedy Trust Chair in Molecular Immunology | The Kennedy Trust for Rheumatology Research | University of Oxford | HRCS22_20525 | No abstract available for this analysis. | Personal | 1fellowships_scholarships
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gen_fb30e657d54aff27c027d377fabd4f11 | Antimicrobials and antimicrobial resistance (AAMR) | Wellcome Trust | University of Nottingham | HRCS22_20539 | No abstract available for this analysis. | Missing/Incomplete | 6project_grants_public
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gen_7d4222d07fab5d1c6a64d018c87b50e7 | A 4 year PhD in theoretical systems biology and bioinformatics | Wellcome Trust | Imperial College London | HRCS22_20553 | No abstract available for this analysis. | Studentships | 1fellowships_scholarships
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gen_8cfc47d53f53de27fa129decb756d2ff | Diamond Capital Award 2021/22 (Diamond FY22/23) | Wellcome Trust | Diamond Light Source | HRCS22_20554 | No abstract available for this analysis. | Infrastructure | 7research_infrastructure
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gen_95a7ad6f98589d3a3d501006bea29ad3 | Alzheimer’s Research UK Drug Discovery Institute 2023: Oxford | Alzheimer's Research UK | University of Oxford | HRCS22_20576 | No abstract available for this analysis. | Infrastructure | 7research_infrastructure
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gen_818cc7c564aa2154c8d986760baf414e | ARUK DRI 2021-22 Commitment | Alzheimer's Research UK | University College London | HRCS22_20582 | No abstract available for this analysis. | Infrastructure | 7research_infrastructure
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gen_d8bc18ea2bd4a8b8c56208d951394773 | Wellcome Trust Four year PhD programme in Stem Cell Biology and Medicine | Wellcome Trust | University of Cambridge | HRCS22_20588 | No abstract available for this analysis. | Studentships | 1fellowships_scholarships
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gen_5ef92cba50dd421404fc2a3a430d94b6 | Wellcome Trust 4-year PhD Programme in Quantitative and Biophysical Biology | Wellcome Trust | University of Manchester | HRCS22_20600 | No abstract available for this analysis. | Studentships | 1fellowships_scholarships
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gen_4607517a10efae93c7cda4e2d44f2f5e | KIR Director salary and research support | The Kennedy Trust for Rheumatology Research | University of Oxford | HRCS22_20610 | No abstract available for this analysis. | Personal | 1fellowships_scholarships
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gen_77d92e9a7628adb155b41e092c9daebc | Mechanisms of inflammatory disease. | Wellcome Trust | University of Birmingham | HRCS22_20629 | No abstract available for this analysis. | Missing/Incomplete | 6project_grants_public
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gen_5422e382c95be38e247a37f5a624a910 | Tissue Repair | Wellcome Trust | University of Edinburgh | HRCS22_20633 | No abstract available for this analysis. | Missing/Incomplete | 6project_grants_public
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gen_77d9989a4272a92f197870ae50b27895 | Infection, Immunology and Translational Medicine 4 year PhD programme. | Wellcome Trust | University of Oxford | HRCS22_20637 | No abstract available for this analysis. | Studentships | 1fellowships_scholarships
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gen_cd8822c3d8350c939513b9fdec9ed6c8 | Molecular and Cellular Basis of Infection | Wellcome Trust | Imperial College London | HRCS22_20654 | No abstract available for this analysis. | Missing/Incomplete | 6project_grants_public
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gen_40d549a089ccdd006d633c804b14339e | Cardiff University - Integrative Neuroscience | Wellcome Trust | Cardiff University | HRCS22_20655 | No abstract available for this analysis. | Missing/Incomplete | 2institutional_funding
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gen_0967ed46e802104428850d0e027e48e6 | Translational Neuroscience - training the next generation of basic neuroscientists to embrace clinical research. | Wellcome Trust | University of Edinburgh | HRCS22_20659 | No abstract available for this analysis. | Studentships | 1fellowships_scholarships
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gen_cdc563d08913a1a6e6a46ceed2ca0f47 | 4 year PhD in Neuroscience | Wellcome Trust | University College London | HRCS22_20669 | No abstract available for this analysis. | Studentships | 1fellowships_scholarships
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gen_06bcffcfaec74710d0ae9796d1f1c6ee | Cell therapies and regenerative medicine. | Wellcome Trust | King's College London | HRCS22_20670 | No abstract available for this analysis. | Missing/Incomplete | 6project_grants_public
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gen_796b7dedd1ac164a8983889bb00e401f | Wellcome Trust Doctoral Training Fellowship Scheme for Clinicians | Wellcome Trust | University of Oxford | HRCS22_20713 | No abstract available for this analysis. | Studentships | 1fellowships_scholarships
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gen_e82061dfcd329e9ba6b4f8d3c2749bfc | UK Biobank Core Renewal Years 6-10 (Joint funding with UKRI, CRUK, WT and DHSC) | British Heart Foundation | University of Oxford | HRCS22_20733 | No abstract available for this analysis | Infrastructure | 7research_infrastructure
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gen_0ffd6981fd94af330e26776c4e45e458 | Joint Global Health Trials Award - round 7 - June 2017 | Wellcome Trust | Medical Research Council | HRCS22_20829 | No abstract available for this analysis. | Infrastructure | 7research_infrastructure
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gen_a772311774d5eaa6248fe93573969db8 | The Wellcome Trust GW4 Clinical Academic Training Programme | Wellcome Trust | University of Bristol | HRCS22_20866 | We propose to create a Wellcome Trust-funded Clinical Academic Training Programme (GW4-CAT) for medical, veterinary and dental trainees across three members of the well-established and successful GW4 Alliance of research-intensive universities: Bristol, Cardiff, and Exeter. Based on our collective experience, we will address the following goals: 1. Recruit and retain trainees from diverse disciplines, backgrounds and clinical specialties across medicine, dentistry and veterinary sciences; 2. Support and encourage trainees to make bold choices with access to cutting edge research environments that will stretch them intellectually and practically exploiting environments that have not ‘traditionally’ been accessed by clinical doctoral trainees; 3. Provide exemplary doctoral and post-doctoral support through linked academic clinical lectureships and mentorship, building a run-through programme to nurture our best graduates so that they are most effectively positioned to win externally-funded post-doctoral fellowships. GW4-CAT will support trainees for almost a decade from pre-PhD through to research independence, provide demonstrable impact on career progression, resilience and ensure significant achievement at more senior levels and independent senior clinical academic positions. Finally, we will use the opportunity provided by GW4-CAT to catalyse the creation of a ‘Centre of Excellence for Clinical Academic Training’ covering the southwest of the UK. | Studentships | 1fellowships_scholarships
