96. Jahrestagung der Deutschen Gesellschaft für Pathologie e. V ...

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FR-013 HPV-genotype distribution in cytological screening, histology and impact of vaccination M . de Jonge 1 , G . Busecke 2 , A . Heinecke 3 , O . Bettendorf 4 1 Institute for Pathology and Cytology Schüttorf/Leer, 2 Medical office of General Medicine, Weener, 3 Department of Medical Informatics and Biomathematics, University of Münster, 4 Insitute of Pathology and Cytology Schüttorf/Leer, Schüttorf Aims. The objective of the research was to investigate the HPV-type distribution in our screening population as well as its correlation to cytological diagnosis and histological outcome, and to calculate the impact of primary HPV vaccination. Methods. HPV genotyping results of 3381 women who attended to the German cervical screening program were retrospectively analysed. The PapilloCheck®-Test was used for HPV genotyping. The distribution of HPV-types with corresponding cytological diagnosis, and – if available – histological outcome, was statistically analysed (SPSS 17.0, SAS9.3, Pearson’s χ2 test). To estimate the possible impact of HPV vaccination on our cohort we calculated the theoretically minimum impact as well as the maximum impact in the prevention of HPV-positive lesions. Results. The HPV-type-distribution showed marked differences among cervical lesions and age. Although HPV-51 was common in all cervical lesions, it was rarely detected as single-type HPV infection in CIN3-lesions. HPV-16 and/or HPV-18 were found in only 58% of the CIN3-lesions, which was still significantly more than the 22% in CIN2-lesions (p
Abstracts detect alterations in histopathological inconspicuous urothelium. Gene expression profiling, TMA technology, promoter methylation analysis, qRT-PCR, aCGH and in vitro studies were performed for the identification and functional characterization of progression-related candidate genes in BC. A comprehensive molecular, immunohistochemical and clinicopathological analysis of a large collection of plasmacytoid BC samples was performed. Results. Deletions on chromosomes 9 and 8p were detected in approx. 10% of normal urothelial samples from BC patients. The most common deleted region was on chromosome 9q33.3. Deletions of chromosome 8p were identified as progression markers for papillary BC. Loss of sFRP1 expression (located on 8p11.21) was found in 35% of BC cases and was caused by gene copy loss and/or promoter methylation. Functional studies revealed an influence of sFRP1 on proliferation, cell viability and migration in papillary BC. Patients with papillary BC and sFRP1 loss showed a significant decreased overall survival which was not relevant in patients with solid tumors. Plasmacytoid BC displayed molecular alterations of advanced, aggressive BC. A complete loss of membranous E-Cadherin un<strong>der</strong>lined the high malignant and metastatic potential of this BC variant. Conclusions. BC is not affecting the complete urothelium. Molecular alterations in the normal urothelium could be origins of multifocal tumor growth and argue for the “field cancerization” theory. Deletions on chromosome 8p and expression loss of sFRP1 might act as entity-specific progression markers for papillary BC. The profile of molecular alterations in plasmacytoid BC might help to find the suitable therapeutic intervention for patients with this highly aggressive BC variant. FR-017 Novel approaches to progressive renal diseases P . Boor1 1RWTH Aachen University, Aachen Aims. Essentially all chronic renal diseases but also repeated or serious acute insults inevitably lead to chronic kidney disease and renal fibrosis. We currently lack effective treatment options for renal fibrosis; the development of an effective therapy would be invaluable virtually for all renal patients. Methods. We have used various in vivo and in vitro models of renal fibrosis. Results. We have identified PDGF-CC, PDGF-DD, C5a and PPAR-α as novel treatment targets in renal fibrosis. By identifying these targets as crucial components of renal tubulointerstitial fibrosis we also uncovered the mechanisms relevant for their actions, including mitogenic effect of PDGF-DD and proinflammatory effects of PDGF-CC on interstitial fibroblasts and effects of C5a/C5aR and PPAR-α on tubular epithelial cells resulting in reduced profibrotic paracrine signaling to interstitial fibroblasts. We verified all of the targets using tools used in, tested for or developed for clinical use. These studies lay an important experimental basis for translating these targets to clinical practice. In this regard, we also showed that serum PDGF-DD is specifically