Academic Writing thesis

Deadline: Monday 8 September 2014, 19:30:00 7 Page(s) - 1925 Words APA with 15 references 25$/1000 words Total budget: 50$ Not negotiable NB: IF our client doesn't raise any issue with 4 day payments shall be sent to the selected freelancer My work is based on genetic progression from Barrett's oesophagous to Oesophageal adenocarcinoma. Have sent my 3 chapters and need help with final discussion. Background: Project 1: Barrett’s oesophagus (BO) is a common premalignant condition in which the normal squamous epithelium of the lower end of the human oesophagus is replaced by a columnar, intestinal phenotype. BO is the predominant risk factor for the development of oesophageal adenocarcinoma (OA). The incidence of BO in Western countries has increased by 30-40 fold in the last 25 years and carries a 0.12% annual risk of developing OA. Therefore, there is a clear clinical need to understand the genetic progression of Barrett’s oesophagus so that we can identify the patients who are at a higher risk of developing OA. Earlier studies into the genetic evolution of BO have lead to the theory that BO is a genetically clonal lesion from which a cancer can arise (Galipeau et al., 1999). However, recent work by Leedham et al. has shown that there are multiple independent clones present; therefore BO is a genetically heterotypic disease. Furthermore, Maley et al. have shown that genetic diversity increases the risk of cancer progression. My plan is to investigate genetic diversity in Barrett’s dysplasia and cancer and analyse which clones progress to cancer. My hypothesis is that the Barrett’s metaplasia-dysplasia-carcinoma (MDC) sequence is characterised by multiple genetically diverse clones in dysplasia but one clone progresses to cancer. Project 2: Around 50% of patients who undergo oesophagectomy for OA develop neo-Barrett’s lesions (neo-BO) over a period of 3-5 years post surgery. This could be due to a field effect, wherein pre-neoplastic cells exist at multiple sites of histologically-normal areas of epithelium. This carries an important clinical implication: apparently normal epithelium surrounding the resection may possess genetic abnormalities that predispose to neo-BO or cancer re-development: so called field cancerization. Project 3: A long-term follow-up up patients with crypt dysplasia showed the development of either synchronous or metachronous traditional dysplasia or cancer on follow-up (Lomo et al., 2006): it was subsequently proposed that dysplasia begins in the bases of the crypts in Barrett’s esophagus and progresses with time to involve the upper portions of the crypts and surface epithelium (Coco et al., 2011). However, it is not yet clear whether, any genetic changes found in the dysplastic cells at the crypt bases are shared by those cells in the upper part of the crypt. PFA the chapters 3,4 and 5