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gen_611e2067bdd672e35496ff7b387be813 | Wellcome Trust Doctoral Training Centre in Public Health, Economics and Decision Science (PHEDS): Assessing the effectiveness and cost-effectiveness of policies and prevention strategies that reduce noncommunicable disease burden and health inequity | Wellcome Trust | University of Sheffield | HRCS22_20881 | With ever scarcer resources for public health policies and programmes, high-quality scientific evidence on the cost-effectiveness and long-term benefits of alternative public health intervention options will become increasingly important for future decision-making. To our knowledge, PHEDS is one of just a handful of Doctoral Training Centres dedicated to Public Health Economics and Decision Science in the world. Wellcome Trust investment will allow us to grow, focus and strengthen ScHARR’s doctoral training in this area, broadening its scientific remit from health behaviours to also include research into the cost-effectiveness of policy options that address the social determinants of health (e.g. economic conditions, housing, employment) to reduce NCD and tackle health inequalities. Through the synergy of several cohorts of PhD researchers conducting cutting-edge research into these challenges at the same time with expert supervision, the programme aims to substantially increase the momentum of scientific discovery. Equipped with 4 years of experience in interdisciplinary collaborative working environments and with strong analytic skills, our graduates will be excellently placed to forge influential careers as leaders in academia and governmental and non-governmental organisations promoting evidence-based decisions about resource allocation in public health and tackling disease burden in the UK and beyond. | Studentships | 1fellowships_scholarships
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gen_e03b26dd8d13f5f18b96a821301eaf3c | Global Health Trials Award – Round 8 - June 2018 | Wellcome Trust | Medical Research Council | HRCS22_20883 | No abstract available for this analysis. | Infrastructure | 7research_infrastructure
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gen_56b74bbf58d4c2a9bc7a6eced93b4506 | One Health Models of Disease: Science, Ethics and Society | Wellcome Trust | University of Edinburgh | HRCS22_20886 | Technological advances in genome editing and animal bioscience have potential for huge societal impact, and are opening up opportunities for the design of new ‘One Health’ models of neurodegenerative, cardiovascular, developmental, and infectious diseases of humans and animals. Such models can transform our approach to understanding pathogenesis, facilitating the development of therapies or preventive measures. However, there is little or no opportunity for graduate student training in relevant state-of-the-art techniques at world-class, purpose-built facilities by leading scientific innovators at the intersection of human and veterinary medicine. Moreover, scientists require training in bioethics and social science to allow them to appreciate the ethical and societal implications of these powerful new approaches. To address this need, we propose a PhD programme in “One Health Models of Disease: Science, Ethics and Society”. This innovative, and versatile programme will combine core training in relevant experimental techniques, bioethics and social sciences relating to One Health, rotation research projects, and internships with academic, industrial, policy and stakeholder organisations, alongside the main PhD project. Students will be supervised by world-leading life scientists addressing important diseases of humans and animals, and social scientists and bioethicists conducting cutting-edge research into the social and ethical dimensions of 21st century science. | Studentships | 1fellowships_scholarships
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gen_4a112b183074d4346516ca9df8e873b4 | Integrative Infection Biology - Mechanisms and Control of Disease | Wellcome Trust | University of Glasgow | HRCS22_20891 | The mission of the proposed IIB Programme is to inspire the next generation of innovative world-class researchers to tackle global infection challenges. We will achieve this by shaping excellent PhD projects that build synergistic collaborations across the University of Glasgow and our partner institutes. Our aim is to give all students an exceptional experience, driving them to build their careers with the ability, confidence and integrity to make transformative contributions to global health. Our principles are promoting inquisitive and rigorous science, imparting technological and analytical skills, and reinforcing personal well-being. Our graduates will be ‘Scientists without Boundaries’ at ease with the implementation of far-reaching interdisciplinary concepts on the local and global stage. The IIB Programme is integrated around Glasgow’s core of global excellence across infectious disease research, including pathogen biology, pathogen-host interaction, epidemiology, ecology and transmission control, encompassing >25 Wellcome Trust-funded investigators. We have partnered with key institutions in Europe and Africa, to offer PhD students exceptional opportunities in all areas of infection biology. UoG funding will add 2 students from Africa each year, making 7 altogether. Students will select projects after laboratory rotations and be fully mentored through to a ‘PhD-Plus Year’ fostering the transition to their post-doctoral career. | Studentships | 1fellowships_scholarships
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gen_28e4e8d88afe966f65c2f99c4a0570e6 | Advanced therapies for regenerative medicine | Wellcome Trust | King's College London | HRCS22_20910 | The goal of the programme is to train a new generation of researchers in the advanced therapies that underpin regenerative medicine, including cell transplantation, gene therapy and endogenous tissue repair. At the heart of this young field is the importance of translating laboratory-based studies to patient benefit. Thus, students will gain knowledge of the underpinning discovery science, and clinical and commercial applications. Moreover, to foster translation we will bring together researchers in different disciplines, so that the students appreciate the creative possibilities of working at the interface between different fields. Supervisors are drawn from across King’s College London, spanning clinical, nonclinical, early, mid-career and senior researchers. The first year comprises three rotations, combined with taught courses and master classes, leading to the award of an MRes. This is followed by three years of focused research. Partner organisations and secondments provide additional training opportunities. From the outset, the programme emphasizes growing as a scientist, exploring post-PhD opportunities, and the scientist in society. Students and their supervisors are seen as partners in a journey, with a special focus on fostering mutual respect and understanding. | Studentships | 1fellowships_scholarships
