{"id":324,"date":"2011-01-11T00:21:51","date_gmt":"2011-01-11T00:21:51","guid":{"rendered":"http:\/\/www.monkeyshines.co.uk\/blog\/?p=324"},"modified":"2011-01-11T00:27:59","modified_gmt":"2011-01-11T00:27:59","slug":"t1dbase-type-1-diabetes-and-my-part-in-its-downfall","status":"publish","type":"post","link":"https:\/\/monkeyshines.co.uk\/blog\/t1dbase-type-1-diabetes-and-my-part-in-its-downfall\/","title":{"rendered":"T1DBase: type 1 diabetes, and my part in its downfall"},"content":{"rendered":"

\nApropos of a new T1DBase<\/a> publication (Burren et al. 2011) (in which I am kindly acknowledged), I thought I’d write a bit about some of the work I did there (Hulbert et al. 2007). I envisage this being the first of maybe three instalments, so before going into detail about the specific projects that I worked on, I’ll explain what T1DBase actually is, and why I’m proud to have worked on the project. For your reading convenience, this post is available as a pdf pdf<\/a>.\n<\/p>\n

\nT1DBase<\/a> is a resource for the type 1 diabetes (T1D) research community, and it has strong ties to the JDRF\/WT Diabetes and Inflammation Laboratory (DIL)<\/a> in Cambridge, which is headed up by John Todd. (When I worked at the DIL we collaborated with the ISB<\/a> and a group at UPenn<\/a>, but this is no longer the case.) Type 1 diabetes is an auto-immune disease, that primarily manifests in childhood, so was formerly known as juvenile diabetes. The symptoms are similar to those of type 2 diabetes, but the aetiology<\/a> is quite different (Todd 2010), and type 1 diabetes is genetically more similar to diseases like rheumatoid arthritis and coeliac disease (Smyth et al. 2008).\n<\/p>\n

\nI worked on T1DBase for three years, from Jan 2006 to Dec 2008, which was a period of massive change in our understanding of the genetics of type 1 diabetes, primarily due to the emergence of genome-wide association studies (GWAS). The DIL was heavily involved in one of the first landmark studies (Todd et al. 2007; Wellcome Trust Case Control Consortium 2007), as part of the WTCCC (Wellcome Trust Case Control Consortium; don’t worry, I think that’s the last of the acronyms). Results from that and subsequent GWAS (e.g. Cooper et al. 2008; Barrett et al. 2009) generated a host of new T1D susceptibility regions, and a better (although still far-from-complete) appreciation of the genetics of this complex disease. (I’ve cited GWAS publications that I was involved in, or that were written by colleagues at the DIL, but T1DBase also gets data from a range of other sources; see the website for more information.)\n<\/p>\n

\nThe people behind T1DBase curate the GWAS results, and make them available as raw data and, more usefully, as region summaries<\/a> that tie to analyses of genes<\/a> and variants (i.e. SNPs)<\/a>, as well as cross-referencing with mouse and rat data. It sounds so simple when you write a sentence like that, but there are, of course, very many challenges involved, both in terms of making sense of a huge amount of biological data, and in working out how to effectively present the results. And that’s not to mention the day-to-day work of maintaining a website, and programming collaboratively and efficiently. I very much enjoyed working on the T1DBase project; I learnt loads, both about disease genetics and programming, and it was always a fun environment to work in (with regular tea breaks, too…) And it was nice to be in a job where, in some small way, I was able to constructively contribute to important and useful research into type 1 diabetes.\n<\/p>\n

\nReferences<\/b><\/p>\n