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Annals of Oncology 1271P ANALYSIS OF PFS AND OS FROM THE SATURN STUDY ACCORDING TO EGFR IHC STATUS USING THE H-SCORE READING METHOD J. Mazières 1 , W. Brugger 2 , F. Cappuzzo 3 , P. Middel 4 , A. Frosch 5 , I. Bara 6 , G. Klingelschmitt 7 , B. Klughammer 8 1 Thoracic Oncology Unit, Larrey Hospital, Toulouse, FRANCE, 2 Haematology/ Oncology, Schwarzwald-Baar Klinikum, University of Freiburg, Villingen-Schwenningen, GERMANY, 3 Oncology, Istituto Toscano Tumori, Livorno, ITALY, 4 Department of Pathology, Targos Advance AG, Kassel, GERMANY, 5 Department of Pathology, Göttingen University Hospital, Gottingen, GERMANY, 6 Global Medical Affairs Oncology, F. Hoffmann-La Roche Ltd, Basel, SWITZERLAND, 7 MDBB Biometrics, F. Hoffmann-La Roche Ltd, Basel, SWITZERLAND, 8 Department of Biomarkers, F. Hoffmann-La Roche Ltd, Basel, SWITZERLAND Background: In the phase III SATURN study, maintenance erlotinib significantly prolonged progression-free survival (PFS) vs placebo in patients (pts) with advanced non-small-cell lung cancer (NSCLC) and non-progressive disease after first-line chemotherapy (Cappuzzo et al, Lancet Oncol 2010). Epidermal growth factor receptor (EGFR) expression analysis by immunohistochemistry (IHC) found no significant difference in PFS (p = 0.63) or overall survival (OS; p = 0.52) with erlotinib by EGFR IHC status (Brugger et al, J Clin Oncol 2011). Recently, Pirker at al. (Lancet Oncol 2012) presented data on EGFR expression as a predictor of OS for first-line chemotherapy plus cetuximab in the phase III FLEX study, using a novel method (H-score) to assign EGFR IHC status. We used this method to reassess samples from the SATURN study. Methods: The H-score method assigns an IHC score to each pt on a continuous scale of 0–300, based on the percentage of cells at different staining intensities (Pirker et al, Lancet Oncol 2012). As per this method, the outcome-based discriminatory threshold IHC H-score for our analysis was set at 200 and existing samples were re-read and classed as low (H-score
MERCK SERONO: Advisor, speaker in symposia, research grant PFIZER: Advisor ROCHE/GENENTECH: Advisor, speaker in symposia. R. Pirker: The author declares the following: Honoraria for Advisory Board and speaker’s fee from AstraZeneca, Boehringer Ingelheim, Merck Serono and Roche. K.J. O’Byrne: The author declares: Payment from Merck Serono in relation to a protocol writing committee and advisory boards and travel costs in related to attendance. Honoraria from Merck Serono associated with presentation of data at satellite/company symposia. K.M. Kerr: Keith Kerr has acted on Advisory Boards and has received speaker’s fees from Merck Serono. He has had similar roles with Astra Zeneca, Roche, Eli Lilly, Daichi Sankyo, Pfizer, Boeringher Ingelheim and Glaxo Smith Klein. S. Störkel: The author has been involved in sponsored research by Merck KGaA. I. Celik: The author is an employee of Merck KGaA. A. von Heydebreck: Teh author is an employee of Merck KGaA and declares stock ownership in this company. F.A. Shepherd: Honorarium from Merck KGaA for presentation at Scientific, Industry-sponsored Satellite Symposium. Provided compensated consultation services to Merck KGaA. 1273P T790M RESISTANT MUTATION IN PLASMA OF ACQUIRED RESISTANT EGFR MUTATED NON SMALL CELL LUNG CANCER (NSCLC) PATIENTS - THE TARZO TRIAL (NCT00503971) N. Reguart 1 , E. Nadal 2 , M.A. Molina 3 , E. Carcereny 4 , C. Queralt 4 , A. Insa Molla 5 , I. Aguirre 6 , M. Taron 7 , D. Isla Casado 8 , R. Rosell 9 1 Medical Oncology, Hospital Clinic Barcelona, BARCELONA, SPAIN, 2 Medical Oncology, Hospital Duran i Reynals (ICO), Barcelona, SPAIN, 3 Laboratoy of Biology Department, Pangaea Biotech, USP Dexeus University Institute, Barcelona, SPAIN, 4 Medical Oncology Service, Hospital Germans Trias i Pujol (ICO), Badalona, SPAIN, 5 Medical Hematology and Oncology, Hospital Clinico Universitario de Valencia, Valencia, SPAIN, 6 Medical Oncology, Hospital Germans Trias i Pujol, Barcelona, SPAIN, 7 Medical Oncology, Hospital Germans Trias i Pujol (ICO), Barcelona, SPAIN, 