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Annals of Oncology between M2 macrophage density and patients outcome (P= 0.724) was found. In multivariate analysis M1/M2 was a positive independent predictor of survival (P= 0.001; HR 0.420, CI95%: 0.22-0.78) whereas grading, histotype and TNM stage were not statistically significant. Conclusion: The M1 macrophage density and in particular M1/M2 ratio, as confirmed in multivariate analysis, is an independent factor that can predict patients survival time in gastric cancer after radical surgery. The role of macrophage phenotype in influencing the gastric cancer prognosis warrant further investigation. Disclosure: All authors have declared no conflicts of interest. 1682P ANTHRACYCLINE-INDUCED CARDIOTOXICITY IN MICE IS PREVENTED BY LATE INA INHIBITION WITH RANOLAZINE, WITH IMPROVEMENT IN HEART FUNCTION, FIBROSIS AND APOPTOSIS N. Maurea 1 , C. Coppola 1 , C. Quintavalle 2 ,D.Rea 3 , A. Barbieri 3 , G. Piscopo 4 , R.V. Iaffaioli 4 , G. Condorelli 2 , C. Arra 3 , C.G. Tocchetti 1 1 Cardiology, National Cancer Institute, Pascale Foundation, Naples, ITALY, 2 Biology and Cellular and Molecular Pathology, Federico II University, Naples, ITALY, 3 Animal Experimental Research, National Cancer Institute, Pascale Foundation, Naples, ITALY, 4 Colorectal Oncology, National Cancer Institute, Pascale Foundation, Naples, ITALY Background: Doxorubicin (DOX) produces a well-known cardiomyopathy through multiple mechanisms, which include, among many, Ca2+ overload due to reduced SERCA2a activity and inappropriate opening of the RyR2, and impaired myocardial energetics. DOX generates Reactive Oxygen and Nitrogen Species (ROS and RNS), posing the heart at increased demand for oxygen, setting the stage for metabolic ischemia that also activates late INa, target of ranolazine (RAN). Here, we aim at assessing whether RAN, diminishing intracellular Ca2+ through inhibition of late I Na, and enhancing myocardial glucose utilization (and/or reverting impairment of glucose utilization caused by chemotherapy) prevents DOX cardiotoxicity. Methods: We measured left ventricular (LV) function with fractional shortening (FS) by echocardiography in C57BL6 mice, 2-4 mo old, pretreated with RAN (370mg/kg/ day, a dose comparable to the one used in humans) per os for 3 days. RAN was then administered for additional 7 days, alone and together with DOX (2.17mg/kg/day ip), according to our well established protocol. Hearts were then excised, mRNA expression was analyzed by qRT- PCR, interstitial fibrosis with picrosirius red staining. By Western blotting, we measured the activation of the apoptotic pathway. Results: After 7 days with DOX, FS decreased to 50 ± 2%, p = .002 vs 60 ± 1% (sham). RAN alone did not change FS (59 ± 2%). Interestingly, in mice treated with RAN + DOX, the reduction in FS was milder: 57 ± 1%, p = 0.01 vs DOX alone. DOX-cardiotoxicity was accompanied by significant elevations in ANP (1000 folds), BNP (500 folds), CTGF (26 folds) and MMP2 (81 folds) mRNAs, while co-treatment with RAN significantly lowered these same genes compared to DOX. The alterations in extracellular matrix remodeling were confirmed by an increase of interstitial collagen with DOX (3.66%), p = .004 vs 2.19% (sham), which was normal in hearts co-treated with RAN (2.02%, p = .0002 vs DOX). Finally, the levels of PARP and pro-Caspase 3 were significantly decreased in DOX (indicating activation of apoptosis) but not in RAN + DOX. Conclusions: In mice, RAN prevents DOX cardiotoxic effects. We plan to test RAN as a cardioprotective agent with other antineoplastic cardiotoxic drugs in mice, and to better characterize the cardioprotective mechanisms of RAN in these settings. Disclosure: All authors have declared no conflicts of interest. 1683P CATUMAXOMAB VERSUS CATUMAXOMAB PLUS PREDNISOLONE IN PATIENTS WITH MALIGNANT ASCITES DUE TO EPITHELIAL CANCER: RESULTS FROM THE CASIMAS STUDY J. Sehouli 1 , P. Wimberger 2 , I.B. Vergote 3 , P. Rosenberg 4 , A. Schneeweiss 5 , C. Bokemeyer 6 , C. Salat 7 , G. Scambia 8 , D. Berton-Rigaud 9 , F. Lordick 10 1 Department of Gynecology, Charite Medical University, Berlin, GERMANY, 2 University of Duisburg-essen, AGO and Department of Gynecology and Obstetrics, Essen, GERMANY, 3 Obstetrics & Gynaecology, University Hospital Gasthuisberg, Leuven, BELGIUM, 4 Onkologiska Kliniken Universitetssjukhuset, University Hospital Linköping, Linköping, SWEDEN, 5 Heidelberg, National Center for Tumor Diseases, Heidelberg, GERMANY, 6 Head of The Department for Oncology, Haematology and Bone Marrow Transplantation, UKE II. Medizinische Klinik und PoliklinikMedizinische Klinik II., Hamburg-Eppendorf, GERMANY, 7 Munich, Hematology Oncology Clinic, Munich, GERMANY, 8 Department of Gynecologic Oncology, Catholic University, Rome, ITALY, 9 Oncology, Centre René Gaducheau, Nantes, FRANCE, 10 Medizinische