1,721,026 research outputs found
Risk assessment in pT1 colorectal cancer
No full textColorectal cancer (CRC) is a common malignancy worldwide and tumour stage is closely related to clinical outcome. A small but significant proportion of submucosal-invasive (ie, pT1) CRC are associated with regional lymph node metastases (LNM) and a worse prognosis. The likelihood of LNM in pT1 CRC needs to be balanced against the operative risk and costs of surgical resection when determining the best patient management. A wide range of histopathological and clinical factors may affect LNM risk in this setting. This script provides a comprehensive overview of the tumour and patient-associated features that have been linked to LNM risk in pT1 CRC. Some of the features are well established within the literature and are included in published guidelines, while others are novel and emerging in nature. Odds ratios for LNM that are associated with key predictive features are provided where appropriate, and published models developed as an aid to the calculation of LNM risk are discussed
CD117/KIT expression in pancreatic adenocarcinoma
No full textObjective: CD117/KIT overexpression is common in neoplasms such as gastrointestinal stromal tumors and predicts clinical response to tyrosine kinase inhibitors. Pancreatic adenocarcinoma has a poor prognosis, and therefore, targeted molecular therapymay be beneficial. Marked differences in the incidence of CD117/KIT expression have been reported in pancreatic adenocarcinoma. The aim of this study was to test the hypothesis that CD117/KIT expression is unusual in pancreatic adenocarcinoma. Methods: CD117/KIT immunohistochemistry was performed on 23 archival pancreatic adenocarcinoma samples using 2 primary antibodies. Results: Satisfactory internal and external positive control labeling was achieved for both primary antibodies. No tumor cell labeling was identified using one primary antibody, whereas all cases showed cytoplasmic CD117/KIT staining with the second. However, CD117/KIT expression was also identified using the latter within nuclei and benign pancreatic epithelium, suggesting that artifactual staining was occurring. Conclusions: Pancreatic adenocarcinoma does not express CD117/KIT as assessed using the primary immunohistochemical antibody usually used in our laboratory for CD117/KIT detection. The variation in reported incidence of CD117/KIT expression in pancreatic adenocarcinoma is because of methodological differences in immunohistochemical technique. Ideally, immunohistochemical studies of this molecule should be combined with mutational status testing of the c-kit gene
Rectal cancer staging post neoadjuvant therapy - how should the changes be assessed?
No full textAims:To compare the utility and reproducibility of tumour regression grade scoring systems during histopathological assessment of rectal cancers resected after neoadjuvant (i.e. pre-operative) chemoradiotherapy. Methods and results:? The histopathological features of tumour regression were assessed independently in 54 rectal cancer resection specimens using three scoring systems: the Tumour Regression Grade (TRG), modified Rectal Cancer Regression Grade (m-RCRG) and RCPath Cancer Dataset (RCPath) methods. Good interobserver agreement was achieved for all three systems (? scores: TRG system 0.719, m-RCRG system 0.734, RCPath system 0.742). Both observers diagnosed complete tumour regression and little/no regression in 11 cases (20% of all cases) and four cases (11% of all cases), respectively. A mean of 5.6 tumour blocks/case were taken and the mean lymph node yield was 8.4/case. Conclusions:? All three scoring systems were usable in a diagnostic setting. The clinical significance of differing degrees of tumour regression is not yet universally agreed and, with this in mind, the m-RCRG system provided the optimum balance between applicability and the accurate recording of low, moderate and high degrees of tumour regression, thus facilitating future clinicopathological studies of moderate and high degrees of tumour regression and clinical outcome
Chemokine expression in IBD. Mucosal chemokine expression is unselectively increased in both ulcerative colitis and Crohn's disease
No full textMucosal changes in inflammatory bowel disease (IBD) are characterized by ulcerative lesions accompanied by prominent cellular infiltrates in the bowel wall. Chemokines are chemotactic cytokines that are able to promote leukocyte migration to areas of inflammation and are also able to initiate cell activation events. They have recently been implicated in the pathophysiology of many disease states. The aim of this study was to detail the degree and distribution of specific chemokines, interleukin (IL)-8, monocyte chemoattractant protein (MCP)-1, -2, and -3, and macrophage inflammatory protein (MIP)-1 and -1, in IBD mucosa. Thirty-nine patients were included, ten controls, 20 ulcerative colitis (UC), and nine Crohn's disease (CD), with a range of disease activity. Colonic mucosal biopsies were collected from UC, CD, and control patients and embedded in glycol methacrylate. Two-micrometre-thick sections were cut and stained using immunohistochemistry for chemokine protein expression. Sections were analysed using a light microscope. Expression of all types of chemokine protein was detected in colonic mucosa from both control and IBD patients. Patterns of staining between IBD patients and controls differed significantly, but CD and UC patients demonstrated similar patterns of staining. Individual chemokine expression was found to be significantly up-regulated in IBD when patients were compared with the non-diseased group in all areas of the mucosal sections. Up-regulated chemokine expression correlated with increasing activity of the disease. It is concluded that human colonic chemokine expression is non-selectively up-regulated in IBD. The results supported the hypothesis that the degree of local inflammation and tissue damage in UC and CD is dependent on local expression of specific chemokines within IBD tissues