increased in patients with mesangioproliferative but not other types of glomerulonephritis. In further studies on renal fibrosis we showed that irrelevant IgG has antifibrotic effects in a model of progressive mesangioproliferative glomerulonephritis resulting in improved survival. We also documented that the renal profibrotic effects of cyclosporine A are mediated by Y-box binding protein-1 (YB-1) and that mesenchymal stem cells might maldifferentiate and induce local fibrotic response in progressive glomerulonephritis in rats. We also pointed out that simple non-pharmacological approaches in diabetic rats, e.g. regular mo<strong>der</strong>ate exercise, reduced renal fibrosis in a very early stage when no functional changes were yet observed. The mechanism seemed to be via improving metabolism and interfering with an important pathogenic pathway in diabetes, the advanced glycation. We have also identified environmental factors, which led to renal but also cardiac fibrosis in healthy rats, i.e. passive smoking and industrial dust 52 | Der Pathologe · Supplement 1 · 2012 particles amozite. These environmental risk factors are external, modifiable and could lead to better monitoring of patients with such (occupational) risk. Conclusions. Still much is to be learned about renal fibrosis. We hope to have uncovered some pieces of this immense puzzle and surely aim to continue to put it together in the future. FR-018 Using genome-wide molecular screening for the identification of new marker and target genes of human hepatocellular carcinoma T . Longerich1 1University Hospital Heidelberg/Institute of Pathology, Heidelberg Aims. To identify new diagnostic and prognostic markers that may be used as therapeutic targets and to develop an oncogenetic progression model of human hepatocellular carcinoma (HCC). Methods. A well-characterized human HCC collection was used for systematic genome-wide screening. Identified potential candidate genes were validated via expression analysis and selected candidates were further characterized in vitro using suitable HCC cell lines. Results. Using a meta-analysis of classical comparative genomic hybridisation (CGH) analysis (24 dysplastic nodules, 871 HCCs) a genomic progression model of tumour dedifferentiation (1q – 8q – 4q – 16q – 13q) was generated. Array-based CGH analysis revealed recurrent chromosomal gains at 1q, 6p, 8q, 17q, 19p, and 20q, while genomic losses were observed at 1p, 4q, 8p, 13q, 16q, and 17p. The mouse double minute homolog 4 (MDM4) that functions as a negative p53 regulator could be identified as a target gene of 1q gains in human HCC. Aetiology-dependent copy number gains and MYC overexpression was detected in viral and alcohol-related HCCs. In contrast, cryptogenic HCCs showed neither 8q24 gains, nor MYC overexpression, nor target gene activation. The role of Polo-like kinase family (PLK) members was analyzed in human HCC. PLK1 levels were upregulated in human HCC, reaching the highest expression in tumours with poorer outcome. PLK1 overexpression resulted from activation of the Ha-Ras/FOXM1/PLK1-axis. In contrast PLK2, PLK3, and PLK4 expression were downregulated in HCC, with the lowest levels being detected in HCC with shorter survival. PLK2-4 down-regulation was paralleled by promoter hypermethylation and/or loss of heterozygosity. Immunohistological analysis revealed that a diffuse sinusoidal expression of Annexin A2 has diagnostic value for the biopsy diagnosis of highly-differentiated HCC and may increase the accuracy of the established diagnostic marker panel (GPC3, GS, HSP70) for HCC detection. Conclusions. Five genomic aberrations allow the generation of a robust progression model of human hepatocarcinogenesis. MDM4 upregulation may result in functional p53-inactivation in HCCs that may allow p53-reactivation as a therapeutic strategy. Differential oncogenic and tumour suppressive roles of Polo-like kinases could be identified in human HCC. Systematic genome-wide screening analysis were used to identify new diagnostic marker and potential oncogenic and tumorsuppressive factors that may be promising future therapeutic targets. FR-019 In situ hybridization in clinical pathology T . Gaiser1 1Philipps-University Marburg, Institute of Pathology, Marburg Aims. Over the last decade in situ hybridization (ISH) has emerged as a powerful clinical and research tool for the assessment of target DNA dosages within interphase and metaphase nuclei. HER2 detection is the widest application for ISH in routine pathology but EGFR ISH or the newly introduced melanoma FISH are further possible applications, which can be additionally improved by computer based analysis systems.