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gen_bc7ee0b2a62dbf63210e2f8be11fcf25 | Optical Biology | Wellcome Trust | University College London | HRCS22_20918 | The ‘Optical Biology’ PhD programme will train future research leaders to answer fundamental questions in biology by exploiting and developing state-of-the-art optical techniques. The programme brings together life scientists, physicists, chemists and computational scientists at UCL, with world-leading industrial and academic partners, to deliver an integrated training programme in the most advanced optical methods and analysis tools. This would be the first UK PhD programme offering multidisciplinary training in the major advanced light-based methods that are transforming all areas of biomedical research. The programme will be based at UCL, a world-leading environment where many major advances in optical techniques for biology have been developed, including ultra-fast 3D 2-photon microscopy, targeted 2-photon optogenetics, low power super-resolution imaging and whole-brain optical mapping. It will also offer students outstanding opportunities to undertake internships and training with our industrial and academic partners, promoting their career development and providing them with attractive post-PhD prospects. Key programme goals: 1. To train researchers capable of developing and using state-of-the-art optical methods and associated analysis techniques. 2. To train researchers to use these methods to address fundamental biological problems. 3. To create researchers who engage, communicate and collaborate effectively with both industry and academia across disciplinary boundaries. | Studentships | 1fellowships_scholarships
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gen_fc172945be1706bccb95482076838e23 | Barts Charity Fixed Term Lecturerships: the Rising Stars programme | Barts Charity | Queen Mary University of London | HRCS22_20919 | Barts SMD at Queen Mary University of London seek funding for a transformational programme to recruit the new generation of lead researchers for the next decade. The proposed plan is to appoint 16 fixed term lecturers (either external or internal) and support them in their career progression towards independence. The results of this project will be: 1) capacity building in junior academic positions (ensuring continuity to the quality of academic research conducted at SMD); 2) higher high quality head counts for REF2021 submission (with positive impact on SMD finances and reputation); 3) consolidation of internal high quality post-docs (avoiding the risk of attraction by other Colleges in London and beyond). Following the Early Career Researchers programme effected in 2013, and the ensuing success, the Barts Fixed Term Lecturerships (also to be referred to as the Barts Rising Stars) programme will support a second round of junior academic recruitment (internal and external) with multiple benefits on the research endeavours in strategic areas for the School. | Personal | 1fellowships_scholarships
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gen_9671e93b4e919ae8d45e1052b6ea6456 | Building research facilities for the future | Barts Charity | Queen Mary University of London | HRCS22_20922 | Barts and The London School of Medicine and Dentistry at Queen Mary University London (SMD) aims to improve the health and wellbeing of people throughout the UK and beyond through research and teaching excellence. Over the past ten years, the SMD has experienced unparalleled growth in research power and research output quality. Researchers in the key strategic areas of cancer, cardiovascular disease, inflammation and preventive medicine have been extremely successful in winning major new grant funding that has huge potential to deliver major patient benefits through translation of research from bench to bedside and into the wider population. This is a very exciting time for SMD. A new phase of growth is planned, aiming to increase the overall research power by recruiting between 50-100 new talents over the next 3-4 years, helping the School continue to grow in breadth and depth within a very competitive London market. This application, requesting £6,460,200 of funds, aims to enhance SMD?s research facilities by optimizing the existing footprint of the Charterhouse Square Campus through an ambitious project of renovation. The SMD is in the fortunate position of being able to expand within the existing campus, unlike many other London universities. Providing new research laboratories equipped to the latest standard, as well as creating additional and bespoke teaching facilities and office space, this proposal supports the Faculty?s ambition of growth. It will ensure the current and ambitiously expanding research programmes are supported, enabling them to reach their full potential to deliver tangible benefits to patients and the community. Providing optimal space to accommodate existing staff and new talent recruited into SMD, will allow them to flourish scientifically and therefore shape the future of research and setting the School in the optimal position for the next Research Excellence Framework (REF2021). The expanded portfolio of research and training activities will enable delivery in terms of translation into patient benefits, high quality publications and further successful grant applications. The School has engaged with all key stakeholders, feasibility studies have already been carried out and a clear plan has been developed to ensure staff and students are fully supported during the renovations which will result in 21st century, high quality research and teaching facilities. | Infrastructure | 7research_infrastructure
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gen_11926f3b63c83927c15fd07ada358618 | Health Priorities in Resource-Limited Settings | Wellcome Trust | University of Liverpool | HRCS22_20926 | This proposal is for the addition of a single post to the existing WT funded Clinical PhD Programme Health Priorities in Resource-Limited Settings at Liverpool. The current Programme supports the development of a cadre of clinician scientists in global health research with aims of: 1. Identifying outstanding individuals 2. Offering them high levels of support and mentorship throughout their PhD 3. Facilitating their onward academic careers as independent researchers and future leaders in research in resource limited settings. The additional post is designed to be more flexible than our current four year posts. It may: a) Last for three OR four years: suiting those with research experience or whose clinical training or domestic requirements prevent a longer fellowship. b) Allow more of the research to be undertaken in the UK. The focus on diseases of Lower/Middle Income Countries (LMIC) will remain, but spending a shorter period abroad may be attractive for those with family or caring responsibilities in the UK. c) Broaden opportunities for veterinary trainees. Many LMIC human health issues are related to animal interactions but opportunities to undertake global health research by veterinary clinicians have been relatively limited. We hope to encourage such research. | Studentships | 1fellowships_scholarships