Klinik III, Staedtisches Klinikum Braunschweig, Braunschweig, GERMANY Purpose: This phase III b study compared catumaxomab with prednisolone (CP) to catumaxomab without prednisolone (C) as 3-hour intraperitoneal (i.p.) infusion in patients with malignant ascites from epithelial cancers. Patients and methods: We randomised 219 patients to receive catumaxomab plus 25 mg prednisolone as premedication (111 pts) or catumaxomab alone (108 pts). Primary endpoint of the study was the composite safety score (CSS) summarizing the worst CTCAE grades for the main TEAEs (pyrexia, nausea, vomiting, and abdominal pain). A potential impact of prednisolone on efficacy was assessed by the co-primary endpoint puncture-free survival (PuFS). Further parameters included overall survival (OS) and time to next therapeutic puncture (TTPu). Results: The primary objective, to demonstrate superiority for safety of the CP arm was not met as the mean CSS was comparable for the two groups (CP: 4.1; C: 3.8 for; p= 0.383). The median PuFS was slightly lower in CP (30 days) compared to C (37 days). However the hazard ratio (HR) for PuFS (HR: 1.130, p = 0.402) as well as the 75% quartiles (CP: 155 days, C: 92 days) were in favour of CP compared to C. The median TTPu was similar in both groups (CP: 78 days; C: 102 days, p= 0.599). The majority of patients (123 pts) had no therapeutic paracentesis prior to death (CP: 54.8%; C; 61.7%, p = 0.297). Median OS was longer for CP (CP: 124 days; C: 86 days, p= 0.186), but lacking statistical significance. Conclusions: The administration of 25mg prednisolone as premedication prior to catumaxomab infusion did not change the safety profile and did not negatively impact the efficacy of catumaxomab. The efficacy results of the CASIMAS study are in concordance with the data of the pivotal study and thus confirm the robustness of the treatment effect of catumaxomab in malignant ascites. The composite safety score after 3-hour infusion time was comparable to that seen in the pivotal study using 6 hours. Disclosure: J. Sehouli: consultant for Fresenius Biotech GmbH. P. Wimberger: consultant for Fresenius Biotech GmbH. I.B. Vergote: consultant for Fresenius Biotech GmbH. P. Rosenberg: financial support for clinical studies from Fresenius Biotech GmbH. A. Schneeweiss: financial support for clinical studies from Fresenius Biotech GmbH. C. Bokemeyer: consultant for Fresenius Biotech GmbH. C. Salat: financial support for clinical studies from Fresenius Biotech GmbH. G. Scambia: financial support for clinical studies from Fresenius Biotech GmbH. D. Berton-Rigaud: financial support for clinical studies from Fresenius Biotech GmbH. F. Lordick: consultant for Fresenius Biotech GmbH 1684P CHARACTERISATION OF A NOVEL ROLE OF MST2 IN CANCER CELL MIGRATION IN THE CONTEXT OF HEAD AND NECK CANCER C. Escriu, F. Watt Medical Oncology, Li Ka Shing Centre, Cancer Research UK, Cambridge Research Institute Addenbrooke’s Hospital, Cambridge, UNITED KINGDOM MST2 has so far been considered a tumour suppressor, however, its expression correlates with poor prognosis in several cancer types. We aimed to understand the unknown mechanism by which these tumours appear more aggressive in the context of head and neck cancers, where MST2 is highly expressed. We tested the role of MST2 in cell migration in automated boyden chambers and scratch wound assays in several early passage oral squamous cell cancer cell lines. Interestingly, cancer cell migration was significantly reduced in knock down cells using short hairpin and short interfering RNA knock down systems. Furthermore, overexpression of wild type MST2 promoted cell migration, whereas overexpression of kinase dead MST2 had a dominant negative effect. In 3D confocal microscopy quantification of inverted matrigel invasion assays MST2 knock down also showed reduced invasion. Trying to characterise this effect further we quantified cell attachment using confocal microscopy and image analysis in different laminin substrate concentrations. MST2 knock down cells showed a reduced cell number attachement and impaired cell spreading ability. Further image analysis of migrating cells revealed, in keeping with the attachment defect, that MST2 knock down cells had larger focal adhesions with lower proportional surface of paxillin phosphorylation than control cells. MST2 knock down cells also required a longer time for actin cytoskeleton recovery after cytochalasin D treatment, suggesting a role in actin polymerisation that could explain the cell-spreading defect. Furthermore, using automated boyden chamber assays, Akt inhibition reduced cell migration over time in a directly proportional manner to cell MST2 expression levels. We are currently testing the effect of MST2 modulation in time to metastasis and survival using a tongue injection xenograft model. We describe here a novel role for MST2 in cell migration, explained by focal adhesion architecture and activity change, and by modulating actin polymerisation. Akt inhibirors can reverse this migration effect, which may lead to MST2 potentially becoming a predictor marker of response to biological therapies in head and neck cancers. Disclosure: All authors have declared no conflicts of interest. 