Developing a 'traffic light' test with potential for rational early diagnosis of liver fibrosis and cirrhosis in the community
No full textBackground: Liver disease develops silently and presents late, with often fatal complications. Aim: To develop a `traffic light' test for liver disease suitable for community use that could enhance assessment of liver risk and allow rational referral of more severe disease to specialist care. Design and setting: Two cohorts from Southampton University Hospital Trust Liver Unit: model development and a validation cohort to evaluate prognosis. Method: A total of 1038 consecutive liver patients (inpatient and outpatient) (development n = 397, validation n = 641) for whom the relevant blood tests had been performed, were followed for a mean of 46 months (range 13-89 months). Blood tests for: hyaluronic acid (HA), procollagen-3 N-terminal peptide (P3NP), and platelet count were combined in a diagnostic algorithm to stage liver disease. Results: A simple clinical rule combined: HA, P3NP, and platelet count into a `traffic light' algorithm, grading the results red - high risk, amber - intermediate risk, and green - low risk. In the validation cohort, no green subjects died or developed varices or ascites (n = 202); in the amber group, 9/267 (3.3%) died, 0/267 developed varices, and 2/267 (0.7%) developed ascites; in the red group, 24/172 died (14%), 24/172 (14%) developed varices, and 20/172 developed (11.6%) ascites. Survival was reduced in red (P<0.001) and amber (P<0.012) groups compared with green. Conclusion: A simple blood test triages liver disease into three prognostic groups; used in the community, it could enhance the management of risk factors in primary care and rationalise secondary care referrals, including the many patients with fatty liver and relatively minor elevations in alanine transaminase
A novel 3' mutation in the APC gene in a family presenting with a desmoid tumour
No full textDesmoid tumours, also known as infiltrative fibromatoses, are rare benign tumours which often recur after local resection and can cause death through local infiltration of vital structures. The estimated incidence in the general population of such tumours is 1-2 per million but in familial adenomatous polyposis (FAP) they occur in up to 15% of cases. Likely precipitating factors include trauma and female sex hormones, since females are more often affected than males. The majority of desmoid tumours in FAP (over 90%) arise in the mesentery of the bowel or in the abdominal wall musculature. In recent years, several families have been described where the predominant phenotype is of desmoid disease and where the colonic phenotype is minimal. We describe another such family with a novel protein truncating mutation in the 3' end of the APC gene
New life for old cellular pathology: A transformational approach to the upcycling of historic e-pathology records for contemporary clinical uses
No full textAims: Cellular pathology (€ e-pathology') record sets are a rich data resource with which to populate the electronic patient record (EPR). Accessible reports, even decades old, can be of great value in contemporary clinical decision making and as a resource for longitudinal clinical research. The aim of this short paper is to describe a solution in a major UK University Hospital which gives immediate visibility and clinical utility to 30 years of e-pathology records. Methods: Over the past decade, we have created a timeline structured and iconographic data framework for the € whole-of-life' visualisation of the entirety of an EPR. We have enhanced this interface with the sequential extraction of 373 342 e-pathology reports from legacy Ferranti (1990-1997) and Masterlab (1997-2004) files. They have been uploaded into our SQL file servers, following appropriate data quality and patient identity reconciliation checks. Results: We have restored a large repository of previously inaccessible e-pathology records to clinical use and to immediacy of access as a foundation element of our timeline structured EPR. This process has also allowed us to populate and validate an EPR-integral breast cancer data system of 20 000 cases with e-pathology records dating back to 1990. Conclusions: The revitalisation of old e-pathology reports into a timeline structured EPR creates preserves and upcycles the investment in pathology reporting which is otherwise progressively lost to clinical use. E-pathology records provide reliable, life-long evidence of critical transition points in individual lives and disease progression for clinical and research use, when they can be instantly accessed. </p
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