Volume 138 • Supplement 1 • February 2012

JOUR NAL OF

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Cancer Research Clinical Oncology 30th German Cancer Congress 22.–25. February 2012 ICC and Messe Berlin

Congress President: Univ.-Prof. Dr. P. Albers

30. Deutscher Krebskongress 22.-25. Februar 2012 Messe und ICC Berlin

Kongresspräsident: Univ.-Prof. Dr. P. Albers

HIJ

Inhaltsverzeichnis

Inhaltsverzeichnis Best of Poster Best of Poster – GI-Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Best of Poster – Hauttumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Best of Poster – Lungentumoren . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 Best of Poster – Lymphome/Leukämien/kindliche Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 Best of Poster – Mammakarzinom/gynäkologische Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . 10 Best of Poster – Molekulare Onkologie. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 Best of Poster – Palliativmedizin/Supportivtherapie. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Best of Poster – Seltene Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Best of Poster – Versorgungsstrukturen/Qualitätssicherung. . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Best of Poster – Urologische Tumoren . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

Discussed Poster Discussed Poster – GI-Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Discussed Poster – Mammakarzinom/gynäkologische Tumoren. . . . . . . . . . . . . . . . . . . . . . . 23 Discussed Poster – Molekulare Onkologie. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 Discussed Poster – Seltene Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Discussed Poster – Supportivtherapie/Palliativmedizin. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Discussed Poster – Versorgungsstrukturen/Qualitätssicherung. . . . . . . . . . . . . . . . . . . . . . . . 33

General Poster GI-Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35 Hauttumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 Lungentumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55 Lymphome/Leukämien/pädiatrische Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57 Mammakarzinom/gynäkologische Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61 Molekulare Onkologie. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .90 Seltene Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106 Supportivmedizin/Palliativtherapie . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119 Urologische Tumoren. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134 Versorgungsstrukturen/Qualitätssicherung. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144

KOK KOK . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151 This supplement was not sponsored by outside commercial interests. It was funded entirely by the publisher.

Autorenverzeichnis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153

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Abstracts J Cancer Res Clin Oncol (2012) [Suppl 1] · 138:2–162 10.1007/s00432-011-1144-4 © Springer-Verlag 2012

30. Deutscher Krebskongress 22.–25. Februar 2012 Messe und ICC Berlin Kongresspräsident Univ.-Prof. Dr. P. Albers

Programmkomitee DKK 2012

Steering Comitee

Adam G (Hamburg), Albers P (Düsseldorf), Bartsch HH (Freiburg), Beckmann MW (Erlangen), Bokemeyer C (Hamburg), Brümmendorf T (Aachen), Bruns J (Berlin), Creutzig U (Hannover), Domagk K (Hamburg), Ehninger G (Dresden), Engers R (Düsseldorf), Enghofer E (Leverkusen), Feyer P (Berlin), Gabbert HE (Düsseldorf), Graeven U (Mönchengladbach), Gschwend J (München), Hallek M (Köln), Hauschild A (Kiel), Hegewisch-Becker (Hamburg), Helbig U (Berlin), Helou A (Bonn), Hofstädter F (Regensburg), Hohenberger W (Erlangen), Hölscher A (Köln), Hübner J (Frankfurt/M), Iro H (Erlangen), Kastenholz H (Bonn), Kerschgens C (Berlin), Kleeberg U (Hamburg), Klingebiel T (Frankfurt), Klinkhammer-Schalke M (Regensburg), Kohlhuber F (Bonn), Kortmann R-D (Leipzig), Kotzerke J (Dresden), Lang H (Mainz), Meier K (Soltau), Nettekoven G (Bonn), Ortmann, O (Regensburg), Paradies K (Hamburg), Propping P (Bonn), Riemann JF (Ludwigshafen), Schadendorf D (Essen), Schirren J (Wiesbaden), Schmidberger H (Mainz), Schmiegel W (Bochum), Schmutzler R (Köln), Singer S (Leipzig), Stummer W (Münster), Thomas M (Heidelberg), Wallwiener D (Tübingen), Weis J (Freiburg), Wesselmann S (Berlin), Wiedenmann B (Berlin), Wiegel T (Ulm), Wiestler O (Heidelberg), Wittekind C (Leipzig), Wolff K-D (München), Wylegalla C (Freiburg), Zeeb H (Bremen)