1685P PROSTATE CANCER STEM CELLS DISPLAY LOWERED ACTIVITY OF THE MTOR PATHWAY AND RESISTANCE AGAINST MTOR INHIBITION CAUSED BY ELEVATED HYPOXIC SIGNALING M. Marhold 1 , E. Tomasich 1 , A. Haschemi 2 , G. Hofbauer 3 , A. Spittler 3 , M. Krainer 1 , P. Horak 1 1 Department of Internal Medicine I, Medical University of Vienna, Vienna, AUSTRIA, 2 Department of Laboratory Medicine, Medical University of Vienna, Vienna, AUSTRIA, 3 ASCTR Core Facility Flow Cytometry, Medical University of Vienna, Vienna, AUSTRIA Tumor-initiating subpopulations of cancer cells, also known as cancer stem cells (CSCs), were recently identified and characterized in Prostate cancer (PCa). We Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds417 | ix539
theorized that the PI3K/AKT pathway and mTOR, one of its main effectors, play a role in CSC maintenance. Moreover, hypoxia was known to be involved in CSC maintenance and to have a regulating effect on mTOR signaling. In our study, we therefore evaluated the effects of mTOR inhibitors on proliferation, assessed the activity of the mTOR pathway and measured the mitochondrial activity as well as levels of radical oxygen species (ROS) of human as well as murine CSCs in vitro. Further, we examined basal levels of mediators of hypoxic signaling such as HIF1α and its effectors.We isolated CSC like cells from the human PCa cell line DU145 and the murine PCa cell line TRAMPC1 using FACS according to their expression of the stem cell markers CD44, CD49f and Sca-1. We used sphere formation assays to confirm stem and progenitor cell properties. Next, we treated the CSC and non-CSC cell populations with mTOR inhibitors under normoxic and hypoxic conditions in order to determine their cell viability at time points up to 72h. Mitochondrial activity was measured using extracellular flux (XF) analysis and levels of ROS were obtained using ROS-specific fluorescent dyes and flow cytometry. Our results suggest that CSC like PCa cells are more resistant to mTOR inhibitors when compared to their non-CSC counterparts. Most interestingly, while the non-CSC population displays higher sensitivity to mTOR inhibitors under hypoxic conditions, the viability of CSCs remains unaffected. Immunoblotting uncovers generally lower mTOR activity in CSCs compared to non-CSCs. Hypoxia leads to a decrease in mTOR activity in both subpopulations, though this effect is stronger in CSC like subpopulations through higher HIF1α-mediated negative feedback in both cell lines studied. At the same time we do not observe alterations in signaling through AR or PI3K downstream effectors besides mTOR, such as AKT. We propose that prostate CSCs might be resistant against mTOR inhibition and that inhibitors targeting multiple kinases along the PI3K/AKT/mTOR axis would be more effective. Our findings could be helpful to assess the impact of mTOR targeted therapy in prostate cancer in light of ongoing clinical trials. Disclosure: All authors have declared no conflicts of interest. 1686P SRC INHIBITION AS A METHOD TO OVERCOME TEMOZOLOMIDE RESISTANCE IN MELANOMA E.J. Jordan 1 , A. Eustace 2 , D.M. Collins 2 , N. O Donovan 2 , J.P. Crown 3 1 Medical Oncology, Mater University Hospital, Dublin, IRELAND, 2 Dublin City University, N.I.C.B, Dublin, IRELAND, 3 Medical Oncology, St Vincents University Hospital, Dublin, IRELAND Background: Malignant melanoma is resistant to chemotherapeutic agents. Src signalling plays a role in many malignancies including melanoma. Src is important in cell adhesion regulation, invasiveness and activating other downstream cellular pathways. Src activity is elevated in melanoma and has potential to provide a treatment target for melanoma. Temozolomide is an oral alkylating prodrug. Dasatinib is a dual Src/Abl kinase inhibitor with antiproliferative activity. AZD0530 is a selective oral Src kinase inhibitor. Methods: We examined the anti-proliferative effects of dasatinib and AZD0530 alone and in combination with temozolomide (TMZ) in melanoma cell lines - MALME, HT144 parent and temozolomide resistant cell lines MALME-TMZ and HT144-TMZ. MALME-TMZ and HT144-TMZ were produced by the pulse method. IC50 and combination proliferation assays were performed using an acid phosphatase-based colourimetric assay. Results: IC50 (50% inhibitory concentrations ± SD) values for TMZ were 338 ±25 µM in HTI44 and 490 ±19 µM in HT144-TMZ. IC50 values for TMZ were 306 ±29 µM in MALME and 515 ±45 µM in MALME-TMZ. Dasatinib was more effective as a single agent in HT144-TMZ (71 ± 8% growth inhibition at 