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| 1 | Polymorphisms of MTHFR and susceptibility to oesophageal adenocarcinoma in a Caucasian United Kingdom population显示文摘AIM:To identify if methylene tetra-hydrofolatereductase(MTHFR)C677T polymorphisms are associated with oesophageal adenocarcnomas in a Caucasian population and to test whether folic acid and homocysteine levels are linked with cancer risk.METHODS:A case control study comprising of 58 non cancer and 48 cancer patients,MTHFR C667T genotyping was made and serum folate,homocysteine and vitamin B12 levels were made.Tumour stage,differentiation and survival was recorded.A P value of less than0.05 was taken to be significant.Theχ2 used to compare discrete variables and the Mantel-Cox was used to compare survival.A P value less than 0.05 was deemed to be significant.RESULTS:MTHFR polymorphisms is associated with an increased risk of several cancers.A link between MTHFR C677T polymorphisms and oesophageal squamous cell carcinoma and gastric cardia adenocarcinoma has been demonstrated in at risk Chinese populations.In a Western European population the role of the MTHFR gene has not previously been investigated in the setting of oesophageal adenocarcinoma.No association between folic acid levels and cancer patients was found.The unstable MTHFR 667 TT genotype occurred in 11%cancers and 7%controls,but statistical significance was not reached,homocysteine levels and folic acid levels were not affected,cancer patients with TT genotype displayed a trend for a shorter survival 7 mo vs 20 mo.Serum vitamin B12 levels were higher in the cancer group.The MTHFR 667 TT genotype is much lower than previous population studies.CONCLUSION:We conclude that serum folic acid and MTHFR polymorphisms are not associated with an increased risk of oesophageal adenocarcinoma,although cancers with unstable TT genotype may indicate a more aggressive disease course. | Richard Keld Manyi Thian Chia Hau Jamil Sajid Narveen Kumar Yeng Ang | 2014 | World Journal of Gastroenterology2014，20，34： | 8 |
| 2 | Targeting key signalling pathways in oesophageal adenocarcinoma:A reality for personalised medicine?显示文摘Cancer treatments are rapidly changing.Curative treatment for oesophageal adenocarcinoma currently involves surgery and cytotoxic chemotherapy or chemoradiotherapy.Outcomes for both regimes are generally poor as a result of tumor recurrence.We have reviewed the key signalling pathways associated with oesophageal adenocarcinomas and discussed the recent trials of novel agents that attempt to target these pathways.There are many trials underway with the aim of improving survival in oesophageal cancer.Currently,phase 2 and 3 trials are focused on MAP kinase inhibition,either through inhibition of growth factor receptors or signal transducer proteins.In order to avoid tumor resistance,it appears to be clear that targeted therapy will be needed to combat the multiple signalling pathways that are in operation in oesophageal adenocarcinomas.This may be achievable in the future with the advent of gene signatures and a combinatorial approach. | Richard R Keld Yeng S Ang | 2011 | World Journal of Gastroenterology2011，17，23： | 6 |
| 3 | Targeting the cell cycle in esophageal adenocarcinoma:An adjunct to anticancer treatment显示文摘Esophageal adenocarcinoma is a major cause of cancer death in men in the developed world.Continuing poor outcomes with conventional therapies that predominantly target apoptosis pathways have lead to increasing interest in treatments that target the cell cycle.A large international effort has led to the development of a large number of inhibitors,which target cell cycle kinases,including cyclin-dependent kinases,Aurora kinases and polo-like kinase.Initial phase Ⅰ/Ⅱ trials in solid tumors have often demonstrated only modest clinical benefits of monotherapy.This may relate in part to a failure to identify the patient populations that will gain the most clinical benefit.Newer compounds lacking the side effect profile of first-generation compounds may show utility as adjunctive treatments targeted to an individual's predicted response to treatment. | Martyn Dibb Yeng S Ang | 2011 | World Journal of Gastroenterology2011，17，16： | 6 |
| 4 | Risk factors for neoplastic progression in Barrett's esophagus显示文摘Barrett's esophagus (BE) confers a significant increased risk for development of esophageal adenocarcinoma (EAC), with the pathogenesis appearing to progress through a 'metaplasia-dysplasia-carcinoma' (MDC) sequence. Many of the genetic insults driving this MDC sequence have recently been characterized, providing targets for candidate biomarkers with potential clinical utility to stratify risk in individual patients. Many clinical risk factors have been investigated, and associations with a variety of genetic, specific gastrointestinal and other modifiable factors have been proposed in the literature. This review summarizes the current understanding of the mechanisms involved in neoplastic progression of BE to EAC and critically appraises the relative roles and contributions of these putative risk factors from the published evidence currently available. | Elizabeth F Wiseman Yeng S Ang | 2011 | World Journal of Gastroenterology2011，17，32： | 5 |