Albers P (Düsseldorf), Beckmann MW (Erlangen), Bokemeyer C (Hamburg), Brümmendorf T (Aachen), Bruns J (Berlin), Graeven U (Mönchengladbach), Hallek M (Köln), Hauschild A (Kiel), Ortmann, O (Regensburg), Schmiegel W (Bochum), Zeeb H (Bremen)

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Gutachter 2012 Al-Batran S (Frankfurt/M.), Albers P (Düsseldorf), Alberti W (Wuppertal), Bamberg M (Tübingen), Barth J (Gießen), Bartsch H (Freiburg), Beckmann M (Erlangen), Belka C (München), Berdel W (Münster), Berking C (München), Biersack H (Bonn), Bokemeyer C (Hamburg), Bosslet K (Penzberg), Branscheid D (Bielefeld), Britzen-Laurent N (Erlangen), Brossart P (Bonn), Budach W (Düsseldorf), Büttner R (Köln), Dartsch D (Hamburg), Debatin K (Ulm), Dunst J (Lübeck), Ebert M (Mannheim), Einsele H (Würzburg), Emons G (Göttingen), Engenhart-Cabillic R (Marburg), Engers R (Neuss), Engert A (Köln), Fehm T (Tübingen), Feyer P (Berlin), Folprecht G (Dresden), Freidank A (Fulda), Friedel G (Gerlingen), Gabbert H (Düsseldorf), Ganser A (Hannover), Geißler M (Esslingen a.N.), Glimm H (Heidelberg), Graeven U (Mönchengladbach), Gutzmer R (Hannover), Hallek M (Köln), Hartenstein R (München), Hartmann J (Kiel), Heike M (Dortmund), Henne-Bruns D (Ulm), Hense H (Münster), Hertenstein B (Bremen), Hillemanns P (Hannover), Hochhaus A (Jena), Hofheinz R (Mannheim), Hohenberger W

Journal of Cancer Research and Clinical Oncology Suppl 1 · 2011

(Erlangen), Hölscher A (Köln), Howaldt H (Gießen), Hübner J (Frankfurt/M.), Jaehde U (Bonn), Jocham D (Lübeck), Jonat W (Kiel), Jordan K (Halle/S.), Kaaks R (Heidelberg), Keller M (Heidelberg), Kiechle M (München), Kimmig R (Essen), Klug S (Dresden), Knüchel-Clarke R (Aachen), Koch U (Hamburg), Köhne C (Oldenburg), Kortmann R (Leipzig), Kreienberg R (Ulm), Krug B (Köln), Kubicka S (Reutlingen), Lang H (Mainz), Lehnert T (Bremen), Lipp M (Berlin), Loquai C (Mainz), Lordick F (Braunschweig), Lorenzen S (München), Lutz M (Saarbrücken), Mackensen A (Erlangen), Marmé D (Freiburg), Meier K (Soltau), Meyer H (Solingen), Meyer T (Ansbach), Miller K (Berlin), Möhler M (Mainz), Molls M (München), Müller R (Köln), Neuhaus P (Berlin), Niederle N (Leverkusen), Oettle H (Friedrichshafen), Ortmann O (Regensburg), Paradies K (Hamburg), Petersen C (Hamburg), Possinger K (Berlin), Propping P (Bonn), Reinacher-Schick A (Bochum), Riemann J (Ludwigshafen), Rödel C (Frankfurt/M.), Schäfer R (Berlin), Schirren J (Wiesbaden), Schlag P (Berlin), Schlegel U (Bochum), Schmidt E (Bremen), SchmidtWolf I (Bonn), Schmieder K (Mannheim), Schmiegel W (Bochum), Schöning T (Heidelberg), Schuler M (Essen), Schütte W Halle/S., Schwarz M (Tübingen), Seufferlein T Halle/S., Singer S (Leipzig), Stahl M (Essen), Stenzl A (Tübingen), Stuschke M (Essen), Tannapfel A (Bochum), Thomas M (Heidelberg), Trarbach T (Essen), Trefzer U (Berlin), Trepel M (Hamburg), Trümper L (Göttingen), Ukena D (Bremen), Unger C (Freiburg), Vanhoefer U (Hamburg), Wecht D (Marburg), Wiegel T (Ulm), Wirth M (Dresden), Wittekind C (Leipzig), Wylegalla C (Freiburg)

GI-Tumoren

Best of Poster – GI-Tumoren

Best of Poster – GI-Tumoren

B2 – 0174 MiR-30a-5p suppresses tumor growth in colon carcinoma by targeting DTL

B1 – 0077 Protein profiling identifies HDAC2 and TXNL1 as aneuploidy-associated markers in colorectal cancer

