2008 Summer Meeting - Leeds - The Pathological Society of Great ...

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S1Virtual slides in research and diagnosisDTreanor 11 Pathology and Tumour Biology, Leeds Institute of Molecular Medicine,University of LeedsVirtual slides are rapidly becoming an essential technology in pathologyresearch and in teaching. While they are less commonly used in diagnosis thetechnology is surely heading in that direction – the integration of digitalimaging in radiology is now complete in the UK.This talk gives an overview of the technology, describes the use of virtual slidesin diagnosis and research, and discusses the advantages and the challenges –technical and otherwise – of virtual slides. Aspects of the virtual slide project atLeeds will be described.In particular aspects of integrating virtual slides into laboratory workflows, useracceptability, and usability will be covered. Further work needed to develop thetechnology in future will also be discussed.S3A Human Protein AtlasFPonten 11 Department of Genetics and Pathology, Uppsala University Hospital,Uppsala, SwedenThe completion of the human genome sequence has opened up a possibility forglobal expression profiling of human tissues and cells, allowing forcomparative studies between normal and disease tissues. A multi-disciplinaryresearch program to create a “Human Proteome Resource” was started in July2003. The aim of the program was to allow for systematic exploration of thehuman proteome using antibody-based tissue proteomics, combining highthroughputgeneration of mono-specific antibodies (affinity-purified) withprotein profiling in human tissues and cells using tissue microarrays.Recombinant protein fragments selected from unique regions called ProteinEpitope Signatures Tags (PrESTs) were used as imunogens to generateantibodies. Analysis of protein expression paterns was performed on tissue andcell microarrays containing >700 spots of normal and cancer tissues as well asin vitro cultured cells.We have used this strategy to construct a comprehensive, antibody-basedprotein atlas for expression and localization profiles in 48 normal human tissuesand 20 different cancers. The results are presented in a publicly availabledatabase (www.proteinatlas.org) containing images and data from proteinprofiling using over 3,000 antibodies. Each image has been manually annotatedand curated by a certified pathologist to provide a knowledge base forfunctional studies and to allow searches and queries about protein profiles innormal and disease tissue . Our results suggest that it should be possible toextend this analysis to a majority of all human proteins thus providing avaluable tool for medical and biological research.S2NCRI/NCI Bioinformatics InitiativeSBell 11 National Cancer Research Institute, Informatics InitiativeAt present, data, services and tools generated via individual cancer researchendeavours are frequently unavailable to the wider research community.Utilising IT ‘grid’ technology, the UK National Cancer Research Institute(NCRI) Informatics Initiative and the National Cancer Institute (NCI) areworking to provide the means to locate and access these datasets, services andtools.The NCRI’s ‘Informatics Platform’ and the NCI’s cancer BiomedicalInformatics Grid (caBIG) are demonstrating the potential of interoperabletechnologies to enhance research, allow re-use of data and potentially allowfaster translation of basic research to new treatments.To exemplify how the Informatics Platform can provide real benefits toclinicians the NCRI Informatics Initiative supported an ‘Imaging andPathology’ demonstrator project.This project drew on the combined expertise of a consortium of leading UKresearch centres to integrate pathology and multi-modal medical image datadrawn from clinical trials of colorectal cancer. The project allowed imagingtechniques to relate diagnostic parameters and features within the images anddata sets to transform that data into clinically relevant information of directbenefit in diagnosis and treatment. The project successfully proved that linkageof imaging data sets was feasible and provided real value to researchers, and isnow being extended further in collaboration with the NCI.The NCRI continues to make progress in the development of a publiclyavailableInformatics Platform to facilitate cancer research. To this end theNCRI Informatics Initiative has the support of the UK Government, charitiesand industry, amongst others.S4Workplace-Based AssessmentEW Benbow 11 University of ManchesterThe Royal College of Pathologists set up a Working Party on Workplace BasedAssessment (WPBA) in May 2006, recognising the importance of WPBA inspecialist medical training, and fulfilling the Postgraduate Medical andEducation Training Board’s (PMETB) standards. WPBAs for pathologytrainees have been under-utilised and poorly recorded, but can provide robustevidence for the Record of In Training Assessment (RITA) process, and for theEnd of Stage Reviews (ESRs) for Senior House Officers, and will continue tosupport the Annual Review of Competence Progression (ARCP) system thathas replaced them.For