Page 2 and 3: Inhalt Der Pathologe · Supplement
Page 4 and 5: Inhalt Der Pathologe · Supplement
Page 6 and 7: Editorial Liebe Kolleginnen und Kol
Page 8 and 9: Kolorektales Karzinom 2 VO-005 Tran
Page 10 and 11: Keynote Lecture VO-014 Genetic dete
Page 12 and 13: (AMACR, FASN, GOLM1, GSP-pi, ERG) t
Page 14 and 15: to assess the correct rate of R1 re
Page 16 and 17: DNA damage, and cytotoxic drugs. Au
Page 18 and 19: HCV-positive formalin-fixed and par
Page 20 and 21: well as MET activation were examine
Page 22 and 23: or BRAF mutation, c-MYC and SIRT1 e
Page 24 and 25: AG Pneumopathologie III DO-032 Remo
Page 26 and 27: immature granulopoiesis showed a st
Page 28 and 29: ned, if well-defined mantle zones,
Page 30 and 31: phomas). Most prominent gains or am
Page 32 and 33: DO-062 Tumor-associated macrophages
Page 34 and 35: DO-080 DOG1: an immunohistochemical
Page 36 and 37: AG Oralpathologie DO-087 Detection
Page 38 and 39: DO-094 Do activated fibroblasts inf
Page 40 and 41: DO-101 Histopathological analysis o
Page 42 and 43: DO-108 Identification of potential
Page 44 and 45: Conclusions. In conclusion, 454 par
Page 46 and 47: subgroup of patients with B-Raf mut
Page 48 and 49: DO-002b Impact of terminologies in
Page 50 and 51: Methods. We performed MCPyV-FISH of
Page 54 and 55: Methods. Three different techniques
Page 56 and 57: (i.e. investment in equipment and e
Page 58 and 59: FR-032 COLD-PCR: a powerful tool in
Page 60 and 61: dissection (MBLND) technique to imp
Page 62 and 63: SO-005 Prevalence of mutations in s
Page 64 and 65: SO-011 Methylation profiling and in
Page 66 and 67: more effective than SAHA alone and
Page 68 and 69: SO-022 Specialized pathology review
Page 70 and 71: SO-027 Ki-67 in mitotic score group
Page 72 and 73: nificantly associated with advanced
Page 74 and 75: liver did not correlate with the mu
Page 76 and 77: AG Paidopathologie II SO-046 Overex
Page 78 and 79: Results. Histomorphology of the ova
Page 80 and 81: p42 and p27 have not yet been inves
Page 82 and 83: SO-068 Recent advances in understan
Page 84 and 85: SO-075 A novel, dual role of CCN3 i
Page 86 and 87: Pancreatic Adenocarcinoma SG-137 Se
Page 88 and 89: sease and 30 colon cancer serum sam
Page 90 and 91: Conclusions. Although CRC is charac
Page 92 and 93: differentiated and TNM stage III or
Page 94 and 95: pressed moderate levels of the prot
Page 96 and 97: FR-P-037 MALDI imaging reveals COX7
Page 98 and 99: in the context of therapy response
Page 100 and 101: on primary cells of wild-type and c
Page 102 and 103:
chemotherapy was recommended and co
Page 104 and 105:
aims are twofold: 1) to verify the
Page 106 and 107:
Results. Her2/neu status in TMAs an
Page 108 and 109:
prognostic impact was found in rect
Page 110 and 111:
provided information on survival ti
Page 112 and 113:
Methods. Biopsy specimens from 430
Page 114 and 115:
the OS rate was 53% for patients wi
Page 116 and 117:
FR-P-098 Immunohistological stainin
Page 118 and 119:
FR-P-104 Histopathological evaluati
Page 120 and 121:
within the earliest morphologic det
Page 122 and 123:
Conclusions. In primary imaging a g
Page 124 and 125:
fibrotic neointma development as we
Page 126 and 127:
FR-P-129 Alpha-1-antitrypsin-PiZ-an
Page 128 and 129:
FR-P-136 The expression of central
Page 130 and 131:
cosa and in the periarterial tissue
Page 132 and 133:
FR-P-149 Combination of Castleman d
Page 134 and 135:
or without different concentrations
Page 136 and 137:
Results. In 18 cases (79%) the caus
Page 138 and 139:
FR-P-168 Autopsy findings in a 2-ye
Page 140 and 141:
FR-P-174 MPGN-like glomerulonephrit
Page 142 and 143:
Poster: Gynäkopathologie und Mamma
Page 144 and 145:
SA-P-011 Genetic aberrations of pre
Page 146 and 147:
Mechanismen, die eine Progression d
Page 148 and 149:
internet server. A network of inter
Page 150 and 151:
Methods. HE-gefärbte Schnittpräpa
Page 152 and 153:
Conclusions. The newly released 450
Page 154 and 155:
and desmoplastic reaction are diffe
Page 156 and 157:
one patient revealed more than 9 mi
Page 158 and 159:
situation, the V600E mutation in th
Page 160 and 161:
SA-P-064 Evolution of molecular pat
Page 162 and 163:
nic markers such as myf4 and MyoD1
Page 164 and 165:
Conclusions. To our knowledge, this
Page 166 and 167:
SA-P-085 Expression of the eukaryot
Page 168 and 169:
Results. The papillary RCC type II
Page 170 and 171:
SA-P-098 Male infertility: assessme
Page 172 and 173:
SA-P-104 Process oriented scientifi
Page 174 and 175:
Conclusions. The IBDW offers a uniq
Page 176 and 177:
L Lasitschka F. DO-046 Lehmann A. F
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96. Jahrestagung der Deutschen Gesellschaft für Pathologie e. V ...

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