*A. Baraniskin1,2, K. Birkenkamp-Demtroder3, A. Maghnouj1, H. Zöllner1, A. Reinacher-Schick2,4, W. Schmiegel2,4, S. Hahn1 1 Ruhr-University, Center of Clinical Research, Bochum, Deutschland, 2 Knappschaftskrankenhaus, Ruhr-University of Bochum, Department of Internal Medicine, Bochum, Deutschland, 3Aarhus University Hospital, Dept. of Molecular Medicine, Aarhus, Dänemark, 4Ruhr-University, Center for Clinical Studies in Oncology, Bochum, Deutschland

*T. Gemoll1,2,3, U. Roblick1,2,3, S. Szymczak4, T. Braunschweig5, S. Becker3, B.-W. Igl4, H.-P. Bruch1, A. Ziegler4, U. Hellman6, M. Difilippantonio7, T. Ried7, H. Jörnvall2, G. Auer3, J. Habermann1,2,3,7 1 University of Lübeck, Department of Surgery, Lübeck, Deutschland, 2 Karolinska Institut, Stockholm, Schweden, 3Karolinska Biomic Center, Stockholm, Schweden, 4University of Lübeck, Institute for Medical Biometry and Statistics, Lübeck, Deutschland, 5University Clinic RWTH Aachen, Institute of Pathology, Aachen, Deutschland, 6Ludwig Institute for Cancer Research, Uppsala, Schweden, 7NCI/NIH, Genetics Department, Bethesda, Deutschland Background. DNA aneuploidy has been identified as prognostic factor for epithelial malignancies. Further understanding of the translation of DNA aneuploidy into protein expression will help to define therapies, prognosis and prevention. We therefore aimed at identifying aneuploidy-associated protein expression. Methods. DNA ploidy assessment by image cytometry identified three diploid and four aneuploid colorectal cancer cell lines. All cell lines were subjected to protein expression profiling by two-dimensional gel electrophoresis. Proteins were identified by mass spectrometry, subjected to Ingenuity Pathway Analysis (IPA), and target proteins were validated by Western Blot. Validated proteins were clinically evaluated by immunohistochemistry using a tissue microarray (TMA). The TMA comprised 47 aneuploid and 31 diploid primary colorectal carcinomas, as well as 19 adjacent normal mucosa specimens. Results. Two independent statistical analyses revealed 64 proteins that were significantly differentially expressed between the diploid and aneuploid cell lines. Of these, 26 proteins could be identified by mass spectrometry and were subjected to IPA. The majority of these proteins interacted in two overlapping high-ranked IPA networks maintaining Cellular Assembly and Organization, Cellular Function and Maintenance, Infection Mechanism, Cell Cycle, and Cellular Growth and Proliferation. Network proteins showed cancer-associated functions of Cellular Assembly and Organization, Cell-To-Cell Signalling, and Cell Death (p10 newly isolated cell lines derived from melanoma brain metastases. Furthermore, immunohistochemical analyses of brain metastases from >10 melanoma patients including matched extracerebral metastases from lung and liver in the same patients for p-ERK, ERK, AKT, p-AKT and PTEN were performed. Results. Growth inhibition was most pronounced with PI3K inhibitors achieving growth inhibition rates of up to 80%. Moreover, PI3K inhibition potently induced apoptosis in cerebral metastatic melanoma cells. Histochemical analysis showed that both cerebral and extracerebral metastases were highly positive for ERK and AKT. p-ERK was seen exclusively at the tumor periphery of both cerebral and extracerebral metastases. Interestingly, most melanoma brain metastases were highly positive for activated AKT, whereas matched extracerebral metastases from lung and liver in the same patients were weakly positive or negative for activated AKT. Moreover, PTEN appeared to be downregulated in brain metastases. Conclusion. Together, these findings suggest that activation of AKT is relevant for the survival and growth of melanoma cells in the brain parenchyma and that inhibition of PI3K-AKT signalling may be a suitable strategy to enhance and/or prolong the antitumor effect of BRAF inhibitors in melanoma brain metastases.