1 µM) and Annals of Oncology MALME-TMZ (60 ± 6% growth inhibition at 1 µM) as compared to MALME (14 ± 10% inhibition at 1 µM) and HTI44 (0 ± 3% inhibition at 1 µM). The combination of dasatinib/TMZ was more effective than TMZ alone in HT144 and HT144-TMZ. AZD0530 increased proliferation in HT144 (25 ± 8% at 1 µM) and HT144-TMZ (35 ± 9% at 1 µM) as a single agent. AZD0530 caused growth inhibition as a single agent in MALME-TMZ (18 ± 6% inhibition at 1 µM) and MALME (4 ± 2% at 1 µM). The combination of AZD0530 and TMZ had no effect in HT144 or HT144-TMZ while AZD0530 combined with TMZ was more effective than TMZ alone in MALME and MALME-TMZ. Conclusion: Dasatinib improved response to TMZ in both the chemotherapy naive and resistant cell line models tested (HT144, HT144-TMZ, MALME, MALME-TMZ). AZD0530 improved response to TMZ in one of the models only– MALME and MALME-TMZ. These in vitro results support further preclinical evaluation of Src Kinase inhibitors in combination with TMZ, and other DNA-targeting agents, particularly in TMZ-refractory melanoma. Disclosure: All authors have declared no conflicts of interest. 1687 VEGF AND VEGF RECEPTORS IN THYMIC EPITHELIAL TUMORS (TET): PATHOLOGICAL FEATURES AND CLINICAL IMPLICATIONS L. Nappi 1 , V. Damiano 1 , M. Marino 2 , T. Gelardi 1 , L. Formisano 1 , P. Federico 1 , E. Matano 1 , L. Puglia 1 , S. De Placido 1 , G. Palmieri 1 1 Medical Oncology, University Federico II, Naples, ITALY, 2 Department of Pathology, National Cancer Institute “Regina Elena”, Rome, ITALY Background: Thymic Epithelial Tumors (TET) are very rare cancers. They derives from Thymic gland and are associated with different clinical syndromes, such as miastenic and Good syndrome and other immunological and paraneoplastic disorders. The principal treatment of these patients is chemotherapy with schedule containing cisplatin characterized by high response rates (60%). Unfortunately some patients do not respond at all and most patients do not achieve long-lasting remission. For these patients have not other therapeutic chances at the moment. There are few data of the efficacy of anti-angiogenetic drugs in TET but new knowledges are emerging on the potential use of this class of drugs in patients with TET on the basis of laboratory and preclinical translational findings. Materials and methods: we investigated the expression of Vascular Endothelial Growth Factor (VEGF) and its receptors (VEGFR1, 2 and 3) in 200 TET arranged in Tissue Micro Array (TMA). We observed both histotype distribution and modulation of angiogenetic factors (both VEGFRs and VEGFs) in TET. Results: we observed that, when compared with the low-grade counterpart, high grade TET (B2, B3 and Carcinomas) contained significantly higher numbers of VEGFA, VEGFC, VEGFD, VEGFR1 and VEGFR2 expressing tumor cells. In addition, in high grade TET, strong positive correlations between staining for VEGFA and those for all other markers were found. In the same tumors, VEGFC staining was not associated with VEGFR1, VEGFR3 and PDGFRB staining and no correlation was obtained between VEGFD and VEGFR1 or VEGFR3 staining. The co-expression in epithelial cells of growth factors and their receptors suggests the presence of autocrine mechanisms in TET. Conclusions: according to our data VEGFs and VEGFRs in TET are potential targets of anti-angiogenesis drugs. Further studies are needed to investigate the potential role of anti-angiogenetic agents. Disclosure: All authors have declared no conflicts of interest. ix540 | Abstracts Volume 23 | Supplement 9 | September 2012
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Annals of Oncology www.annonc.oxfor
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subscriptions A subscription to Ann
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Annals of Oncology Official Journal
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The European Society for Medical On
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Audit Committee Chair: Fortunato Ci
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Familial cancer Judith Balmaña, Ba
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ESMO 2012 Congress Travel Grants 47
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Exhibitors The following companies
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ESMO Fellowships, 1989-2011 The Eur
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Ondrej Gojis, Czech Republic 2008-2
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abstracts hpv biology and implicati
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abstracts the characterization of l
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abstracts description of intra-tumo
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prevent cell death. It is anticipat
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22IN TARGETING THE HOST IN TNBC G.
