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

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Poster: Gynäkopathologie und Mammapathologie I SA-P-005 HER2 status in breast cancer remains stable with FISH (fluorescence in situ hybridisation) but is highly variable with IHC (immunohistochemistry) methodology in view of 10 years experience Z . Varga 1 , C . Ramach 2 , B . Padberg 3 , H . Moch 1 , A . Noske 1 1 University Hospital Zurich, Institute of Surgical Pathology, Zürich, Switzerland, 2 County Hospital St . Gallen, Institute of Pathology, St . Gallen, Switzerland, 3 Institute of Pathology, County Hospital Graubünden, Chur, Switzerland Aims. Gold standard methodology in HER2 status determination in breast cancer is still a debated issue. Advantage of IHC analysis over timeconsuming and experience-requiring FISH methodology can be strongly influenced by pre-analytical differences and interpretational-issues. Methods. We analysed 6000 consecutive HER2-FISH tests in breast cancer in 10 years (2001 to 2011) and compared stability of amplification-rate with immunohistochemical 3+ positivity. Four years long (2001–2004) FISH tests were performed in all 3+ and 2+ cases and in some of the 1+ and negative (0) cases. For 6 years (2005–2010) HER2 status was determined with “only FISH” testing. For one year (2011) all cases were tested with both IHC and FISH. Results. Between 2001 and 2004, 61% of 3+ IHC was amplified with FISH (amplification-rate varied from 50%, 67%, 53% and 77%). In 2011, 86% of 3+ IHC cases were amplified with FISH. FISH amplification rate varied between 15–17% in 2005–2008 and 11–13% in 2009–2011 (due to modified ASCO criteria of HER2/CEP17 ratio from
Abstracts SA-P-008 Correlation of anti-PHH3 positive mitoses to pathological response in neoadjuvantly treated breast cancer S . Timme 1 , M . Becker 2 , E . Stickeler 2 , P . Bronsert 1 , L . Reischuck 2 , L . Bogatyreva 3 , D . Hauschke 3 , A . zur Hausen 4 , M . Werner 1 1 Institute of Pathology, University Medical Center, Freiburg, 2 Department of Obstetrics and Gynecology, University Medical Center Freiburg, Freiburg, 3 Institute of Medical Biometry and Medical Informatics, University Medical Center, Freiburg, 4 Department of Pathology, GROW, School for Oncology and Developmental Biology, Maastricht University Medical Center, Maastricht, Netherlands Aims. We evaluated breast cancer (BC) core biopsies taken before neoadjuvant chemotherapy (NACT) by immunohistochemistry using anti-PhosphohistoneH3 antibody (PHH3) to determine the mitotic count. The data were correlated to clinicopathological parameters including intrinsic subtypes as well as the histopathological regression of resected tumour specimens after NACT with Epirubicin/Cyclophosphamide (EC) and Taxotere. Methods. 72 patients with either triple negative (21/72) or luminal type (51/72) BC obtained NACT with EC and Taxotere. Thereafter, tumour regression was analyzed in resection specimens using a semiquantitative score from 0 (no effect) to 4 (no cancer cells) according to Sinn et al. (1994). Pathological complete response (pCR) was defined as no residual invasive carcinoma (score 3+4). In 16/72 cases (22.2%) pCR occurred; 9/16 (56.25%) were TNBC and 7/16 were luminal type BC (ER and/or PrR+/ HER2−). In the pre-treatment biopsies immunohistochemical stainings with PHH3 were performed and mitotic figures were evaluated in 10 high power fields (HPF). The number of mitoses detected by PHH3 was correlated to different clinicopathological parameters determined before treatment (intrinsic subtype, WHO-type, grading, tumour size and nodal stage) and to regressive changes/pCR after therapy by univariate statistical analyzes (using SPSS v 18). Results. The number of PHH3-detected mitoses correlated significantly with the tumour grading (p=0.001), but there was no correlation with WHO-type, tumour size or nodal stage. PHH3/10 HPF differs significantly between the two intrinsic subtypes (p=0.003). PHH3 expression alone was no predictor for pCR (p=0.399). But tumours with 11 or more mitoses/10 HPF achieved significantly more often pCR than those with under 11 mitoses/10 HPF (p=0.031). Furthermore, luminal type BC with 11 or more mitoses/10 HPF and also TNBC had significantly more frequent pCR than luminal type BC with under 11 mitoses/10 HPF (p=0.016). Conclusions. Strong proliferating BC (11 or more mitoses/10 HPF) have significantly more pCR compared to low proliferating tumours (under 11 mitoses/10 HPF) after NACT with EC and Taxotere. Furthermore, mitoses detected by PHH3 are a discriminator for luminal type BC to predict pCR, because luminal type BC under 11 mitoses/10 HPF rarely reach pCR. Thus, the determination of mitoses by PHH3 may be recommended especially for luminal type BC before NACT with EC and Taxotere. SA-P-009 Transitions between flat epithelial atypia and low-grade ductal carcinoma in situ of the breast S . Aulmann1 , F . Mietzsch1 , R . Penzel1 , P . Schirmacher1 , H .P . Sinn1 1University of Heidelberg, Institute of Pathology, Heidelberg Aims. Flat epithelial atypia (FEA) of the breast typically is a localised alteration involving only few, neighbouring terminal ducto-lobular units (TDLUs). However, occasionally there are cases with extensive FEA and morphological evidence of direct transitions between FEA and classical ductal carcinoma in situ (DCIS). Methods. To investigate the relationship of FEA and DCIS in these cases, we microdissected multiple foci of the respective lesions in a series 142 | Der Pathologe · Supplement 1 · 2012 of 10 cases and performed comparative allelotyping using a panel of 14 LOH markers. In addition, phylogenetic tree models were calculated on the basis of mitochondrial DNA sequencing to visualise the clonal relationship of the different lesions. Results. FEA and lg-DCIS shared the majority of chromosomal imbalances, loss of diverging alleles was not detected in any of the 10 cases. mtDNA sequencing and phylogenetic tree clustering revealed direct transitions between FEA and lg-DCIS in all 10 cases. However, in three patients, additional foci of FEA were present which were not directly related to the rest of the FEA and the lg-DCIS. Conclusions. In conclusion, our data demonstrate the presence of direct transitions between FEA and lg-DCIS and support the interpretation of foci of FEA as part of the lg-DCIS in those unusual cases in which multiple areas of FEA are interspersed with areas of classical lg-DCIS and direct transitions of both lesions are apparent. SA-P-010 Different cytoplasmic and nuclear PARP expression patterns in hereditary and non-hereditary breast cancer M .