histopathology trainees, methods include Case-based Discussion (CbD),Direct Observation of Practical Skills (DOPS) and Evaluation of ClinicalEvents (ECE), together with multi-source feedback gathered on-line with e-PATH SPRAT. CbDs assess decision making, and the application of medicalknowledge in individual cases. DOPS evaluate the capacity of trainees tocomplete day-to-day routine tasks, with immediate feedback about strengthsand weaknesses. ECEs look at integration of simple skills into complex tasks,such as presentations at multidisciplinary team meetings or clinicopathologicalcorrelation. The e-PATH SPRAT is 3600 appraisal, where characteristics arerated on a standard form, completed on line by several raters; this includes selfassessment.Education research in clinical disciplines shows that formative WPBA canchange trainees’ behaviour. The commitment of trainers, properly trained, iscrucial: anything less risks generating a lot of pointless box-ticking.88 Summer Meeting (194 th ) 1–4 July 2008 Scientific Programme
S5The MRCPath Autopsy ExaminationSLucas 11 Guy's, King's & St Thomas' School of MedicineThe MRCPath examination changed radically in 2005, with the Autopsy andHistopathology/Cytopathology modules separated and becoming noncontingent.The revised full-day autopsy exam enabled a fuller evaluation ofcandidates, but suffers from lack of standardisation in all the three sections(autopsy dissection & presentation, laboratory diagnosis, viva).Along with problems from 1) increasing difficulties in providing training inautopsy procedures and the associated 2) introduction of Autopsy OptionalTraining (AOT) in the near future, and 3) organising autopsy centres within theexam time frame, a new format has been consulted upon and (in general)agreed. The new exam is for those trainees not opting out of autopsy practice.In outline this will be:A. a workplace based assessment (WPBA) of actual autopsy dissectioncompetence• undertaken after stages A+B of training, at the mutual convenience of traineeand assessors• at the trainee’s home mortuary, or the regional examiner’s if appropriate• assessed by the local educational supervisor plus a visiting regional examiner• to be completed within 3 hours, including write up and documentation ofcause of deathB. Once a trainee has satisfied this WPBA, a centralised part 2 examinationwith all candidates in one place, undertaken twice a year. This includes:• critical evaluation of autopsy reports• viva on communication skills & medico-legal aspects• microscopy and gross diagnosis of autopsy material• biochemical, toxicological and microbiological evaluation• questions on autopsy practice• case interpretation and cause of deathS7The Molecular Pathology of Cervical NeoplasiaCS Herrington 11 University of St AndrewsIt is now accepted that almost all cervical neoplasia is causally associated withhigh-risk human papillomavirus (HPV) infection. However, HPV infection isnot sufficient for the development of neoplasia and other factors are involved.HPV integration has emerged as an important factor in the progression of HPVassociatedneoplasia and the effects of integration, notably loss of HPV E2expression and up-regulation of HPV E6 and E7 expression, can lead to manyof the molecular features associated with the development of high-gradeintraepithelial and invasive squamous and glandular lesions, for exampletelomerase activation and chromosome abnormalities. Sites of frequentchromosome abnormality include 3q, 5p and 20q, all of which have beenassociated with gain and/or elevated expression of specific genes, for examplethe telomerase gene TERC, the microRNA processor Drosha, and DNAmethyltransferase 3B (DNMT3B) respectively. This is consistent with thesequential methylation of several tumour suppressor gene promoters, notablyMGMT, during the progression of HPV-transfected keratinocytes to anchorageindependence. Thus, both genetic and epigenetic changes appear to beimportant in the progression of HPV-associated neoplasia, driven by the effectsof HPV infection and integration.S6Chromosomal Instability in Colorectal Adenoma toCarcinoma Progression & Early Detection of ColorectalCancerGA Meijer 11 VU University Medical Centre, Amsterdam, The NetherlandsColorectal adenomas are commonly found in individuals over 60 years of age,and only a minority of colorectal adenomas progress to adenocarcinomas. Thisis progression is mostly associated with overt chromosomal instability (CIN). Incontrast to the less frequently occurring microsatellite instability, which iscaused by failing DNA mismatch repair, the mechanisms underlying CIN incolorectal adenoma to carcinoma progression are still largely obscure.We have investigated the patterns of CIN in colorectal adenoma tocarcinoma progression by measuring DNA copy number changes witharrayCGH. Amongst others, frequent DNA copy number alterations onchromosomes 13q and 20q turned out to affect mRNA and miRNA expressionof multiple genes like AURKA and the miRNA cluster mir-17-92.Apart from mutations and DNA copy number alterations, also promoterhypermethylation is an important factor in colorectal carcinogenesis. Whencomparing promoter