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abstracts a paradigm shift in early
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abstracts how can medical oncologis
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feasibility), but by how high the c
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abstracts re-inventing the medical
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abstracts emerging diagnostic and t
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abstracts biologically based treatm
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abstracts molecular targets in mali
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abstracts melanoma therapy: from fr
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diagnosis and can also be used for
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analysis at 11 months median follow
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mouse model of Kras mutant NSCLC. I
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abstracts subtyping soft tissue sar
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abstracts key topics in supportive
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ESMO-CSCO Joint Symposium: Building
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ESMO-EANM-ESR Joint Symposium: Imag
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ESMO-ESTRO Joint Symposium: Innovat
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ESMO-MASCC Joint Symposium: Integra
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ESO Society Symposium: Celebrating
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Results: TIMP-1 expression was incr
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will benefit from this targeted the
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cytomegalovirus (CMV). Analysis of
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functional consequences of Endoglin
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elationship between the ROR score,
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183P EPIDERMAL GROWTH FACTOR RECEPT
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Plasma adiponectin level on the pre
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Table: 198P PFS OS Median, mo HR Me
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204P EVALUATION OF PTEN AND PIK3CA
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Material and methods: We searched P
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Results: The median concentration o
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Table: 226P Methods: Pts were rando
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However, additional analysis sugges
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number of biomarkers have been trie
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Table: 248O 249PD PROTEOMIC PREDICT
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Conclusions: BW and serum Ctrough o
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261P BREAST CANCER SUBTYPES AND OUT
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90 mg/m2-cyclophophamide 600 mg/m2
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to 9 weeks after dosing. Trastuzuma
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Patients and methods: We reviewed d
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sector patients. The aim of this st
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Linear Logistic Model with Relaxed
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Results: The median CTC fold change
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312: Table: Chemotherapy uptake wit
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abstracts breast cancer, locally ad
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Results: 8 trials (2092 pts) with 1
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absolute difference of median value
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Novartis, Genentech, and sanofi-ave
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Results: Three RCTs with 1023 patie
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collected from all patients for det
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355P FIRST REPORT OF LONG-TERM RESP
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361P A RETROSPECTIVE ANALYSIS OF PL
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publications and aggregated in a me
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Thus the primary aim to target BCSC
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383 WHY DO WOMEN WITH BREAST CANCER
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Results: We evaluated 76 pts with M
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more than 6 cycles of capecitabine.