Best of Poster – Hauttumoren B8 – 0489 Validation of a fresh-tissue based prognostic gene signature in formalin-fixed, paraffin-embedded melanomas *G. Brunner1, L. Suter1, H.-J. Schulze2, C. Berking3, A. Heinecke4, J. Atzpodien5 1 Hauttumorzentrum Hornheide-Münster, Tumorforschung, Münster, Deutschland, 2Hauttumorzentrum Hornheide-Münster, Dermatologie, Münster, Deutschland, 3LMU München, Dermatologie und Allergologie, München, Deutschland, 4WWU Münster, Medizinische Informatik und Bioinformatik, Münster, Deutschland, 5Hauttumorzentrum Hornheide-Münster, Onkologie, Münster, Deutschland Melanoma incidence is rapidly increasing – with a doubling rate of 10– 20 years. Precision and reliability of conventional histopathological and clinical staging, however, remain limited in predicting clinical outcome. On the other hand, complementary molecular prognostic markers are not yet available. We have recently identified, for the first time, a prognostic gene signature expressed in fresh-frozen primary melanomas (n=135), which is associated with overall survival (multivariate Cox regression analysis: p=0.0004, hazard ratio 3.83). The clinical value of a signature-based risk score is its ability to identify patients at low risk, not identified by conventional AJCC staging, and to define risk patients in need of adjuvant therapies. The purpose of this study was to establish analysis of the signature genes in formalin-fixed, paraffin-embedded (FFPE) melanoma tissue and to validate prognostic significance.

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Abstracts We developed a sensitive and robust methodology to analyze and normalize gene expression in FFPE tissue samples (some of them more than 20 years old): Total RNA was prepared from FFPE sections matching the above fresh-frozen primary melanomas (131 out of 135), quality-controlled, and transcribed into cDNA. Human reference RNA was included as an internal standard. Following pre-amplification of the cDNA, expression of the nine signature genes (KRT9, KBTBD10, DCD, ECG2/SPINK7, PIP, SCGB1D2, SCGB2A2, COL6A6, HES6) and of four house-keeping genes (18S rRNA, GAPDH, GUSB, BPNT1) was quantified by real-time PCR using TaqMan assays specific for short amplicons. Gene expression data were normalized, in two steps, to correct for interassay technical variability (based on the reference RNA data) as well as for inter-sample variability of RNA quality (based on the data for the house-keeping genes). Significance of correlation of FFPE gene expression data (CT values or estimated mRNA copy numbers) with data from matched fresh-frozen tissue samples (two-sided t-test) or with patient overall survival (univariate Cox regression analysis; clinical follow-up data up to 273 months) was evaluated. The majority of FFPE primary melanomas (125 out of 131) yielded mRNA of sufficient quality. In matched pairs of FFPE and fresh-frozen tissue samples, there was significant correlation of expression of all nine signature genes. Significance of correlation was higher with CT values (r=0.19–0.58; p=0.001–0.05) than with estimated copy numbers. Expression of 7 out of the 9 genes in FFPE melanomas (CT values or estimated copy numbers) was significantly associated with overall survival (p=0.0001–0.07). Thus, our prognostic melanoma gene signature was successfully transferred from fresh-frozen onto FFPE tissue samples. This greatly increases clinical applicability of a gene-signature based prognostic risk score and, in addition, allows the retrospective prognostic analysis of primary melanomas.

Lungentumoren Best of Poster – Lungentumoren B9 – 0198 Hypofractionated image-guided breath-hold radiotherapy of pulmonary tumors and metastases – clinical results A. Frauenfeld1, *J. Boda-Heggemann1, C. Weiss2, U. Attenberger3, K. Siebenlist1, F. Schneider1, F. Wenz1, F. Lohr1 1 University Medical Center Mannheim, University of Heidelberg, Department of Radiation Oncology, Mannheim, Deutschland, 2University Medical Center Mannheim, University of Heidelberg, Abteilung für Medizinische Statistik, Biomathematik und Informationsverarbeitung, Mannheim, Deutschland, 3University Medical Center Mannheim, University of Heidelberg, Institute of Clinical Radiology and Nuclear Medicine, Mannheim, Deutschland Purpose. Stereotactic Ablative RadioTherapy (SABR) of stage I–II tumors has been shown to be a highly effective treatment modality with low toxicity. It is also a non-invasive therapy option for lung metastases. Outcome and toxicity were retrospectively evaluated in a single-institution patient cohort who had undergone hypofractionated image-guided breath-hold lung SBRT. Patients and methods. 50 lesions of 43 patients with NSCLC (n=27, St. I– IV including patients with controlled brain metastases or local relapse) and lung metastases of various primary tumors (n=16) were consecutively treated with image-guided breath-hold SBRT. After an initial dose finding phase, patients were irradiated with a regimen of 5×12 Gy. Dose calculation was performed with collapsed cone algorithm in 60% of the lesions. Breath hold was performed with Active Breathing Control

