This year ESRT will be participating in the 20th Funraisers Dragon Boat Festival, on Saturday, 9th September 2017 at Bewl Water near Lamberhurst in Kent. This will be out seventh year in a row participating and we hope to have three boats competing and raising funds for us this year too! In previous years the charity has raised over £60,000 towards realising its aims and we hope that this year will be just as successful. The Body Shop Tunbridge Wells store will again be on hand to provide all competitors at the event with back and hand massages to ease the 'pain' of rowing! If you would like to know more about the charity's participation email us now @ [email protected]

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We’ve been fundraising for over two years, and so far we’re amazed by the progress we’ve made. We’re hugely indebted to our wonderful fundraisers across the UK and the world who have donated, or helped support us in any other way, and this page is a little update to thank the people who’ve gone out of their way to raise funds for us. Below is a summary of all of the people or organisations that have helped us reach where we are now! August 2011 HSBC’s Sports Association was the first fundraiser we received money from – a £750 donation from their Summer Ball. This was hugely important, in allowing us to set up for our first organised fundraiser – the Dragon Boat Festival 2011. September 2011 The Dragon Boat Festival! We have to say a huge thank you to all the volunteers, participants, and sponsors of our launch event, which helped us raise another £13,000 for research. To see how it went, click here.

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Research published today in Science journal demonstrates a genetic link between Ewing's Sarcoma, melanoma (skin cancer) and glioblastomas (brain cancer). Researchers at Georgetown University School of Medicine, Washington, found defective copies of a gene called STAG2 in 21% of Ewing's Sarcomas, 19% of glioblastomas and 19% of melanoma. A researcher said "mutations in STAG2 appear to be a first step in the transformation of a normal cell into a cancer cell." This research may open up an opportunity to develop new drugs which target cells wih defective STAG2. Theoretically, this could prevent some cancers forming. One of the lead researchers, Professor Todd Waldman of Georgetown University, said that having identified mutations of STAG2 in a "substantial fraction of Ewing's Sarcoma tumours, [we] can begin to develop strategies to specifically kill cells with mutated STAG2 genes" which would hopefully allow treatments to "kill the cancer cells but spare the patient's normal tissue." The concept of the research is based around the idea of aneuploidy, which is a hallmark of most cancers. Aneuploidy is an abnormal number of chromosomes in cells, which it is believed can trigger the development of tumours. Researchers in the study found a range of tumour types harboured deletions or inactivations of STAG2. STAG2 is effectively a gene which controls the separation of chromatids during cell division. Researchers found that deliberately inactivating STAG2 in normal cells led to chromosomal defects and aneuploidy. They also went further with regard to glioblastoma, by correcting mutant aspects of the cells, which resulted in increased chromosomal stability - thus the number of chromosomes was less likely to become abnormal. STAG2 encodes a sub-unit of cohesin, which is a protein complex involved in regulation of the inner workings of every human cell. Specifically, it is required for cohesion of sister chromatids after DNA replication, which occurs whenever cells replicate. Previous studies have shown that the deletion of chromosomes under the control of STAG2 have been observed in other cancer studies. In all of the instances where a Ewing's Sarcoma tumour was studied, there were somatic (tumour specific) mutations. The mutations in the STAG2 gene were consistent with functional inactivation. Researchers then attempted to treat the mutation with a DNA inhibitor, which led to minimal or no re-expression of STAG2 in samples derived from a female patient. This led them to believe that the "wild-type" allele of STAG2 was on the inactivated X chromosome. The fact the treatment had little effect suggests that chromosomal inactivation was responsible for the single-hit inactivation of STAG2 - that is, a single mutational event caused the inactivation of STAG2 in these chromosomes. Researchers observed "robust STAG2 expression" in noraml tissues, however, a significant number of the three cancer types studied demonstrated a "completely lost expression of STAG2". Furthermore, adjacent stroma, endothelial cells and lymphocytes were STAG2 positive, which supports the conclusion of researchers that STAG2 inactivation is tumour specific in nature. Part of the study also involved inducing STAG2 inactivation in cells to determine the effect this would have upon healthy cells. STAG2 proficient cells demonstrated virtually perfect chromatid cohesion, which was effectively cancelled by knocking out the STAG2 gene. Conversely, when STAG2 deficient chromatids were corrected, defects in chromatid cohesion were largely reverted (corrected). Imaging of untreated asynchronous cells revealed several deficiencies in STAG2 deficient cells, which is a characteristic of aneuploid divisions. This led researchers to conclude that STAG2 inactivation resulted in altered chromosomal counts (that is, aneuploidy itself) in these cancer cells. The conclusion of the study, published in Science, is that "STAG2 is likely to function as a "caretaker" tumour suppressor gene that, when inactivated, results in chromosomal instability." This study demonstrates the sorts of discoveries that can be made when funding is available for researchers. The finding that 21% of Ewing's Sarcoma tumours demonstrate STAG2 deficiency means this research has the potential to affect treatment of 1 in 5 Ewing's Sarcoma sufferers, statistically a huge number. With thanks to Professor Todd Waldman of Georgetown University for providing a copy of the study.

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