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406TiP PHASE II TRIAL OF PRIMARY SY
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abstracts CNS tumors 410O CONDITION
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Conclusions: Our data suggested tha
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Conclusions: As in other cancer typ
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432 GAMMA KNIFE RADIOSURGERY AS A M
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abstracts developmental therapeutic
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1PR), but no responses were seen in
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RO and Cd, as well as PD data for c
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and vulvar Ca), and 11 SDs were obs
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knowing HLA-A status double-blindly
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Acquired-resistance to EGFR inhibit
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474P PHASE 1 STUDY OF THE SELECTIVE
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TST is active in breast and gastric
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Treatment-induced shedding of circu
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Methods: Either co-cultures of peri
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501 PRECLINICAL DATA INVESTIGATING
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509TiP LUX-LUNG 8: A RANDOMIZED, OP
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(P = 0.64). Synchronous BBC was sig
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abstracts gastrointestinal tumors,
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Disclosure: M. Lee: I am an employe
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plus intravenous Bev(7.5mg/kg q 21d
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anti-EGFR treatment. The present st
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patients harboring a T/T genotype t
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551P ADJUVANT CHEMOTHERAPY (AC) USE
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experienced significantly more ≥
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functioning scales. Exploratory ana
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oxaliplatin (100 mg/m 2 )/raltitrex
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572P PANERB STUDY: WHICH CATEGORY O
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Results: 92/114 patients were preop
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585P CHANGES IN THE INTESTINAL ENVI
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592P PHASE II TRIAL OF COMBINED CHE
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minutes. In a previous study, 30-mi
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Patients and methods: Chemotherapy-
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612P ARE PATIENTS WITH RESECTABLE R
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Conclusions: AMPK and ACC activatio
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of surgical monotherapy in patients
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Table: 632 633 AFLIBERCEPT/FOLFIRI
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factors play the determining role i
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Abstract withdrawn in exceptional c
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were respectively 10.6 vs 8.5 vs 3.
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Results: 20 gastrointestinal cancer
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abstracts gastrointestinal tumors,
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Day 8. A second identical course wa
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proven in stage I GC. The aim of th
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Conclusions: Longer OS to FOLFOX wa
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692P PRELIMINARY SAFETY DATA FROM A
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subgroup. Taking into consideration
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Results: Three years of adjuvant im
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considered sufficient to give an 80
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721P FIRST-LINE TREATMENT WITH FOLF
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after Gem-based therapy. The additi
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735P RADIOGRAPHIC PARAMETERS IN PRE
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validate the revised AJCC 7th stagi
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Results: Among 862 MM we identified
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Results: Frequently reported advers
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gastric cancer patients with CNS me
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discriminate the prognosis of HCC p
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prospective, non-interventional stu
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abstracts genitourinary tumors, non
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787O EXTERNAL VALIDATION OF THE ASS
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patient preference for P over S, an
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798PD OPEN-LABEL PHASE II TRIAL OF
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Hb, PS and LM. Median PFS for patie
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may have led to reduced dose and sh
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Results: 1,622 patients were identi
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RCC) was designed to address an unm
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Patients and methods: This is a sin
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treatment at week 4, and week 12 by
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effective in second or further line
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Conclusions: In pts with RCC treate
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using Drug inCode ® pharmacogeneti
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Table: 857P standard, but is not av
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efused HDCT. Of 23 patients, 20 com
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we identified 49 and 220 patients w
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879 TREATMENT OF PATIENTS WITH META
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Median overall survival (OS) was 26
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abstracts Genitourinary tumors, pro
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and week 13 BPI-SF Q3 scores), 28%
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Working Group (PCWG)-2 guidelines r
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atio HR 0.39; CI 0.18, 0.83, p = 0.
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We observed tumor responses and pro
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Here we report emerging data from t
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928P LHRH AGONIST-INDUCED SUPPRESSI
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Disclosure: S. Oudard: Has acted as
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939P NEOADJUVANT SIPULEUCEL-T IN LO
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945 BONE TURNOVER MARKERS AND POTEN
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952 SEQUENTIAL ANDROGEN DEPRIVATION
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managed in a multidisciplinary (MD)
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or hypercalcemia at screening; prio
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meeting. The prevalence of LGSC is
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Table: 975PD Continued AMG 386 + pa
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physicians in the U.S. and Europe.