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(ABC®, Elekta), daily imaging with EPIDs and repeat breath hold cone-beam CT. The data were evaluated retrospectively regarding overall survival (OS), progression-free-survival (PFS), progression pattern and local control (LC). Radiation parameters and follow-up CT images were analysed. Results. BED2 (Biologically Effective Dose) was 87±20  Gy (median 83 Gy). 30 lesions were treated with a BED2 of 90 Gy. Median follow-up was 15 months. Median OS was 20 months, without significant difference in patients with primary lung tumor or metastases. Actuarial 1-year OS-rate was 67%; 2-years OS rate 43%, respectively. 27% of the patients died on non-disease related reason (cardiovascular events or infections). Actuarial 1-year PFS-rate was 42%, 2-years PFS rate 28% without significant difference in patients with primary lung tumor or metastases. Site of progression pattern was predominantly distant (60% distant metastases and 32% mediastinal lymph nodes). Actuarial 1-year LC-rate was 90%, 2-years local control rate 85%. 95% of the lesions treated with a BED2 >90 Gy was controlled locally after one year. Local progression was observed in only 5 cases, mainly in the initial dose finding phase, in one patient with an extremely large PTV and in one patient with an only retrospectively recognised pleural invasion of the irradiated lesion. Clinically apparent pneumonitis (requiring treatment) was present in 23% of the cases. No patient experienced fatal toxicity. Conclusions. Despite the unfavorable patient selection, high local control rates could be achieved. If a reasonably high BED2 can be applied, image-guided breath-hold SBRT is an effective non-invasive treatment modality with a high local control rate and relatively low toxicity in patients with inoperable lung tumors and lung metastases. As disease progression was mainly outside the treated area, systemic therapy has to be improved.

Best of Poster – Lungentumoren B10 – 0290 First screening round results from the German component LUSI of the European trial on the efficacy of multislice CT for the early detection of lung cancer, and the perspective of the European trial in view of the results of the US NLST trial *N. Becker1, E. Motsch1, M.-L. Groß1, C.P. Heussel2, H. Dienemann3, P. Schnabel4, M. Eichinger5, D.-E. Optazaite5, M. Puderbach5, J. Tremper5, S. Delorme5 1 Deutsches Krebsforschungszentrum, Epidemiologie von Krebserkrankungen, Heidelberg, Deutschland, 2Thoraxklinik, Radiologie, Heidelberg, Deutschland, 3Thoraxklinik, Chirurgie, Heidelberg, Deutschland, 4Universität, Medizin/Pathologie, Heidelberg, Deutschland, 5Deutsches Krebsforschungszentrum, Radiologie, Heidelberg, Deutschland After closure of the recruitment period of the German Lung Cancer Screening Intervention Trial (LUSI) in 2011 the study comprises 4052 participants, randomised into 2029 subjects in the multislice-CT (MSCT) screening arm and 2023 into the „usual care“ control arm. The early recall rate for suspicious nodules requiring further examination ranges currently around 27%. Nineteen lung cancers have been detected (detection rate 0.9%). Related to all early recalls, the positive predictive value was about 3%, and related to the immediate recalls about 35%. The subsequent screening rounds started in October of the years 2008 (2nd round) to 2011 (5th and final round) having led so far to the identification of eight, two, two and 0 further lung cancers, respectively. In overall 41 surgical interventions, 15 were benign and 26 malignant. Among the lung cancers detected in the screening arm 22 were adenocarcinoma, 5 squamous cell carcinoma, two a small-cell carcinoma and two a carcinoid. One interval cancer has so far been observed (an adenocarcinoma).

The study contributes to the European multicenter study comprising studies from the Netherlands and Belgium (NELSON, 15422 participants), Denmark (4104 participants), Italy (DANTE, 2472; ITALUNG, 3206; MILD, 3997) and Germany (LUSI, 4052). The scope is to demonstrate an at least 25% reduction of lung cancer mortality by MSCT. However, in 2011, the National Lung Screening Trial (NLST) conducted in the USA, provided after an average follow-up of 6 years a significantly reduced lung cancer mortality by MSCT screening in comparison to chest X-ray in the control group. Nevertheless, the European studies decided to continue their trials and to conduct a first common evaluation in 2012 for several reasons, e.g.: (a) an early visible benefit can disappear after prolonged follow-up due to postponement of cause-specific death in the screening group, (b) harmful side effects, especially overdiagnosis, cannot be properly assessed in comparison to a control group with another screening modality (chest X-ray), (c) efficient screening modalities are still undefined such as, risk-related selection of the appropriate target population, appropriate management of suspicious nodules, screening intervals etc, as to be outlined in the presentation.