hypermethylation and DNA copy number changes indifferent stages of colorectal carcinogenesis, promoter hypermethylationoccurred earlier. In addition, also specific associations between DNA copynumber alterations and promoter hypermethylation occurred like promotermethylation of GATA-4 and p16INKA4 that were inversely related tochromosomal loss at 15q11-21 and gain at 20q13 respectively (P values: 3.8 x10-2 and 4.5 x 10-2 respectively).Current challenge is to translate this knowledge into approaches formolecular early diagnosis of colorectal cancer, like stool DNA based tests.Methylation markers already have yielded promising results, but we also havegenerated pilot data for detecting DNA copy number alterations in stool derivedDNAS8Occult Lymphoproliferative DisordersAS Jack 11 HMDS, St James's Institute of Oncology, LeedsThe use of sensitive flow cytometric and molecular diagnostic tests has led tothe detection of low level lymphoproliferative disorders in increasing numbersof healthy individuals. In the case of CLL it is estimated that around 3% of theadult population may be affected and a similar proportion can be shown to havea paraprotein. There is less Information on the prevalence of other forms ofoccult lymphoproliferative disorder, but it is clear that low levels of B-celllymphoproliferative disorders with non-CLL phenotypes are also relativelycommon. This is consistent with the frequent detection of t(14;18) by sensitivePCR in healthy individuals. Clonal T-cell lymphoproliferative disorders,usually with a cytotoxic T-cell large granular lymphocyte (LGL) phenotype, arealso frequently encountered in the investigation of lymphocytosis detected onroutine blood counts.The detection of these conditions in the course of other forms of medicalinvestigation and treatment raises a number of important issues. If the patienthas Diffuse Large B-cell Lymphoma the possibility that disease has arisen bytransformation of an underlying indolent lymphoma will need to be addressedand this may have prognostic implications. In other patients the detection of anoccult lymphoproliferative disorder may cause significant anxiety and requirefollow up commensurate with the risks of disease progression. Finally, theclinical consequences and disease associations of clonal T-LGL disorders arewell recognised. In contrast, the possible health effects of the more numerousB-cell disorders remains poorly understood.Summer Meeting (194 th ) 1–4 July 2008 Scientific Programme89
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PROGRAMME ACKNOWLEDGEMENTSPublished
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PROGRAMME QUICK REFERENCE TABLES -
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SCIENTIFIC SESSIONS INFORMATIONSLID
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GENERAL ARRANGEMENTSSOCIAL ACTIVITI
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Detailed Programme - Tuesday 1 July
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Detailed Programme - Tuesday 1 July
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Detailed Programme - Wednesday 2 Ju
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Detailed Programme - Thursday 3 Jul
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Detailed Programme - Friday 4 July
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ACKNOWLEDGMENTSas at the time of go
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AbstractsPlenaryNote: Presenter’s
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PL5Identification of Key Breast Can
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P1Distinction of Fibroadenoma & Phy
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P9Mistletoe should be reserved for
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P17Specimen Handling of Screen-Dete
Page 38 and 39: P25Mib1 Tumour Growth Fraction Asse
Page 40 and 41: P33What is the Real Incidence of HE
Page 42 and 43: P41MCPH1, a potential predictor for
Page 44 and 45: P49CTEN positively regulates cell m
Page 46 and 47: P57Meta-clustering of Small Intesti
Page 48 and 49: P65Colovesical Fistula - Complicate
Page 50 and 51: P71Ciliated foregut cyst of gallbla
Page 52 and 53: P79Evaluation of survivin expressio
Page 54 and 55: P87Incompletely Differentiated (Unc
Page 56 and 57: P95Ovarian Neuroblastoma Arising Wi
Page 58 and 59: P103Biopsy Pathology in HIV in the
Page 60 and 61: P111YY1 is a Prognostic Marker in F
Page 62 and 63: P119Ossifying Fibromyxoid Tumour of
Page 64 and 65: P127The effect of inhaled carbon di
Page 66 and 67: P135Clinical significance of miR-21
Page 68 and 69: P143Streamed Internet Video for Pat
Page 70 and 71: P151P153The Central & Northern Rese
Page 72 and 73: P159Immunohistochemistry Biomarker
Page 74 and 75: P167Presence of stem cell traits in
Page 76 and 77: P175Systematic Random Sampling with
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Page 80 and 81: O9Development and characterisation
Page 82 and 83: O17Regulation of the Adenomatous Po
Page 84 and 85: O253 Dimensional Pathology with Vir
Page 86 and 87: O33Molecular Genetic Profiling of O
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