| 5 | Gastric endoscopic submucosal dissection as a treatment for early neoplasia and for accurate staging of early cancers in a United Kingdom Caucasian population显示文摘AIM To investigate the efficacy of endoscopic submucosal dissection(ESD) at diagnosing and treating superficial neoplastic lesions of the stomach in a United Kingdom Caucasian population.METHODS Data of patients treated with or considered for ESD at a tertiary referral center in the United Kingdom were retrieved for a period of 2 years(May 2015 to June 2017) from the electronic patient records of the hospital. Only Caucasian patients were included. Primary outcomes were curative resection(CR) and were defined as ESD resections with clear horizontal and vertical margin and an absence of lympho-vascular invasion, poor differentiation and submucosal involvement on histological evaluation of the resected specimen. Secondary end-points were reversal of dysplasia at 12 mo endoscopic follow-up and/or at the latest follow up. Change in histological diagnosis pre and post ESD was also analysed.RESULTS Twenty-four patients were initially identified with intention to treat. 19 patients were eligible after mapping gastroscopy and ESD was attempted on a total of 25 ESD lesions, 4 of which failed and had to be aborted mid-procedure. Out of 21 ESD performed, en-bloc resection was achieved in 71.4% of cases. Resection was considered complete on endoscopy in 90.5% of cases compared to only 38.1% on histology. A total of 6 resections were considered curative(28%), 5 noncurative(24%) and 10 indefinite for CR or non-CR(24%). ESD changed the histological diagnosis in 66.6% of cases post ESD. Endoscopic follow-up in the 'indefinite' group and CR group showed that 50% and 80% of patients were clear of dysplasia at the latest follow-up respectively; 2 cases of recurrence were observed in the 'indefinite'group. Survival rate for the entire cohort was 91.7%.CONCLUSION This study provides early evidence for the efficacy of ESD as a therapeutic and diagnostic intervention in Caucasian populations and supports its application in the United Kingdom. | Aisha Sooltangos Matthew Davenport Stephen McGrath Jonathan Vickers Siba Senapati Kurshid Akhtar Regi George Yeng Ang | 2017 | World Journal of Gastrointestinal Endoscopy2017，9，12： | 3 |
| 6 | Immunohistochemical assessment of NY-ESO-1 expression in esophageal adenocarcinoma resection specimens显示文摘AIM:To assess NY-ESO-1 expression in a cohort of esophageal adenocarcinomas.METHODS:A retrospective search of our tissue archive for esophageal resection specimens containing esophageal adenocarcinoma was performed,for cases which had previously been reported for diagnostic purposes,using the systematised nomenclature of human and veterinary medicine coding system.Original haematoxylin and eosin stained sections were reviewed,using light microscopy,to confirm classification and tumour differentiation.A total of 27 adenocarcinoma resection specimens were then assessed using immunohistochemistry for NY-ESO-1 expression:4 well differentiated,14 moderately differentiated,4 moderatepoorly differentiated,and 5 poorly differentiated.RESULTS:Four out of a total of 27 cases of esophageal adenocarcinoma examined(15%)displayed diffuse cytoplasmic and nuclear expression for NY-ESO-1.They displayed a heterogeneous and mosaic-type pattern of diffuse staining.Diffuse cytoplasmic staining was not identified in any of these structures:stroma,normal squamous epithelium,normal submucosal gland and duct,Barrett’s esophagus(goblet cell),Barrett’s esophagus(non-goblet cell)and high grade glandular dysplasia.All adenocarcinomas showed an unexpected dot-type pattern of staining at nuclear,paranuclear and cytoplasmic locations.Similar dot-type staining,with varying frequency and size of dots,was observed on examination of Barrett’s metaplasia,esophageal submucosal gland acini and the large bowel negative control,predominantly at the crypt base.Furthermore,a prominent pattern of apical(luminal)cytoplasmic dot-type staining was observed in some cases of Barrett’s metaplasia and also adenocarcinoma.A further morphological finding of interest was noted on examination of haematoxylin and eosin stained sections,as aggregates of lymphocytes were consistently noted to surround submucosal glands.CONCLUSION:We have demonstrated for the first time NY-ESO-1 expression by esophageal adenocarcinomas,Barrett’s metaplasia and normal tissues other than germ cells. | Stephen J Hayes Keng Ngee Hng Peter Clark Fiona Thistlethwaite Robert E Hawkins Yeng Ang | 2014 | World Journal of Gastroenterology2014，20，14： | 0 |
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