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989P PHASE II STUDY OF COMBINATION
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elated with stage, nodal involvemen
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1004P CASE CONTROL STUDY ON TWO DIF
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eight patients who had infertility
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abstracts head and neck cancer 1016
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same CT/RT; Arm B2: 3 cycles of ind
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induction chemotherapy in the treat
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patients. We have developed a rando
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evaluated by the screening instrume
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morbidities that radiation would le
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Conclusions: Through adequate selec
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abstracts hematological malignancie
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anthracyclines in vitro. A favorabl
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1076P RITUXIMAB PLUS SUBCUTANEOUS C
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than the standard target of ≥2.5
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Patients: From November 2002 to May
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lymphadenopathy and multiple cutane
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prospective non-interventional stud
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Funding: GSK Biologicals Disclosure
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survival rates of 13-25% (Prieto et
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high response rates and prolonged p
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GlaxoSmithKline, Merck Sharp & Dohm
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advisor for Merck Sharp & Dohme, an
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or cutaneous melanoma. A survival u
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systemic therapy or were intolerant
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abstracts neuroendocrine tumors and
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morbidity, with G3 tumors behaving
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pts. Poorly differentiated endocrin
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Adenocarcinoma was present in 25 pa
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Method: Endobronchial ultrasound gu
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widely used by single agent or plat
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disease after surgery were treated
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stage IIIA NSCLC, EML4-ALK fusion-p
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1200P CONCOMITANT CHEMORADIATION GI
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Patients and methods: The study was
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months (95% CI:13-25). The PFS and
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maintenance therapy had favourable
Page 401 and 402:
abstracts non-small cell lung cance
Page 403 and 404:
Ingelheim, GSK Biologicals (compens
Page 405 and 406:
1234PD RANDOMIZED PHASE III TRIAL O
Page 407 and 408:
GlaxoSmithKline (myself, compensate
Page 409 and 410:
1243P IDENTIFICATION OF MICRORNA (M
Page 411 and 412:
N-arm n=34 P-arm n=32 All n=66 Male
Page 413 and 414:
1255P POPULATION BASED EVALUATION O
Page 415 and 416:
1262P DISTINCT SPREAD OF EGFR MUTAT
Page 417 and 418:
1268P VISUAL DISTURBANCES IN PATIEN
Page 419 and 420:
MERCK SERONO: Advisor, speaker in s
Page 421 and 422:
Conclusions: These data from SAiL a
Page 423 and 424:
NSCLC diagnosis and time of BM diag
Page 425 and 426:
1291P PHASE I/II DOSE-FINDING STUDY
Page 427 and 428:
Network utilization of WBCGF in the
Page 429 and 430:
1303P COST EFFECTIVENESS OF PEMETRE
Page 431 and 432:
Results: The patients’ characteri
Page 433 and 434:
EGFR mut at exons 18, 19, 21, and K
Page 435 and 436:
Methods: EML4-ALK fusion was screen
Page 437 and 438:
Results: The median survival time (
Page 439 and 440:
enefit from sustained EGFR blockade
Page 441 and 442:
epresented by 19 pts (32%) female,
Page 443 and 444:
and at least one prior course of ch
Page 445 and 446:
Methods: NSCLC patients with radiog
Page 447 and 448:
1367TiP LONG-TERM ERLOTINIB THERAPY
Page 449 and 450:
Austria, Czech Republic, Finland, G
Page 451 and 452:
were every 6 weeks (wk) (S1), every
Page 453 and 454:
Advantage enrollees (83% vs. 25%) [
Page 455 and 456:
Results: Based on 10,000 simulation
Page 457 and 458:
cancer tumors 12%, Germ cell tumor
Page 459 and 460:
Material and methods: 50 lung cance
Page 461 and 462:
1414TiP IMPLEMENTATION OF CANCER RE
Page 463 and 464:
abstracts palliative care 1422O EFF
Page 465 and 466:
Method and results: A total of 317
Page 467 and 468:
1436P SURVEY ON MODELS OF INTEGRATI
Page 469 and 470:
care unit (PCU) at the National Can
Page 471 and 472:
Characteristic No. % Total 63 1 st
Page 473 and 474:
hysterectomised-9.10% and cervix ca
Page 475 and 476:
abstracts psycho-oncology 1462PD IN
Page 477 and 478:
events, tumour response, and surviv
Page 479 and 480:
abstracts sarcoma 1477O ADHESION TO
Page 481 and 482:
1481PD A PHASE II STUDY OF DOVITINI
Page 483 and 484:
1488P ORGANISATION OF SARCOMA PATIE
Page 485 and 486:
Patients and methods: From August 2
Page 487 and 488:
chemotherapy respectively. At a med
Page 489 and 490: of this group Those with relapsed d
Page 491 and 492: 1515 PREDICTORS OF SURVIVAL IN ADOL
Page 493 and 494: abstracts small cell lung cancer an
Page 495 and 496: emaining receiving either CAV or to
Page 497 and 498: 1533P EXPRESSION OF WILM⍰TUMOUR G
Page 499 and 500: more than 3 months after first line
Page 501 and 502: lower recurrence rate of NE. Pegfil
Page 503 and 504: egimens (HR = 2.5, p < 0.001). Phys
Page 505 and 506: 1561P PREDICTIVE DIAGNOSTICS FOR RE
Page 507 and 508: Methods: A prospective multicentre
Page 509 and 510: Table: 1574P Pharmacokinetic parame
Page 511 and 512: Novartis and unrestricted research
Page 513 and 514: studies have shown that chemotherap
Page 515 and 516: (Grade 1) and moderate to severe (G
Page 517 and 518: declined to relatively lower level
Page 519 and 520: 1609P PHYSICAL ACTIVITY (PA) AND PH
Page 521 and 522: patients were admitted to the oncol
Page 523 and 524: Dicarbamin 100 mg/day on day 5 befo
Page 525 and 526: Results: Anemia was detected in 83.
Page 527 and 528: important to carry out randomized s
Page 529 and 530: abstracts translational research 16
Page 531 and 532: expression. Then, we analyzed PB sa
Page 533 and 534: Table: 1657P TH BV + TH HR (95% CI)
Page 535 and 536: BRAF mutations. Circulating free DN
Page 537 and 538: 1671P PHASE I CLINICAL TRIAL OF CAN
Page 539: 1678P PREDICTIVE VALUE OF TWO PHENO
Page 543 and 544: Material and methods: 101 patients
Page 545 and 546: overexpressing and 232 had triple n
Page 547 and 548: author index author index A Aamdal
Page 549 and 550: author index Badran A. ix288 (874)
Page 551 and 552: author index Bösmüller H. ix209 (
Page 553 and 554: author index Chen A. ix319 (966O) C
Page 555 and 556: author index De Droogh E. ix452 (13
Page 557 and 558: author index Esposito G. ix209 (618
Page 559 and 560: author index Geiges G. ix306 (930P)
Page 561 and 562: author index Hartono S. ix70 (155P)
Page 563 and 564: author index Iwasaki H. ix542 (1694
Page 565 and 566: author index Kodaira M. ix90 (228P)
Page 567 and 568: author index Lichtensztejn D. ix350
Page 569 and 570: author index Martinez A. ix496 (153
Page 571 and 572: author index Morishita N. ix432 (13
Page 573 and 574: author index Okamoto N. ix432 (1320
Page 575 and 576: author index Piau S. ix456 (1401P)
Page 577 and 578: author index Rodríguez Rodríguez
Page 579 and 580: author index Scoggins C.R. ix371 (1
Page 581 and 582: author index Stern L. ix272 (823P)
Page 583 and 584: author index Trypaki M. ix429 (1308
Page 585 and 586: author index Whitmore J.B. ix310 (9
Page 587 and 588: subject index subject index A AAV-H
Page 589 and 590: subject index ix115 (316TiP), ix116
Page 591 and 592:
subject index diffuse large B-cell
Page 593 and 594:
subject index (1033P), ix340 (1036P
Page 595 and 596:
subject index medical information,
Page 597 and 598:
subject index (612P), ix214 (633),
Page 599 and 600:
subject index RCC, ix274 (830P) re-
Page 601 and 602:
subject index TR-FRET, ix84 (206P)
Page 603 and 604:
drug index drug index 1248P, 1250P,
Page 605 and 606:
translational research index transl
Page 607 and 608:
Page 609:
show all

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