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gen_47d847706fabd7fb4577c1bbd4eaa1a3 | Neuro-Immune Interactions in Health and Disease | Wellcome Trust | King's College London | HRCS22_20927 | Cross-talk between the nervous and immune systems is critical for survival, and disrupted neuro-immune communication is observed in many debilitating conditions, including chronic inflammatory, neurodegenerative and psychiatric diseases. Yet, research and training in neuro-immune interactions is generally conducted in discipline-specific silos. We propose to accelerate ground-breaking interdisciplinary research and knowledge sharing by instituting a unique PhD training programme in Neuro-Immune Interactions in Health and Disease. We will deliver: • World-class scientific training, provided in a flexible, student-led fashion, by internationally leading investigators, using state-of-the-art technologies, cutting-edge science and supervision methods (Assessment, Feedback and Development (AFD) meetings, PhD Progress Committees). • Extensive skills training to transition students in and out of the Programme – individually tailored and formalised in a personal development plan (PDP). • A diverse and inclusive training environment, reflected in our Programme Management Board (PMB), supervisors, recruitment and partnership plans. • An open and positive research culture, including training in research integrity, data sharing, bespoke mental health provisions and zero-tolerance of bullying and harassment. • A new generation of scientists with the knowledge, skills and networks to drive world-leading neuro-immune research, who can excel equally in academic and non-academic professions. Searchable keywords: share, sharing, world-class, flexible, positive, diverse, inclusive, skills training, mental health | Studentships | 1fellowships_scholarships
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gen_60f2b0ab7bae097f00cbf1325b6d9d26 | WT-MRC Clinical Research Training Fellowship Partnership | Wellcome Trust | Medical Research Council | HRCS22_20929 | Wellcome funding will allow the MRC to appoint an extra 5 CRTFs between 2017-2021. | Studentships | 1fellowships_scholarships
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gen_bdd56fbc8b6f92d1139289884b85a114 | UK Biobank - Core Renewal | Wellcome Trust | UK Biobank | HRCS22_20932 | No abstract available for this analysis. | Infrastructure | 7research_infrastructure
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gen_01c85db05b0ae0279953e89044dc0b14 | GW4-CAT PhD Programme for Health Professionals | Wellcome Trust | University of Bristol | HRCS22_20945 | Building on our Wellcome-funded Clinical Academic Training Programme (GW4-CAT) that uniquely supports Medical, Dental and Veterinary professionals; we will deliver a scheme that combines world class PhD training with exit to mentored post-doctoral positions with protected research time, open to all health professions (GW4-CAT-HP). Capitalising on the world class facilities and absolute commitment of the universities of Bath, Bristol, Cardiff and Exeter (Great Western 4 - GW4), and our partner NHS Boards and Trusts and Vet School, our objectives for GW4-CAT-HP are to: 1. Recruit talented Fellows from diverse disciplines and clinical specialties, supporting them to make bold choices by accessing the wide range of world-class cutting-edge research environments across GW4 where they will be stretched intellectually and practically. 2. Foster a positive and inclusive research culture, through robust equality, diversity and inclusion (EDI) practice and enabling the highest standards of research integrity through support and formal training. 3. Ensure, through bespoke and structured long-term support and mentoring, that all our Fellows secure externally funded post-doctoral support and linked clinical academic posts provided in partnership with our NHS Trusts, Boards and Vet School, to achieve research independence and retain excellent researchers in clinical academia. | Studentships | 1fellowships_scholarships
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gen_147068a0ab98206d560feca07ef76783 | 4Ward North PhD Programme for Healthcare Professionals | Wellcome Trust | University of Manchester | HRCS22_20952 | Our programme will deliver excellent doctoral training for all healthcare professions. We are building a comprehensive inter-disciplinary programme across biomedical discovery and experimental medicine, reaching into our leading skills in physical sciences, engineering and computational/data science. We have fully refreshed our partnership across the Universities of Leeds, Manchester, Newcastle and Sheffield; seven out of eight new directors are new. We have forged fresh partnership with the Alan Turing Institute, integrated our comprehensive ties with industry, and deepened our links to the Francis Crick Institute. We have coalesced features that define our best research culture and developed a thoughtful approach to equality, diversity and inclusion to ensure we capture talent, regardless of background or profession. The training will be valuable to fellows, supervisors and directors alike and set best-practice that will permeate our partner organisations. We are particularly proud of a new initiative with the Nuffield Foundation/STEM Learning to host 16-19 year olds as part of widening participation in higher education and scientific research. This programme is important to us. We need a research-intensive workforce trained to the highest standards equipped to innovate for a surrounding population with some of the greatest health needs and reduced life expectancy in the UK. | Studentships | 1fellowships_scholarships
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gen_07ac50c481226dcdc9e8b9468fbabfa2 | Health advances in underrepresented populations and diseases (HARP) PhD Programme (“HARP PhD programme”) | Wellcome Trust | Queen Mary University of London | HRCS22_20962 | Underrepresentation of patient groups and diseases in research is both a cause and a consequence of health inequality. People may be underserved by healthcare and underrepresented in research due to 1) social inequalities related to demographic and protected characteristics, 2) marginalisation related to socioeconomic, lifestyle or legal factors, or 3) health status e.g. mental health, or rare diseases. Disease mechanisms, phenotyping and novel therapeutics are often studied in homogeneous populations with chronic underrepresention of certain groups. If studies fail to include these groups, outputs will be less accurate, relevant or effective in underrepresented populations, thereby exacerbating health inequalities. To tackle these problems and redress these inequalities we will support fellows’ individual and specific training needs so that they are more able to manage career transitions and have the confidence to apply their imagination to bold research with populations and in diseases that will benefit the most from their efforts. This DTP will: 1. Recruit the best and most motivated fellows from a diverse range of applicants into a progressive research culture environment. 2. Conduct world-class research with underrepresented populations supported by specific training 3. Tackle barriers to Academic Transitions: i. (optional) Pre-Doctoral Training Phase ii. Bespoke Career Development Programme iii. Post-Doctoral Support Phase | Studentships | 1fellowships_scholarships
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gen_885438ced25d9dc8c4d02a7c30f61231 | PhD Programme for Primary Care Clinicians | Wellcome Trust | Queen Mary University of London | HRCS22_20965 | This doctoral programme for Primary Care Clinicians aims to increase research capacity across contemporary primary care to create future research leaders who will develop innovative and evidence based practice and policy to improve population health and support the NHS. Five clinical PhDs per year for five years (in total approximately 18 GPs and 7 other primary health care clinicians) will be hosted across 10 NIHR School for Primary Care (SPCR) members, building on our successful previous Wellcome PhD programme. The NIHR SPCR represents the leading departments of academic primary care in England and provides extraordinary critical mass enabling a broad and inclusive supervisory pool, access to databases, international expertise and bespoke training. Doctoral students will have supervisors across two consortium members and will join 45 NIHR SPCR doctoral students appointed from 2021-2026 to form a supportive cohort of peers who have the opportunity for regular contact at training meetings and our very successful Annual Trainees Event. Equality and diversity are core values underpinning the Programme which promotes the development of networking and collaboration, builds strong and experienced research groups and provides a rich, supportive research environment for doctoral students to develop into successful clinical academics and future research leaders. | Studentships | 1fellowships_scholarships