8 Oncology Service, Hospital Clínico Universitario Lozano Blesa, Zaragoza, SPAIN, 9 Medical Oncology, Hospital Germans Trias i Pujol (ICO)Oncology, Badalona, SPAIN Background: EGFR-mutant NSCLC patients (pts) ultimately overcome resistant to tyrosine kinase inhibitors (TKIs). Among resistant mechanisms secondary EGFR T790M is the most frequent and account 50% of tumors. Previous data suggest that tumors with acquired T790M at post-progression biopsy specimen may have a more favorable prognosis and indolent progression. However, tumor re-biopsies at progression sites are scare in NSCLC patients and blood samples are a non-invasive method that may help to identify resistant mechanisms. Material and methods: Pts with advanced NSCLC harboring EGFR mutations (Exon 19 and 21) and acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) were eligible. All patients where included in a phase II trial (TARZO) and treated with erlotinib 150 mg PO daily plus oral vorinostat 400 mg QD on days 1–7 and 15–21 in a 28-day cycle. Blood samples were required at study entry. We aim to determine the feasibility and incidence of T790M resistant mutation from plasma DNA from patients by mutation from cell free circulating DNA from patients using a 5 0 nuclease PCR assay (TaqMan assay) with a FAM MGB-labeled probe for the wild-type and a VIC MGB-labeled probe for the mutant sequence in the presence of a protein nucleic acid (PNA) clamp, which was designed to inhibit the amplification of the wild-type allele (Pangaea Biotech SL patent). Results: Twenty-five pts were included in the trial. From those, nineteen plasma specimens were obtained and used for DNA extraction. Overall T790M resistant mutation was detected from plasma DNA in 36.8% of the samples (7/19). There were no differences according patient characteristics (gender/ECOG-PS, smoking habits, number of previous treatments) or type of sensitizing mutation in tissue (Exon 19, L858R) and the presence of T790M. Median time to progression (TTP) and survival (OS) for the entire cohort was 2.4 months (IC 95% 1.2-3.6) and 13.2 months (IC 95% 2.23-26.9 months). Median TTP and OS were 2.4 vs 1.8 (p 0.076) and 13.7 vs 3.7 (p 0.095) in patients without and with T790M respectively. Conclusions: T790M mutation is a common feature of resistant acquired EGFR mutated NSCLC patients and can be detected using plasma DNA. Disclosure: All authors have declared no conflicts of interest. 1274P ALK AND EGFR MUTATION ANALYSIS IN A PHASE II TRIAL OF CISPLATIN/PEMETREXED IN JAPANESE PATIENTS WITH ADVANCED NON-SQUAMOUS NON-SMALL CELL LUNG CANCER N. Yanagitani 1 , K. Kaburaki 1 , F. Ohyanagi 1 , K. Kudo 1 , A. Horiike 1 , N. Motoi 2 , K. Takeuchi 2 , Y. Ishikawa 2 , T. Horai 1 , M. Nishio 1 1 Thoracic Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, JAPAN, 2 Pathology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, JAPAN Background: Recently, ethnic differences and genotypes such as EGFR mutation or fusion gene (ALK translocation) are important factors in non-small cell lung cancer (NSCLC) treatment. Pemetrexed (P)/cisplatin (C) is one of the standard treatments Annals of Oncology for advanced non-squamous (Nsq) NSCLC. However, the efficacy of the CP regimen has not been well examined in Japanese Nsq NSCLC patients; furthermore, the difference in efficacy between genotypes was not thoroughly examined. Therefore, the present study was conducted to evaluate the efficacy of the CP regimen in Japanese Nsq NSCLC patients, and to determine whether EGFR mutation and ALK translocation impacted the treatment. Methods: This study was conducted from May 2009 to December 2010. Patients were eligible for this study if they had histologically or cytologically confirmed recurrent or metastatic Nsq NSCLC previously untreated with chemotherapy, an ECOG performance status of 0 or 1, life expectancy of more than 12 weeks, and adequate organ function. Patients received C (75 mg/m2) plus P (500 mg/m2) on day 1 every 3 weeks. Of the 50 patients initially enrolled, 49 were evaluated, and 43 tumor samples were available for analysis. Most