Best of Poster – Lungentumoren B11 – 0436 The role of sleeve resections in advanced nodal disease of NSCLC *J. Schirren1, M. Eberlein2, A. Fischer3, S. Bölükbas1 1 Dr. Horst Schmidt Klinik, Thoraxchirurgie, Wiesbaden, Deutschland, 2 Carver College of Medicine, Division of Pulmonary, Critical Care and Occupational Medicine, Iowa City, USA, 3Dr. Horst Schmidt Klinik, Anästhesie und Intensivmedizin, Wiesbaden, Deutschland Objective. The aim of this study was to contrast the short-term and longterm results of sleeve resections in centrally located non-small cell lung cancer (NSCLC) depending on limited nodal disease (N0/N1, LND) and advanced nodal disease (N2/N3, AND). Methods. All NSCLC-patients undergoing sleeve resections for centrally located NSCLC were reviewed from our prospective database between January 1999 and December 2008. Patients’ characteristics, morbidity, mortality, locoregional recurrence, distant recurrence and survival were analyzed corresponding to LND and AND. Results. One-hundred seventy sleeve resections out of 213 consecutive sleeve resections were performed for ventrally located NSCLC (LND: n=120; AND: n=50). There were no statistically differences between the both groups for age (LND: 61.8±12.4 vs. 60.8±9.6 years), gender, co-morbidities, type of sleeve resection (bronchial vs. bronchovascular), number of dissected lymph nodes (LND: 40.0±12.4 vs. 36.7±14.0), histology and completeness of resection (LND: 96.7% vs. 98.0%), respectively. More patients had induction chemotherapy in AND group (p=0.049). Similar short-term results were monitored with regard to morbidity rate (LND: 34.2%, AND: 44.0%), secondary pneumonectomy (LND: 1.7%, AND: 4.0%) and mortality rate (LND: 5.0%, AND: 6.0%), respectively. Better 5-year-survival rate and mean survival were observed in LND (LND: 80.8 months; AND: 37.7 months; p=0.014; LND: 67%; AND: 42%). In the long-term, more distant metastases were identified in AND group (26.0% vs. 14.2%, p=0.079) in comparison of identical locoregional recurrence (LND: 1.7%; AND: 0%). Mean time to the development of distant metastases was similar (LND: 19.1 months; AND: 12.4 months; p=0.2) in event of metastazing. Conclusions. Lymph node involvement is a negative prognostic factor with regard to long-term survival. Sleeve resections in AND are not associated with higher morbidity and mortality. Sleeve resections in AND are correlated with promising long-term survival and unexpected high local control of the disease as a result of high complete resection rates. Further investigation for the systemic control of the disease is warranted because of high rates of distant failure.

Best of Poster – Lungentumoren B12 – 0475 Prognostic value of estrogen (ESR-1) receptor expression in curatively resected non-small cell lung cancer (NSCLC) *W. Brückl1, J. Ficker1, A. Hartmann2, R. Wirtz2 1 Klinikum Nürnberg, Medizinische Klinik 3, Nürnberg, Deutschland, 2Universität Erlangen, Institut für Pathologie, Erlangen, Deutschland Background. Despite undergoing complete resection of NSCLC, 33% and 77% of patients with stage IA and IIIA, respectively, die within 5 years. The benefit of adjuvant chemotherapy (aCTx) is only modest, whereas such treatment is associated with adverse effects and predictive factors are of utmost importance. We recently could show a better outcome in estrogen (ESR-1) receptor expressing tumors in the palliative treatment of metastatic NSCLC (Brueckl et al., Proc ASCO 2011). The main objective of this study was to test, whether ESR-1 expression is of prognostic/ predictive value in the curative setting as well. Methods. Affymetrix microarray data from N=138 non-metastatic NSCLC patients undergoing curative resection were retrieved from a data base (Lee et al., Clin Cancer Res 2008) and used as a test set to hypothesize that ESR-1 expression in the tumor is of prognostic value in curatively resected NSCLC. Baseline data according to ERS-1 status were compared with the use of chi-square tests and in a multivariate logistic model including all variables with p values