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gen_72e57da7bc10b769f4b088a2ab0fb23f | Diamond Operating Award 2021/22 (Diamond FY22/23) | Wellcome Trust | Diamond Light Source | HRCS22_20973 | No abstract available for this analysis. | Infrastructure | 7research_infrastructure
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gen_410026c8037f9fe2b1dbf27b309b04a8 | Funding towards Cambridge Heart and Lung Research Institute (HLRI) | British Heart Foundation | University of Cambridge | HRCS22_20975 | No abstract available for this analysis | Infrastructure | 7research_infrastructure
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gen_744fe88ffd5f058fa2159a5447043ec2 | EMBL-EBI expansion: response to the exponential increase in life science data | Wellcome Trust | EMBL - European Bioinformatics Institute | HRCS22_20977 | No abstract available for this analysis. | Infrastructure | 7research_infrastructure
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gen_2ccbbc05552a5bbd5d86aacccc8383a7 | Sanger Supplementary Award 2021-2023 | Wellcome Trust | Wellcome Sanger Institute | HRCS22_21020 | No abstract available for this analysis. | Infrastructure | 7research_infrastructure
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gen_ee045bdd8f44a02ce3f2e8e91ef77e7f | Evaluating the Impact of Beyond Words Book Clubs on the Health and Wellbeing of People with Learning Disabilities | Arts and Humanities Research Council | The Open University | HRCS22_21141 | Abstract not available | Studentships | 1fellowships_scholarships
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gen_c7c7aa231a6e0a2438890a6bfd3f8078 | A bioarchaeological examination of the impact of early life stress on later health outcomes using procrustean assessment of dental fluctuating asymmetry | Arts and Humanities Research Council | University of Sheffield | HRCS22_21142 | Abstract not available | Studentships | 1fellowships_scholarships
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gen_8d8bcc571c1680c20a0f20b9d39aabed | Musician's health and wellbeing: a study of health literacy and promotion in higher education | Arts and Humanities Research Council | Royal College of Music | HRCS22_21143 | Abstract not available | Studentships | 1fellowships_scholarships
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gen_31c64b28002cc8ed6d88f085a2c5bc97 | False Teeth for the Masses: Artificial Technologies, Prostheses and Commodities in Britain, 1848 - 1948 | Arts and Humanities Research Council | University of Kent | HRCS22_21144 | Abstract not available | Studentships | 1fellowships_scholarships
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gen_e01275a3bc3952cad18fa0085506a791 | Where Nobody Can Follow (Memoir as Catharsis) | Arts and Humanities Research Council | Queen's University Belfast | HRCS22_21145 | Abstract not available | Studentships | 1fellowships_scholarships
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gen_aa1d6dcfad4a420951c13d7c9865f6ab | Hive minds and pathological collaborations: are mental illnesses socially extended? | Arts and Humanities Research Council | University of Edinburgh | HRCS22_21146 | Abstract not available | Studentships | 1fellowships_scholarships
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gen_84672b5ccc7eb0055cd13743a31fa743 | Explaining the Youth Anxiety Epidemic: Towards a New Social Theory of Anxiety | Arts and Humanities Research Council | University of Birmingham | HRCS22_21147 | Abstract not available | Studentships | 1fellowships_scholarships
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gen_dd097061dc859e0f14a918459a79dc75 | Searching for Meaning: meeting cancer patients' desire for spiritual care through the arts | Arts and Humanities Research Council | University of St Andrews | HRCS22_21148 | Abstract not available | Studentships | 1fellowships_scholarships
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gen_f2d83ef0adec8d78cc6a75bf5946371f | Are people with psychopathy morally responsible for the harm they cause: A philosophical account of psychopathy and moral responsibility | Arts and Humanities Research Council | University of Birmingham | HRCS22_21149 | Abstract not available | Studentships | 1fellowships_scholarships
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gen_7d781a27ebe12944fac7675f65424eba | Accelerating Cognitive Therapy Implementation On a National Scale (ACTIONS) | Innovate UK | 365 Health Solutions Limited | HRCS22_21152 | Depression and anxiety cause untold misery on our citizens' lives and severely reduce both life expectancy and opportunity, affecting 1 in 6 people in any given week and 25% in their lifetime. Over 10 million episodes of common mental health problems were recorded in 2020\. The London School of Economics state that mental health costs the UK economy £118bn annually while Deloitte estimate a £45bn cost to employers of the resulting workplace absenteeism and presenteeism. Focusing on people with Mild and Moderate Depression and/or Anxiety this project assesses a novel delivery model that encourages the self-management of mental wellbeing, using advanced computing to integrate secure, data-driven digital and human interventions. It removes the need to wait for treatment, meets minimum outcomes of the IAPT initiative and provides evidence to enable further investment to upscale our solution UK-wide. For individuals this proposal will: * Eliminate waiting times * Provide an alternative to being prescribing antidepressants * Be acceptable to the individual * Be acceptable to Practitioners and Therapists * Broaden patient choice * Increase self-management of mental health care It will also * Meet the published outcomes of existing IAPT services * Be delivered at or below the price point of existing IAPT services * Provide a long-term solution that is scalable and affordable on a National, Regional or Local basis * Identify what investment would be required to deliver this The outcomes of this project will transform how services for depression and anxiety will be provided in the future by placing the knowledge, tools and opportunity into the hands of the individual so that they can achieve recovery in the time they currently wait to be seen by existing services This will bring about significant social and economic benefit to both the individual and the nation. | Missing/Incomplete | 0business_rnd_innovation