patients were male (80%), and 80% of the patients had adenocarcinoma. The primary endpoint was the response rate that was evaluated. according to RECIST. EGFR mutation was examined using PCR-based methods, and the ALK fusion protein was examined using a highly sensitive IHC method in the available tumor specimens. Results: The objective response rate and disease control rate in all patients were 44.9% and 79.6%, respectively. The median progression-free survival was 4.4 months, and the 1-year survival was 73.5%. Toxicities were mild; no new toxicity profile was identified. Among the 43 samples, the following mutations were identified: 9 EGFRm (21%), 5 ALK (12%), and 29 wild-type (67%). Objective response was observed in 6 (66.7%) EGFRm, 2 (40%) ALK (+), and 13 (44.8%) wild-type mutations. Conclusion: Although the CP regimen demonstrates consistent efficacy in Japanese Nsq NSCLC patients, EGFR mutation and ALK translocation may have impacted this treatment. Disclosure: All authors have declared no conflicts of interest. 1275P UPDATED SAFETY AND QUALITY OF LIFE (QOL) RESULTS OF PARAMOUNT STUDY: MAINTENANCE PEMETREXED (PEM) PLUS BEST SUPPORTIVE CARE (BSC) VS PLACEBO (PBO) PLUS BSC IMMEDIATELY FOLLOWING INDUCTION TREATMENT WITH PEM PLUS CISPLATIN (CP) FOR ADVANCED NONSQUAMOUS NON-SMALL CELL LUNG CANCER (NS-NSCLC) J. Pujol 1 , L. Paz-Ares 2 , M. Dediu 3 , M. Thomas 4 , P. Bidoli 5 , J. Corral 2 , N. Chouaki 6 , C.M. Visseren-Grul 7 , A. Zimmermann 8 , C. Gridelli 9 1 Thoracic Oncologic Unit, Montpellier Academic Hospital, Hospital Arnaud de Villeneuve, Montpellier, Montpellier, FRANCE, 2 Medical Oncology, Hospital Universitario Virgen del Rocío, Seville, SPAIN, 3 Medical Oncology, Institute of Oncology Bucharest, Fundeni Clinical Hospital Alexandru Treistoreanu, Bucharest, ROMANIA, 4 Department of Thoracic Oncology, University of Heidelberg, Thoraxklinik Heidelberg, GERMANY, 5 Medical Oncology, Azienda Ospedaliera S. Gerardo U.O. Oncologia Medica, Monza, ITALY, 6 Medical Department, Eli Lilly, Paris, FRANCE, 7 Oncology Europe, Eli Lilly, RA Houten, NETHERLANDS, 8 Oncology, Eli Lilly and Company, Indianapolis, IN, UNITED STATES OF AMERICA, 9 Medical Oncology, UO Oncologia Medica “S.G. Moscati Hospital”, Avellino, ITALY Objectives: The PARAMOUNT trial showed that continuation maintenance therapy with pem after induction therapy with pem plus CP significantly reduced the risk of disease progression (HR = 0.62) and death (HR = 0.78) in patients (pts) with advanced NS-NSCLC. The purpose of this abstract is to present the updated safety and patients’ QoL results from the continuation maintenance treatment of the PARAMOUNT trial. Methods: In this phase III, randomized, double-blind, PBO-controlled study, 939 pts were treated with pem (500 mg/m 2 ) plus CP (75 mg/m 2 ) on day 1 of four 21-day cycles. Patients (n = 539) who had not progressed and had an Eastern Cooperative Oncology Group performance status (PS) of 0/1, were randomized (2:1; stratified for PS, induction response, and disease stage) to maintenance pem (500 mg/m 2 ,day1) plus BSC (n = 359) or PBO plus BSC (n = 180) until disease progression. All pts received vitamin B 12, folic acid, and dexamethasone. All randomized pts were qualified for the maintenance phase safety analyses, which included summaries of the incidence of adverse events by maximum Common Terminology Criteria Adverse Events, version 3, grade. All enrolled patients that had provided baseline and at least 1 subsequent measurement for EuroQol 5-dimensional (EQ-5D) scale were included in the analysis of patient-reported outcomes. Results: Safety and the QoL analyses in the continuation maintenance therapy will be presented. Conclusions: The long-term and low-grade toxicities of continuation maintenance therapy with pem will be discussed. Disclosure: C.M. Visseren-Grul: Employed by and own stock in Eli Lilly and Company. L. Paz-Ares: I have advisory board relationship and honararia to disclose with Eli Lilly and Company, Bayer, Roche, Pfizer. I. M. Dediu: Advisory Board - Eli Lilly and Company. M. Thomas: Advisory Board - Eli Lilly and Company Corporate Sponsored Trial - Eli Lilly and Company. N. Chouaki: Employed by and own stock in Eli Lilly and Company. A. Zimmermann: Employed by and own stock in Eli Lilly and Company. J. Pujol: Advisory Board - Eli Lilly and Company. C. Gridelli: ix418 | 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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Page 411 and 412: N-arm n=34 P-arm n=32 All n=66 Male
