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

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SO-027 Ki-67 in mitotic score groups of the Nottingham Grading System for breast cancer C . Focke 1 , D . Gläser 1 , K . Finsterbusch 1 , T . Decker 1 1 Dietrich-Bonhoeffer-Klinikum Neubrandenburg, Department of Pathology, Neubrandenburg Aims. The 2011 St. Gallen Consensus suggested the addition of Ki-67 for defining proliferation and thus the difference between luminal A and B clinicopathological subtypes. Whereas a Ki-67 cut-off of 14% is cited from literature it became obvious from the discussion that no standardized methodology or cut-off definition for Ki-67 is available so far. To estimate the capability of immunohistochemically quantified Ki-67 rates to discriminate the Nottingham Grading System (NGS) mitotic score groups and to determine respective cut-offs in breast cancer (BC). Methods. We retrospectively analyzed routinely H&E stained slides of 50 invasive BC (9 G1, 23 G2, and 18 G3). Immunohistochemistry for Ki-67 was done prospectively according to an in house protocol, evaluated in a national interlaboratory trial for quality assurance in immunohistochemistry. To rate Ki-67, 100 tumor cells within an area of the “hot spot “ were evaluated by counting all stained nuclei regardless of intensity. We used the mitotic activity index (MAI) per mm2 as gold standard for proliferation measurement. By assessing the MAI ranges within the mitotic score subgroups of the Nottingham Grading System (NGS) we determined respective MAI cut-offs. Using these MAI cut-offs we adjusted the observed Ki-67 rates. Results. Whereas the cut-offs of MAI for NGS mitotic scores 1, 2, and 3 were 0–32, 33–70, and 71–582, respectively, the resulting ranges of Ki-67 were 7–30%, 13–54%, and 33–98%. The median Ki-67 rates for NGS scores 1–3 came out with 21 (SD±7.5), 41 (SD±11), and 59 (±18.8), respectively. Conclusions. Whereas there is obviously a trend of higher Ki-67 rates in NGS score groups with higher MAI, our data indicate that 1) it was not possible to discriminate the NGS mitotic score groups by using Ki-67 rates, 2) the cited cut-off of
Abstracts SO-031 Decentral gene expression analysis to predict outcome of ER+/ Her2− breast cancer – results of a proficiency testing program for the EndoPredict assay C . Denkert 1 , R . Kronenwett 2 , W . Schlake 3 , K . Bohmann 2 , R . Penzel 4 , K .E . Weber 2 , H . Höfler 5 , U . Lehmann 6 , P . Schirmacher 4 , K . Specht 5 , M . Rudas 7 , H . Kreipe 6 , P . Schraml 8 , G . Schlake 3 , Z . Bago-Horvath 7 , F . Tiecke 3 , Z . Varga 8 , H . Moch 8 , M . Schmidt 9 , J . Prinzler 1 , D . Kerjaschki 7 , B .V . Sinn 1 , B .M . Müller 1 , M . Filipits 10 , C . Petry 2 , M . Dietel 1 1 Charité University Hospital, Institute of Pathology, Berlin, 2 Sividon Dignostics GmbH, Köln, 3 Institute of Pathology, Gelsenkirchen, 4 University of Heidelberg, Institute of Pathology, Heidelberg, 5 Technical University Munich, Institute of Pathology and Pathological Anatomy, München, 6 Medizinische Hochschule Hannover, Institute of Pathology, Hannover, 7 Medical University of Vienna, Institute of Pathology, Austria, 8 University Hospital Zurich, Institute of Surgical Pathology, Zürich, Switzerland, 9 University of Mainz, Department of Gynecology and Obstetrics, 10 Medical University of Vienna, Institute of Cancer Research, Austria Aims. Gene expression profiles provide important information about the biology of breast tumors and can be used to develop predictive tests. However, the implementation of quantitative RNA-based testing in routine molecular pathology has not been accomplished, so far. The EndoPredict assay has recently been described as a quantitative RT-PCR-based multigene expression test to identify a subgroup of hormone-receptor positive tumors that have an excellent prognosis with endocrine therapy only. To transfer this test from bench to bedside it is essential to evaluate the testperformance in a multicenter setting in different molecular pathology laboratories. In this study, we have evaluated the EndoPredict assay in seven different molecular pathology laboratories in Germany, Austria and Switzerland. Methods. A set of ten formalin-fixed paraffin-embedded tumors from patients with breast cancer was tested in the different labs. The Endo- Predict score (EP score) ranging from 0 to 15 was calculated and patients were classified into low or high risk for the occurrence of distant recurrence using a validated cut-off. The variance and accuracy of the Endo- Predict assays were determined using predefined reference values. Results. Extraction of a sufficient amount of RNA and generation of a valid EP score was possible for all 70 study samples (100%). The EP scores measured by the individual participants showed an excellent correlation with the reference values, respectively, as reflected by Pearson correlation coefficients ranging from 0.987 to 0.999. The Pearson correlation coefficient of all values compared to the reference value was 0.994. All laboratories determined EP scores for all samples differing not more than 1.0 score units from the pre-defined references. All samples were assigned to the correct EP risk group, resulting in a sensitivity and specificity of 100%, a concordance of 100%, and a kappa of 1.0. Conclusions. Taken together, the EndoPredict test could be successfully implemented in all seven participating laboratories and is feasible for reliable decentralized assessment of prognosis in luminal breast cancer. 70 | Der Pathologe · Supplement 1 · 2012 SO-032 Cyclin D1 gene amplification is rarely heterogeneous in breast cancer E . Burandt1 , M . Grünert1 , A . Lebeau1 , M . Choschzick1 , V . Müller2 , C . Bokemeyer3 , R . Simon1 , G . Sauter1 , F . Jänicke2 , W . Wilczak1 1University Medical Center Hamburg-Eppendorf, Department of Pathology, Hamburg, 2University Medical Center Hamburg-Eppendorf, Department of Gynecology, Hamburg, 3University Medical Center Hamburg-Eppendorf, Department of Internal Medicine II, Oncology Center, Hamburg Aims. Amplification of Cyclin D1 (CCND1) occurs in about 10–20% of breast cancers and has been suggested to predict resistance to anti-hormonal therapy. As the diagnostic accuracy of predictive biomarkers can be substantially limited by regional expression differences within tumors, heterogeneity of CCND1 amplification was assessed in this study. To assess heterogeneity, a novel tissue microarray based analysis platform was developed. Methods. To comprehensively asses the