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gen_9b6fab808d77633fda76f960c04c56b6 | AI Driven Review for Scientific Accuracy in Life Sciences | Innovate UK | 3six Health Limited | HRCS22_21155 | The life science industry in the United Kingdom operates by codes of ethics which govern set compliance guidelines for all materials and activities to ensure they are delivered in a responsible, professional, transparent manner and are appropriate for use. Codes cover promotion of medicines and devices to healthcare professionals and other decision makers to ensure they are kept up-to-date on the latest treatments available for patients. The availability of accurate up-to-date information is vital for appropriate use and approvals of all activities and materials adhere to standard operating procedures. Although codes are self-regulating, there is strong support given by the industry and any complaint made against a company is treated as a serious matter which can result in not only reputational damage but also hefty fines and full company audits. Each activity must be checked for medical factual accuracy and obtain a final medical signatory for approval of use. The more activities a company undertakes, the more items will require review and approval which creates an increase of pressure on the compliance approval system. Currently this is a manual based process which uses a vast amount of time from highly-skilled individuals. The AI Driven Review for Scientific Accuracy in Life Sciences project will consist of a written master piece of Pseudocode which will enable us to partner with a software company to implement as a bolt on module to their established software. Having identified a number of risk elements based on the UK Code of Practice we will write code to identify risk elements within a piece of promotional material. Each piece of code will identify a risk element e.g. it will identify and match job bag codes, ensure no hanging comparisons, check specific regulatory requirements such as the black triangle, ensure images do not contain sexual imagery etc. Not only will this speed up the process, it will also reduce any human based errors. By automating this service it will allow companies to better manage their highly-skilled employees time on projects where they provide the most value to their business. Streamlining the compliance review and approval process will enable the industry to fast track activities and materials which will mean a quicker entry to market and provide agility, whilst reducing missed opportunities or postponements previously caused by human based pressures. | Missing/Incomplete | 0business_rnd_innovation
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gen_029c31d21b0e7b801f8ef335fa8665d7 | Structural characterization of thin carbon films on high-current silicon field emitters | Innovate UK | Adaptix Limited | HRCS22_21171 | Adaptix is a SME based at the Oxford University Science Park that develops low-cost, low-dose, portable 3D x-ray sources. The core technology is a 'Distributed Array' that digitises the source, replacing a single high-power tube with a multitude of addressable low-power emitters in conjunction with modern Flat Panel Detectors). Thus 2D diagnostics is replaced with 3D (digital tomosynthesis) in the acute care setting (A&E, ICU), and into Primary Care, improving initial diagnosis overall. Adaptix is currently selling its units for veterinarians, and is expanding its technology for the Non-Destructive Evaluation applications and for its biggest market, ortho x-ray imaging, chest and dental. For some applications it needs to increase the brightness of its panel x-ray source, e.g in chest imaging, because of the thickness of the human chest, with overlaying different types of tissue, bone, muscle etc. The development of the emitters' array by novel etching and coating technologies is Adaptix' current priority. For the theoretical background we are collaborating with leading experts in the modelling and characterization of field emitters from the Universities of Tartu and Lyon in France. Preliminary experiments on an inert coating on the silicon emitters held very promising results in terms of the improved current emission (3x) and its stability. In collaboration with the University of West Scotland and STFC in Daresbury we are investigating various methods for the fabrication of this inert coating. Initial results exhibit a huge variation in the performance of the emitters. We ascribe this to the film composition and structure, known to vary a lot among different coating techniques, but we have not the means to characterise that. The increased current emission (2-3X) and the improved lifespan that we observe in some of the coated samples would be a real game changer for our technology and open new markets for us. Analytical tools to characterise the exact structure and composition of the coatings are not easily available and Adaptix does not have the acute scientific know-how, analysis or facilities for the required measurements. In collaboration with NPL we hope to be able to understand the composition of our coatings. With this we aim for reproducible, stable results. An additional goal is also to develop a method for quality control in our production facility. | Missing/Incomplete | 0business_rnd_innovation
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gen_b15225a7bb618bdbc4321d4245460e86 | Validation of novel chemiresistive sensors for environmental monitoring | Innovate UK | Advanced Material Development Limited | HRCS22_21180 | Nitrogen dioxide pollution is associated with diseases such as stroke, chronic obstructive pulmonary disease and asthma, while ammonia emissions significantly contribute to several well-known environmental problems. Remote monitoring of rising levels of both nitrogen dioxide and ammonia are essential to be able to reduce mandated emissions and monitor compliance and ultimately save lives. The development of low-powered, sensitive, and selective chemiresistive gas sensors for monitoring of key pollutants is essential for public and environmental health considerations. The use of novel nanomaterials for battery-operated highly sensitive sensing devices is gaining commercial interest so more accurate environmental monitoring can be carried out. **By capitalising on the skills and expertise of outstanding UK scientists and capabilities of cutting-edge facilities will enable us to test the performance of our devices using a dedicated certified instrumentation.** Utilising the National Physical Laboratory (NPL) gas testing facilities, advanced quantitative analysis will ensure greater validation of our sensing products. Investigating the quantified, traceable interaction of gases with our sensor platform will enable Advanced Material Development (AMD) Ltd. to advance several sensing application technologies for various clients both in the UK and the US. Well-controlled experiments generate data which opens further commercial opportunities. Once successful, this adds considerable value to the company and increases our ability for full product development and commercialisation. | Missing/Incomplete | 0business_rnd_innovation