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Page 421 and 422: Conclusions: These data from SAiL a
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Page 427 and 428: Network utilization of WBCGF in the
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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 (
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Page 441 and 442: epresented by 19 pts (32%) female,
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Page 445 and 446: Methods: NSCLC patients with radiog
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Page 459 and 460: Material and methods: 50 lung cance
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care unit (PCU) at the National Can
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Characteristic No. % Total 63 1 st
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hysterectomised-9.10% and cervix ca
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abstracts psycho-oncology 1462PD IN
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events, tumour response, and surviv
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abstracts sarcoma 1477O ADHESION TO
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1481PD A PHASE II STUDY OF DOVITINI
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1488P ORGANISATION OF SARCOMA PATIE
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Patients and methods: From August 2
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chemotherapy respectively. At a med
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of this group Those with relapsed d
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1515 PREDICTORS OF SURVIVAL IN ADOL
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abstracts small cell lung cancer an
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emaining receiving either CAV or to
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1533P EXPRESSION OF WILM⍰TUMOUR G
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more than 3 months after first line
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lower recurrence rate of NE. Pegfil
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egimens (HR = 2.5, p < 0.001). Phys
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1561P PREDICTIVE DIAGNOSTICS FOR RE
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Methods: A prospective multicentre
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Table: 1574P Pharmacokinetic parame
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Novartis and unrestricted research
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studies have shown that chemotherap
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(Grade 1) and moderate to severe (G
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declined to relatively lower level
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1609P PHYSICAL ACTIVITY (PA) AND PH
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patients were admitted to the oncol
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Dicarbamin 100 mg/day on day 5 befo
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Results: Anemia was detected in 83.
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important to carry out randomized s
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abstracts translational research 16
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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 and 540:
1678P PREDICTIVE VALUE OF TWO PHENO
Page 541 and 542:
theorized that the PI3K/AKT pathway
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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