-L . Klauke1 , N . Hoogerbrugge1 , J . Budczies2 , P . Bult1 , J .H .J . van Krieken1 , C . Denkert2 , B .M . Müller2 1Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands, 2Charité Hospital, Institute of Pathology, Berlin Aims. High cytoplasmic poly (adenosine diphosphate-ribose) polymerase (PARP) expression in non-hereditary breast cancer correlates with an aggressive tumor pattern and a poor long-term prognosis. Our study was designed to compare cytoplasmic and nuclear PARP expression between hereditary and non-hereditary breast cancer. Methods. Tissue micro arrays containing 39 familiar and 39 non-hereditary formalin-fixed, paraffin embedded breast cancer tumor samples were immunohistochemically analyzed for cytoplasmic (cPARP) and nuclear (nPARP) PARP expression. Stained slides were digitized and evaluated using the VM Slide Explorer. The intensity and percentage of positive tumor cells were used to calculate an immunoreactive score (IRS), which was divided into three subgroups defined as low (IRS 0–2), intermediate (IRS 3–4) and high (IRS 6–12) expression. The mean age at diagnosis in patients with familiar breast cancer was about 45±11 years and in patients with non-hereditary breast cancer about 65±12.1 years. Results. cPARP and nPARP expression patterns were significantly different in hereditary and non-hereditary breast cancer. cPARP expression in hereditary breast cancer was low in 33.3%, intermediate in 25.6% and high in 41.0% of cases. In contrast, cPARP in non-hereditary breast cancer was low in 59.0%, intermediate in 25.6% and high in 15.4% of cases. Statistical analysis showed that cPARP expression was significantly higher in hereditary compared to non-hereditary breast cancer (p=0.008, χ2-test for trends). Hereditary breast cancer showed a significant lower intermediate nPARP expression (23.1%) than non-hereditary breast cancer (59.0%; p=0.005, χ2-test). Conclusions. PARP expression in hereditary and non-hereditary breast cancer differs significantly, which might be related to the higher frequency of BRCA1 or 2 mutations in hereditary breast cancer and is compatible with a role of PARP-1 in DNA repair and genomic stability. Because patients with hereditary breast cancer have a poor long-term prognosis and show very often an aggressive tumor pattern the overall higher cPARP expression found in this subgroup suggests that high cPARP expression might be correlated with an aggressive tumor pattern and a poor longterm prognosis.
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Inhalt Der Pathologe · Supplement
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Inhalt Der Pathologe · Supplement
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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
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well as MET activation were examine
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or BRAF mutation, c-MYC and SIRT1 e
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AG Pneumopathologie III DO-032 Remo
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immature granulopoiesis showed a st
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ned, if well-defined mantle zones,
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phomas). Most prominent gains or am
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DO-062 Tumor-associated macrophages
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DO-080 DOG1: an immunohistochemical
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AG Oralpathologie DO-087 Detection
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DO-094 Do activated fibroblasts inf
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DO-101 Histopathological analysis o
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DO-108 Identification of potential
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Conclusions. In conclusion, 454 par
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subgroup of patients with B-Raf mut
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DO-002b Impact of terminologies in
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Methods. We performed MCPyV-FISH of
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FR-013 HPV-genotype distribution in
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Methods. Three different techniques
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(i.e. investment in equipment and e
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FR-032 COLD-PCR: a powerful tool in
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dissection (MBLND) technique to imp
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SO-005 Prevalence of mutations in s
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SO-011 Methylation profiling and in
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more effective than SAHA alone and
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SO-022 Specialized pathology review
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SO-027 Ki-67 in mitotic score group
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nificantly associated with advanced
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liver did not correlate with the mu
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AG Paidopathologie II SO-046 Overex
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Results. Histomorphology of the ova
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p42 and p27 have not yet been inves
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SO-068 Recent advances in understan
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SO-075 A novel, dual role of CCN3 i
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Pancreatic Adenocarcinoma SG-137 Se
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sease and 30 colon cancer serum sam
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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 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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