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gen_44d13ebdc19359853aa34c069fa183b8 | UK market access strategy for AlphaBiomics’ novel precision medicine diagnostic test RxSelex™ | Innovate UK | Alpha Biomics Ltd | HRCS22_21199 | **HEALTHCARE CHALLENGE:** Immune-mediated diseases are lifelong illnesses characterized by an abnormal reaction of the body's immune system, known as inflammation. Examples are Crohn's disease (CD) and ulcerative colitis (UC). People who experience severe disease whose activity cannot be controlled with the usual medication are typically treated with a biologic drug to stop inflammation. This type of medicine is made of materials also found in living organisms. Typically, individuals with the same disease are initially treated with the same type of biologic drug. However, individual patients respond very differently to the same biologic drug. Some may benefit, whereas others do not, or have unwanted side effects. The continued need for hospital visits and uncertainty of treatment success has been especially difficult for these immuno-compromised patients during the COVID-19 pandemic. **ALPHABIOMICS' SOLUTION:** The gut microbiome (the large and complex community of typically harmless bacteria in our intestines) has an important influence over biologic drug response. AlphaBiomics is developing a non-invasive at-home test for CD and UC patients that predicts a person's likely response to biologic drugs as a group. This test, called RxSelex(tm), measures important gut microbiome components found in a patient's stool. Once this diagnostic test is ready for use, it will be sold to the NHS. **FAST PROJECT AIM:** The NHS is currently undergoing major changes in how health and care services are planned, obtained, paid for, and delivered. New Integrated Care Systems (ICSs) have been established to aggregate providers and commissioners of NHS services across a geographical area with local authorities and other local partners to collectively plan health and care services to meet the needs of regional population. NHS reorganisation into ICSs is changing adoption and ordering pathways including for diagnostic tests like RxSelex(tm). The aim of this project is to develop a clear roadmap for NHS adoption and dissemination of RxSelex(tm) that fits the novel ICS structure. **FAST WORK PLAN:** AlphaBiomics will engage the expert consultancy Hardian Health to deliver this roadmap. Hardian will review publicly available information regarding adoption and purchasing of diagnostic tests. They will also estimate the number of IBD patients in the UK who will benefit from RxSelex(tm). Hardian will then interview experts to confirm or update their findings and then summarise the results in a roadmap. | Missing/Incomplete | 0business_rnd_innovation
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gen_618cc489a56ed10a8ef3d1e8453df856 | Easel, Virtual Reality stress-relief | Innovate UK | Animorph Ltd | HRCS22_21206 | In the UK, 79% of adults frequently experience work-related stress, which is one of the key causes of 17.9 million working days lost each year, costing UK employers up to £45 billion. Easel, is a stress-relieving Virtual Reality (VR) application for employees working in high-stress environments. The app applies scientific findings with cutting-edge, yet easily available technology, to creatively address workplace stress with a compelling mental well-being product. Easel reduces stress by transporting the player to a distant, safe, underwater world where they can foster a caring relationship with an other-worldly sea creature. The player's ability to move around freely and initiate rich interactions within the calming and audiovisually enchanting world provides a soothing sense of control. The player uses gaze and hand gestures to navigate the ocean, and interacts with their sea-animal companion in a variety of ways, including feeding, playing, and cleaning up their environment. At the start and end of each session the player self-reports their well-being rating, developing their profile over time. Our product is based on scientific research in stress- and pain-relief through nurturing animals and how VR can facilitate it. Interacting with an animal in VR has been documented as hugely beneficial, even surpassing the effectiveness of morphine for pain reduction. Despite the promising results of medical prototypes in clinical settings, almost none are commercially available. In the absence of evidence-based and accessible solutions on the market, we want to create a cutting-edge, compelling solution for large enterprises to start with, next offer it to public sector institutions and eventually roll it out to individual customers. The project will deliver three main outputs: 1. A detailed market assessment. 2. A beta version of the Easel VR app. 3. A white paper evaluating the app's effectiveness. | Missing/Incomplete | 0business_rnd_innovation
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gen_4befc4fba135079b4569abe2a73bbfcb | The development and assesment of an innovative Health and Medical Aid. | Innovate UK | Atec Medical Devices Ltd | HRCS22_21230 | Having seen and experienced the challenges and issues when changing an incontinence pad of my step father who suffered from dementia and stroke. I thought there must be some sort of aid. This first hand experience of the issue of clothing getting in the way when changing a patient's incontinence pad particularly when they suffer from dementia and are unable to lift and hold up the clothing, and seeing my mother struggle to help him. I thought there has to be some sort of aid, I searched extensively but there is not an aid. The aid's potential benefits include: * That assists a health professional to carry out certain duties far more effectively. * Efficient and time saving * That improves the safety of both patient and carer * That can give a patient greater independence * That can give a patient a sense of dignity So this led me to design and develop the Apparel Aid. The project's objective is to take the design and basic prototype of the aid, and develop working prototypes that are functional and durable in a variety of sizes for both female and male. These prototypes will then be assessed by a Health and Social Care establishment. | Missing/Incomplete | 0business_rnd_innovation
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gen_177faeb5342a5124af84c4bda1b8c672 | Beanbag App - Beta Version | Innovate UK | Beanbag Health Limited | HRCS22_21246 | **Overview** Beanbag Health is a purpose-driven business aiming to transform support for young people suffering with eating disorders through a highly empowering approach, avoiding an overly clinical look and feel, and placing emphasis on peer support as much as clinical input. The Beanbag digital app will support people to manage their own journey of recovery, change their behaviours and maintain their recovery through four features: 1\. Safe, supportive peer community 2\. Self-serve content platform drawing from evidence-based treatments 3\. Behaviour change support and just in time adaptive interventions. 4\. Recovery coaches to guide users through treatment programmes. **Project Vision and objectives** This project will develop our working prototype into a beta version that we can test with users at scale. The beta version will be our minimum viable product and part of our critical path to raising further investment and also to trialling our product with the NHS and private clinics. Our prototype was developed through extensive codesign and user testing since January 2022 and will continue to generate insights through to year end. However, the prototype does not integrate the various product components well and many processes need to be run manually by the Beanbag team so we can only accommodate a low number of users. The beta app will be a substantial improvement in user experience and introduce basic just-in-time adaptive interventions to shift behaviours. It will also provide scalability, by automating various processes currently done manually and incorporating a robust quality and clinical risk management system to comply with NHS commissioning requirements. **Details of how innovative** Not only will our product be evidence-based; it will have an empowering and approachable look and feel. This is very different from a traditional purely clinical service as it provides relatable, non-judgmental but trustworthy support that can be digested in small, immediately actionable steps as well as opportunities for deeper psychological support. Our app will be the first online guided CBT for eating disorders commercially available anywhere in the world and the first eating disorder app to use just-in-time adaptive interventions. The combination of peer community with treatment also makes us distinctive. | Missing/Incomplete | 0business_rnd_innovation