three-dimensional molecular composition of breast cancers, a “heterogeneity TMA” was constructed containing 8 different tissue cylinders from as many different cancer containing tumor blocks as possible (at least 4) from 147 primary breast cancers. Additional tissue samples were taken from 1–4 corresponding nodal metastases from 35 of these patients. CCND1 amplification was assessed by dual labeling fluorescence in situ hybridization (FISH). Results. The analysis revealed amplification in 28 of 133 (21.05%) patients with informative FISH results. CCND1 amplification was significantly associated with high tumor grade (p=0.042). The preference of ER positive tumors (p=0.061) was not statistically significant. No association was found between CCND1 amplification and tumor type (p=0.307), stage (p=0.540) and PR expression (p=0.871). A discordant Cyclin D1 amplification status was initially detected in 6 out of 28 (21.43%) amplified tumors by TMA analysis. Re-testing on large sections confirmed CCND1 heterogeneity in only 3 of them. Discordant results of the other cases were due to variable interpretation of the TMA cores within the borderline range (CCND1/centromer 11 ratios between 1.7 and 2.3). Overall CCND1 genetic heterogeneity was observed in 3 out of 133 informative tumors (2.3%). No discrepancies were detected between 22 primary tumors and their matched lymph node metastases. Conclusions. The high degree of homogeneity seen for CCND1 amplification suggests that this alteration represents an early event in breast cancer development in a small subset of breast cancers. Thus, CCND1 status determined in a core biopsy is highly representative of the entire tumor and appropriate for predicting treatment outcome if applicable. SO-033 Prognostic relevance of AIB1 (NCoA3) amplification and overexpression in breast cancer E . Burandt1 , G . Jens1 , F . Holst1 , F . Jänicke2 , V . Müller2 , C . Bokemeyer3 , W . Wilczak1 , L . Terracciano 4 , R . Simon1 , G . Sauter1 , A . Lebeau1 1University Medical Center Hamburg-Eppendorf, Department of Pathology, Hamburg, 2University Medical Center Hamburg-Eppendorf, Department of Gynecology, Hamburg, 3University Medical Center Hamburg-Eppendorf, Department of Internal Medicine II, Oncology Center, Hamburg, 4University of Basel, Department of Pathology, Basel, Switzerland Aims. AIB1 is an estrogen receptor co-activator, know to be amplified in a fraction of breast cancers. Aim of this study was to test the potential clinical significance of AIB1 expression levels and its relationship with ER alpha expression, tumor phenotype and prognosis. Methods. To analyze AIB1 expression and amplification immunohistochemistry and Fluorescence in situ hybridization (FISH) was performed on a pre-existing breast cancer tissue microarray (TMA) containing tumor samples of 2197 breast cancer patients. Results. AIB1 expression was found in 60% of our tumors including 29% weak, 7% moderate and 24% strong expressors. AIB1 expression was sig-
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Inhalt Der Pathologe · Supplement
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Inhalt Der Pathologe · Supplement
Page 6 and 7:
Editorial Liebe Kolleginnen und Kol
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Kolorektales Karzinom 2 VO-005 Tran
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Keynote Lecture VO-014 Genetic dete
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(AMACR, FASN, GOLM1, GSP-pi, ERG) t
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to assess the correct rate of R1 re
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DNA damage, and cytotoxic drugs. Au
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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 52 and 53: FR-013 HPV-genotype distribution in
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 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
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within the earliest morphologic det
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Conclusions. In primary imaging a g
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fibrotic neointma development as we
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FR-P-129 Alpha-1-antitrypsin-PiZ-an
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FR-P-136 The expression of central
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cosa and in the periarterial tissue
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FR-P-149 Combination of Castleman d
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or without different concentrations
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Results. In 18 cases (79%) the caus
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FR-P-168 Autopsy findings in a 2-ye
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FR-P-174 MPGN-like glomerulonephrit
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Poster: Gynäkopathologie und Mamma
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SA-P-011 Genetic aberrations of pre
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Mechanismen, die eine Progression d
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internet server. A network of inter
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Methods. HE-gefärbte Schnittpräpa
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Conclusions. The newly released 450
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and desmoplastic reaction are diffe
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one patient revealed more than 9 mi
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situation, the V600E mutation in th
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SA-P-064 Evolution of molecular pat
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nic markers such as myf4 and MyoD1
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Conclusions. To our knowledge, this
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SA-P-085 Expression of the eukaryot
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Results. The papillary RCC type II
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SA-P-098 Male infertility: assessme
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SA-P-104 Process oriented scientifi
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Conclusions. The IBDW offers a uniq
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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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