- Total grants
- Total funders
- Total recipients
- Earliest award date
- 20 Nov 1998
- Latest award date
- 18 Jan 2019
- Total GBP grants
- Total GBP awarded
- Largest GBP award
- Smallest GBP award
- Total Non-GBP grants
LifeLines 20 Apr 2016
This is the expansion of a project supporting volunteers aged 50 plus to run activities for vulnerable older people to improve health and well-being. These have previously included art classes, creative writing, yoga and computer club. The group will expand across the city, recruiting more volunteers, supporting more than 800 new people and establishing a Menâ€™s Network to encourage older men to socialise regularly. It will also extend its HealthLink scheme to help older people get to medical appointments.
Kilkeel RBL - Saving Our Community Venue 22 Oct 2015
The group is a community and voluntary based organisation providing a range of services and activities to the local community. They received a grant of Â£10,000 to make improvements to their venue so that it can be used for more classes and activities.
Towards improving access and facilities for disabled people at the Forest Hall Ex-Servicemen's Institute.
Grant awarded to Community Service Volunteers (Training and Enterprise NE) (Tyne & Wear) 13 Jul 2004
To provide daycare services to older people living in high rise flats in Newcastle.
10,000 UK genome sequences: accessing the role of rare genetic variants in health and disease. 14 Dec 2009
We propose a series of complementary genetic approaches to find new low frequency/rare variants contributing to disease phenotypes. These will be based on obtaining the genome wide sequence of 4000 samples from the TwinsUK and ALSPAC cohorts (at 6x sequence coverage), and the exome sequence (protein coding regions and related conserved sequence) of 6000 samples selected for extreme phenotypes. Our studies will focus primarily on cardiovascular-related quantitative traits, obesity and related m etabolic traits, neurodevelopmental disorders and a limited number of extreme clinical phenotypes that will provide proof-of-concept for future familial trait sequencing. We will analyse directly quantitative traits in the cohorts and the selected traits in the extreme samples, and also use imputation down to 0.1% allele frequency to extend the analyses to further sample sets with genome wide genotype data. In each case we will investigate indels and larger structural variants as well as SNPs, and use statistical methods that combine rare variants in a locus or pathway as well as single-variant approaches. We will make the sequence data we obtain available for further research purposes, empowering many additional research directions both on these samples and by imputation on further samples from the UK and beyond.
Identification of genes predisposing to tuberculosis in a Russian population and genetic analysis of the host-pathogen interaction. 01 Apr 2009
To discover human genes predisposing to TB we propose to undertake a genome-wide association scan (GWAS) in the Russian (5,000 TB patients and 5,0000 controls) and Ghanaian (2,010 TB patients and 2,346 controls) collections established by the TB-EUROGEN consortium. We will genotype these samples in the Wellcome Trust Sanger Institute using Affy 6.0 array comprising 906,600 single nucleotide polymorphisms (SNPs) and more than 946,000 probes for the detection of copy number variation (CNV). We wil l test TB association of these variants and will undertake meta-analysis of the Russian and Ghanaian data and an additional Gambian dataset comprising 1,400 TB cases and 1,400 controls previously genotyped by the Wellcome Trust Case Control Consortium and will compare TB-associated variants in the European and African populations. Additional follow-up of the variants associated with TB exclusively in the European (Russian) population will be done in 2,532 TB patients and >30,000 controls from Ic eland. Once we complete a GWAS and meta-analyses, we will undertake analysis of interaction between human genes predisposing to TB and M. tuberculosis strains in the Russian and Ghanaian collections to dissect population-specific effects in TB.
Population genomics of the mouse. 06 Oct 2009
The mouse is the leading model mammal in genetics and biomedical research, yet little is known about how variation in its genome translates to variation in reproductive fitness. This is important because the fitness effects of nucleotide variants are closely related to the nature of quantitative genetic variation, such as susceptibility to genetic disease in humans. We propose to study the population genetics of Mus m. castaneus, a highly variable subspecies from the ancestral range of the house mouse subspecies complex. We shall generate accurate, whole genome nucleotide polymorphism data for the genomes of a sample of wild-caught individuals. Using this data in conjunction with the mouse genome annotation and the rat genome, we shall apply new methods developed by the PI and others that analyse within population polymorphism and between species divergence to infer the fitness consequences of nucleotide variation. We propose to estimate the frequency distributions of effects of new mu tations for both coding and noncoding DNA, and the frequency of adaptive substitutions in the genome. We shall analyse the spatial correspondence between selected-site divergence and neutral diversity to estimate both the rate and strength of selection associated with selective sweeps.
Clinical responses to anticancer therapeutics are often restricted to a subset of cases. Accumulating evidence indicates that response often correlates with a specific tumour genotype. Therefore, response rates could be substantially improved by directing treatment towards genetically-defined subsets of patients most likely to benefit. Toward this goal, we propose a scientific strategic alliance between investigators at Massachusetts General Hospital (MGH) and the Wellcome Trust Sanger Institute (WTSI) to "personalise" cancer therapy by identifying in vitro, prior to clinical trial, tumour cell genotypes that predict sensitivity to anticancer agents. We aim to expose approximately 1,000 cell lines derived from a broad spectrum of cancer classes to several hundred known and potential anticancer therapeutic agents correlating responses with genomic copy number information, cancer gene mutation data and expression data. Correlations between genotype or expression and response will then be validated in clinical specimens and will subsequently inform the design of clinical studies in which patients are stratified on the basis of a tumour genotype prior to treatment. The collaboration will develop and share the experience in automated high throughput exposure of cancer cell lines to small molecules at MGH and the background in large scale genotyping, sequencing and informatics at WTSI.