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gen_6156df380e3da40dd3ccac67faaa6590 | Brining the SMART revoloution to bodyweight fitness training. | Innovate UK | Bgr Training Limited | HRCS22_21252 | BGR Training is a fitness company with a mission to bring the SMART revolution to bodyweight fitness training. The company has recently launched its first innovation, The BGR: the ultimate 3-in-1 fitness tool that enables anyone to workout anytime and anywhere using their bodyweight with a portable pull-up bar, single and grips, and gymnastic rings. The company has experienced sales at a global level from birth by selling into 47 different countries and capturing the attention and interest of industry giants such as Echelon, The NFL, and Reebok. Following the successful launch of its first innovation, The BGR, the company is now preparing for the future of fitness by innovating to create bespoke fitness technology that will transform The BGR to become smart, connected, and data generating before extending the applications of the technology throughout the fitness equipment industry. 'RepTek' is the company's pre-emptive response to the inevitable digitisation of the industry. However, RepTek is no regular piece of fitness technology. RepTek has been designed to aid fitness users in their journey to achieve their fitness goals by analysing their performance -- the key to progression. RepTek will then use the stored information to create and evolve a bespoke and personalised workout on the user's behalf -- acting like a personal trainer. The feasibility of RepTek has been proven using a Scottish Enterprise SMART Feasibility award, developing RepTek to TRL4\. The objectives of this project were achieved, demonstrating that RepTek possesses a significant competitive advantage for the company and that it can bring true innovation to an increasingly homogenised space. The company is now seeing Innovate UK funding to develop the technology further to TRL6\. Achieving a TRL6 position will enable the company to produce a significantly improved demonstrator prototype, reduce the time and cost of achieving the MVP stage, engage with stakeholders, and identify the appropriate. Allocating resources to the development of what's been described as '_next-generation fit-tech'_ at an early stage in the company's development carries risk. Ultimately, the purpose of this project is to carry on the momentum of the SMART Feasibility project and to de-risk the business proposition in the eyes of an investor. | Missing/Incomplete | 0business_rnd_innovation
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gen_0e5673ff76ef12ff3b96f92407d22831 | Enabling biological manufacturing at scale | Innovate UK | Biokind Ltd | HRCS22_21260 | Engineering Biology allows sustainable biomanufacturing of foods, chemicals, plastics etc., from engineered microbes via fermentation, helping achieve Net Zero by reducing our reliance on fossil fuel- and animal-based systems. Reaching a truly impactful scale however is severely hampered by the current manufacturing systems. This project will develop a prototype for a new paradigm in Advanced BioManufacturing scale-up. | Missing/Incomplete | 0business_rnd_innovation
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gen_6762b6ac4747d187608d6867ad72a853 | Characterisation of BiologIC’s 3D printed biocomputer platform for advanced therapies, cellular agriculture and diagnostics | Innovate UK | Biologic Technologies Limited | HRCS22_21261 | BiologIC Technologies is developing the first world's biocomputer leveraging foundational IP and the latest additive manufacturing (3D printing) technologies. The first generation of the biocomputer is being developed to advance applications in diagnostics, advanced therapies, new vaccines and cultured meat and is designed to power the next generation of synthetic biology at scale. We use 3D printing as the fabrication process of the biocomputer platform. Multi-material 3D printing enables digital blending of materials (polymers and elastomers) that lets us produce a single system that integrates fluidics, electronics, optics and pneumatics into a single system. One of the challenges in bringing these systems to regulated markets such as manufacturing of advanced therapies is controlling the materials. BiologIC has developed proprietary knowhow regarding biocompatibility of the 3D printed system across each layer of its technology. Previous work has shown that BiologIC's post-processing methodologies can efficiently increase the biocompatibility of the 3D printed systems enabling molecular and cellular biology applications although further optimisation is desirable. By collaborating with external expertise through this project BiologIC will characterise the 3D printed components necessary for the further development of the biocomputer platform that will enable a paradigm shift in the production of synthetic biology, advanced therapies and diagnostics. | Missing/Incomplete | 0business_rnd_innovation
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gen_08ece2112402eb180074e37939ed0ac7 | Intelligent monitoring of home health devices to track, label and alert changes in heart health. | Innovate UK | Brimstage Engineering Solutions Ltd | HRCS22_21282 | As healthcare systems (e.g. NHS) have become increasingly stressed and the expectation of what these healthcare systems can deliver has become greater(Increasingly, CQC requires evidence that good care is being provided), there has been a significant migration of health and medical devices into the home. It is also vital to balance the range of relevant information with a simplicity of presentation to allow easy assimilation by clinicians or indeed by autonomous systems (that can generate appropriate alerts/messages when necessary). As healthcare data is relative to the patient, it is important to track changes over hours, days, months and years without increasing the workload of the clinician. This work will address this issue by developing a novel intelligent monitoring algorithm to detect subtle changes in complex physiological signals enabling autonomous alert triggering, early intervention and informed decision making in real time and in long term monitoring. The novel algorithm will be suitable to be embedded directly in a smart device (e.g. a smart watch), a standalone IOT hub, or in the cloud as part of a larger digital health framework. The funding will be used to validate the methodology. The results from this work will be used as 'proof of concept' to show that the method works and would be suitable to scale. This work will be delivered by Dr John Kenny, an expert in intelligent monitoring, from Brimstage Engineering Solutions Ltd | Missing/Incomplete | 0business_rnd_innovation
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gen_bdb880e2e8f6a642f82387c97eace49d | BeSecAT: Blockchain-enabled Secure and Resilient Supply Networks for Advanced Therapies Medicinal Products | Innovate UK | Cardiff University | HRCS22_21294 | Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details. | Missing/Incomplete | 6project_grants_public
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