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| 1 | Genetic risks and familial associations of small bowel carcinoma显示文摘Adenocarcinoma of small intestines(SBA) is a relatively rare malignancy with poor outcomes due to delayed diagnosis.Fifty percent of patients have metastases on presentation and therefore early detection and treatment offers the best long term outcomes.Certain genetic polyposis syndromes and familial diseases are associatedwith increased risks for SBA.These include familial adenomatous polyposis(FAP),Lynch syndromes(LS),Juvenile polyposis syndrome,Peutz-Jeghers syndrome,Crohn's disease(CD) and celiac disease.Mutations in APC gene,Mismatch repair genes,STK11 gene,and SMAD4 gene have been implicated for the genetic diseases respectively.While there are no specific inherited genetic mutations for CD,genome-wide association studies have established over 140 loci associated with CD.CpG island mutations with defects in mismatch repair genes have been identified in celiac disease.Significant diagnostic advances have occurred in the past decade and intuitively,it would seem beneficial to use these advanced modalities for surveillance of these patients.At present it is debatable and no clear data exists to support this approach except for established guidelines to diagnose duodenal polyps in FAP,and LS.Here we discuss the genetic alterations,cancer risks,signaling mechanisms and briefly touch the surveillance modalities available for these genetic and clinical syndromes.English language articles from Pub Med/Medline and Embase was searched were collected using the phrases 'small-bowel adenocarcinoma,genetics,surveillance,familial adenomatous polyposis,lynch syndromes,Peutz-Jeghers syndrome,juvenile polyposis syndrome,CD and celiac disease'.Figures,tables and schematic diagram to illustrate pathways are included in the review. | Santosh Shenoy | 2016 | World Journal of Gastrointestinal Oncology2016，8，6： | 9 |
| 2 | Field cancerisation in colorectal cancer:A new frontier or pastures past?显示文摘Despite considerable advances in our understanding of cancer biology, early diagnosis of colorectal cancer remains elusive. Based on the adenoma-carcinoma sequence, cancer develops through the progressive accumulation of mutations in key genes that regulate cell growth. However, recent mathematical modelling suggests that some of these genetic events occur prior to the development of any discernible histological abnormality. Cells acquire pro-tumourigenic mutations that are not able to produce morphological change but predispose to cancer formation. These cells can grow to form large patches of mucosa from which a cancer arises. This process has been termed 'field cancerisation'. It has received little attention in the scientific literature until recently. Several studies have now demonstrated cellular, genetic and epigenetic alterations in the macroscopically normal mucosa of colorectal cancer patients. In some reports, these changes were effectively utilised to identify patients with a neoplastic lesion suggesting potential application in the clinical setting. In this article, we present the scientific evidence to support field cancerisation in colorectal cancer and discuss important limitations that require further investigation. Characterisation of the field defect is necessary to enable early diagnosis of colorectal cancer and identify molecular targets for chemoprevention. Field cancerisation offers a promising prospect for experimental cancer research and has potential to improve patient outcomes in the clinical setting. | Abhilasha Patel Gyanendra Tripathi Kishore Gopalakrishnan Nigel Williams Ramesh P Arasaradnam | 2015 | World Journal of Gastroenterology2015，21，13： | 0 |
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