Our focus will be on viral infections in Vietnam with special emphasis on zoonotic viruses: these are relatively under-studied and viruses of animal origin are the dominant source of emerging infectious diseases in humans. WT-VIZIONS: 1. Establish a model consortium focused on an integrated approach to human and animal health in a country at the epicenter of emerging infectious diseases. 2. Quantify the epidemiology and burden of disease (focus on viral zoonoses) in i) patients hospitalized w ith one of four clinical syndromes; ii) infections in a cohort of high risk individuals occupationally exposed to animals; with targeted sampling from domestic animals and wildlife in association with (i)/(ii). 3. Elucidate the origin, nature, and burden of infectious diseases of unknown origin in the human study populations; 4. Characterize genetic diversity within virus populations on either side of the species-barrier to understand cross-species transmission and disease emergence; 5. Ident ify socio-demographic, environmental and behavioural drivers for disease emergence; 6. Provide a platform and resource for complimentary research on human and animal pathogens, and nonviral zoonoses. The results will inform the design of surveillance for infectious disease, and the opportunity to conduct detailed investigations of outbreaks, especially zoonotic diseases, occurring during the study period.
Quantifying disease burden in patients with cancer using tumour-specific genomic rearrangements 26 Feb 2010
Cancer is caused by the accumulation of genetic damage (mutations) in cells within a particular organ. These mutations are only found in the cancerous cells and therefore could be used to track the malignancy during treatment. Advances in DNA sequencing allow the high-throughput identification of these mutations from any cancer sample in a clinically relevant time-frame. As tumour cells die, they release their DNA into the bloodstream. Dr Peter Campbell, Wellcome Trust Sanger Institute and colleagues propose to use the new generation of genetic sequencing technologies to identify a particular class of mutations caused by the abnormal rearrangement of chromosomes in patients with breast cancer and colorectal cancer.From these rearrangements, the team will develop assays to detect DNA from each patient's cancer that has been released into the bloodstream. Such assays will be highly specific (minimal risk of falsely positive results) and sensitive (capable of detecting one copy of tumour DNA in many millilitres of blood). The programme will measure the amount of disease using blood samples collected before surgery, after surgery, during chemotherapy and at regular time-points post-therapy. Dr Campbell and colleagues will therefore be able to assess the ability of this approach to identify high-risk patients before treatment begins, to monitor response to treatment and to predict cancer relapse before it is clinically apparent.
DNA in all cells is prone to mutagenesis, with somatic mutations making key contributions to human diseases such as cancer and neurodegenerative diseases, and to aging itself. Mutations are the consequence of exogenous or endogenous mutagenic influences (including radiations and DNA-damaging chemicals) and also result from enzymatic DNA modifications or low fidelity DNA synthesis by specialized DNA polymerases. Mutations are generally prevented by the cellular DNA-repair machinery and defective functioning of this machinery can markedly increase mutation rates. Different mutational processes leave different, characteristic signatures of somatic mutations on the exposed cellular genome. Notably, recent analyses of cancer genomes have revealed several novel mutational signatures, the biological bases of which are predominantly unknown. To define somatic mutational processes operative in cells, and in particular their influences on human disease, we propose to systematically survey, at th e genome-wide level, mutational signatures generated by exposures to known or putative human carcinogens, defective DNA repair/editing processes or dysfunction of other cellular processes. These studies will provide a set of mutational signatures with known underlying causes for subsequent matching to signatures found in normal or diseased human cells and will expand our knowledge of how various cellular components influence mutagenesis.
A Powerful, Genome-Wide Association Scan for Susceptibility Genes for late-onset Alzheimer's disease. 19 Sep 2007
This project aims to identify novel susceptibility genes for late-onset AD (LOAD) using high-throughput genome-wide approaches investigating over 500,000 variants, to test for genetic association, in a powerful sample of approximately 10,000 well characterised, LOAD cases and controls, which comprises the largest genetic association study currently undertaken. The study is timely and economical, exploiting samples collected through other funding, reducing genotyping costs without adversely affecting power through a staged design and bringing together genuine expertise in genotyping, clinical assessment and statistical analysis in the UK. First, we will select 1000 LOAD cases and 1000 matched controls from the MRC Genetic Resource and genotype on the Illumina platform using the HumanHap550 Beadchip. 30,000 SNPs showing evidence of association will be selected for further study in independent case-control samples comprising 1964 LOAD cases and 942 controls, from the Alzheimer's Research Trust (ART) and the MRC LOAD samples. A customised SNP Chip will be constructed of the selected SNPs and the samples genotyped on the Illumina platform. Finally, a meta-analysis of selected SNP's will be undertaken and the genes/variants which show the strongest evidence for conferring susceptibility for LOAD will be further genotyped in 4976 association based samples provided by US collaborators.
RBL Portstewart Branching Out 26 Apr 2018
The group, based in Portstewart, are using a grant of £6,500 to replace their hall’s heating system and improve its insulation, making it more usable for community events.
The impact of WW1 on Dartford and its residents
Grant to Little Newcastle Community Association in conjunction with Royal British Legion, Pembrokeshire 30 May 2014
Interpreting World War 1 through Commemoratives