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Annals of Oncology 95% CI and curves were compared with log-rank test. The study had the ethical approval. Results: 1905 pts were screened and 252 pts (13%) were treated with 3 TTs. The median age was 60 yrs (range 52–68), 73% were male, 96% underwent nephrectomy and 38% were metastatic at diagnosis. At 1 st line, the Motzer class was good, intermediate, and poor in 48%, 47% and 5% of pts, respectively. PFS for type and line of therapy are reported in the table below. The TTSF was 36.4 (30.5–42.2) vs. 30.6 (26.5–34.6) mos (p = 0.11), and the OS was 52.1 (41.6–62.6) vs. 36.3 (31.2–41.4) mos (p = 0.01), for TKIàTKIàm-TOR and and TKIàm-TORàTKI, respectively. TTSF for SU-SO-EV was 36.5 vs. 30.4 mos for SU-EV-SO (p = 0.011). When stratified by ECOG-PS before 3 rd line or baseline MSKCC, TS maintained its independent prognostic role (p = 0.002 and p = 0.004, respectively). Conclusions: Only few patients received 3 lines of TTs. The sequence sunitinib-sorafenib-everolimus was associated with a better TTSF and OS as compared to the sequence sunitinib-everolimus-sorafenib. Therapy 1 st line 2 nd line 3 rd line % PFS % PFS % PFS Sunitinib 60 10.1 31 11.2 8 14.1 Sorafenib 25 13.1 35 7.7 28 5.2 Pazopanib 2 6.4 0 / 0 / Bevac. + IFN 11 11.3 0 / 1 4.3 Everolimus 0 / 30 4.7 55 6.9 Temsirolimus 2 5.1 3 5.6 5 2.6 Other 0 / 0 / 3 3.2 TOTAL 100 11.6 100 6.8 100 6.2 Disclosure: All authors have declared no conflicts of interest. 819P IMPLEMENTATION OF TARGETED THERAPY IN DENMARK FOR PATIENTS WITH METASTATIC RENAL CELL CARCINOMA: RESULTS FROM THE DANISH RENAL CANCER GROUP (DARENCA) STUDY-2 A.V. Soerensen 1 , F. Donskov 2 , G.G. Hermann 3 , N.V. Jensen 4 , H. Spliid 5 , E.Q. Bergan 6 , K. Fode 2 , P.F. Geertsen 1 1 Department of Oncology, University Hospital of Copenhagen Herlev, Herlev, DENMARK, 2 Department of Oncology, Aarhus University Hospital, Aarhus, DENMARK, 3 Department of Urology, University Hospital of Copenhagen Rigshospitalet, Copenhagen, DENMARK, 4 Department of Oncology, Odense University Hospital, Odense, DENMARK, 5 Section for Statistics, Informatics and Mathematical Modelling, Technical University of Denmark, Kongens Lyngby, DENMARK, 6 Denmark, Pfizer, Ballerup, DENMARK Background: Treatment options for metastatic renal cell carcinoma (mRCC) have expanded since the introduction of targeted therapies. The impact of these new treatment options on overall survival in a complete national cohort of patients is unclear. Objective: To analyze Overall Survival (OS), Progression Free Survival (PFS) and Time to Treatment Failure (TTF) in a complete national cohort of patients. Design, setting and participants: All Danish patients with mRCC starting first line treatment with immunotherapy, TKIs or mTOR-inhibitors between 2006 and 2010 were included. Baseline and outcome data were collected retrospectively. Untreated patients referred for treatment were also assessed. Outcome measurements and statistical analysis: OS, PFS and TTF was calculated using the Kaplan-Meier method. Differences between OS and treatment year were assessed using the log rank test. Differences in distributions were tested with the Chi-square test. Results and limitations: Between 2006 and 2010, a total of 1073 patients were referred. Of these, 759 patients received first line treatment and 314 received no systemic treatment. The proportion of treated patients increased from 64% in 2006 to 75% in 2010 (p = 0.02). In 2006 22% received targeted therapy and this increased to 75% in 2010 (p < 0.00001). In 2006 21% of first line patients received second line treatment compared to 41% in 2010 (p = 0.01). From 2006 to 2010 we observed an improved median OS from 11.5 to 15.7 months (p = 0.03), improved median PFS from 4.1 to 5.5 months (p = 0.001) and an improved median TTF from 3.1 to 4.9 months (p = 0.006) for first line treatment. The untreated population of 314 patients had a median OS of 3.1 months from date of metastatic disease with no significant change from 2006 to 2010. Conclusions: In a complete national cohort of patients, implementation of targeted therapy has resulted in improved treatment options and outcome for patients with mRCC. Disclosure: A.V. Soerensen: has received a research grant/funding from Pfizer. F. Donskov: has received a research grant from Novartis. E.Q. Bergan: Employee of Pfizer Denmark Aps. All other authors have declared no conflicts of interest. 820P SUNITINIB GLOBAL EXPANDED-ACCESS TRIAL IN METASTATIC RENAL CELL CARCINOMA (MRCC) – FINAL RESULTS M.E. Gore 1 , C. Porta 2 , S. Bracarda 3 , G.A. Bjarnason 4 , S. Oudard 5 , S. Lee 6 , L. Crino 7 , T.M. Kim 8 , K. Fly 9 , C. Szczylik 10 1 Department of Medicine, Royal Marsden Hospital NHS Foundation Trust, London, UNITED KINGDOM, 2 Medical Oncology, IRCCS San Matteo University Hospital Foundation, Pavia, ITALY, 3 Ospedale San Donato, Medical Oncology Arezzo, Arezzo, ITALY, 4 Division of Medical Oncology, Sunnybrook Odette Cancer Centre, Toronto, ON, CANADA, 5 Medical Oncology, Georges Pompidou Hospital and Rene Descartes University, Paris, FRANCE, 6 Oncology, Seoul National University Hospital, Seoul, KOREA, 7 Medical Oncology, S. Maria della Misericordia Hospital, Perugia, ITALY, 8 Medical Oncology, Seoul National University Hospital, Seoul, KOREA, 9 Oncology, Pfizer Inc., Groton, CT, UNITED STATES OF AMERICA, 10 Oncology, Military Medical Institute, Warsaw, POLAND Background: Sunitinib had a manageable safety profile and encouraging efficacy in a global expanded-access mRCC study (ClinicalTrials.gov, NCT00130897; Pfizer) initiated prior to regulatory approval, in patients (pts) ineligible for other trials (Gore et al, 2009). Here we report final results. Methods: Pts aged ≥18 yrs with treatment-naïve or previously treated mRCC received oral sunitinib on the approved 50 mg/day 4-wk-on/2-wk-off schedule. Safety was assessed regularly and tumor measurements were done as per local standard practice using RECIST-defined response. Analyses included all pts who received ≥1 dose of sunitinib. Results: 4,577 pts were enrolled. From July 2005 to November 2011, 4,543 pts received treatment, including poor prognosis pts with brain metastases (7%), Eastern Cooperative Oncology Group performance status (ECOG PS) ≥2 (14%), non-clear cell RCC (12%) and age ≥65 yrs (33%). Median treatment duration was 7.5 mths and median follow-up was 13.6 mths. 4,298 pts (95%) discontinued; reasons included lack of efficacy (37%), death (20%) and adverse events (AEs; 15%). The most common treatment-related AEs of any grade were diarrhea (47%), fatigue (40%), nausea (36%), decreased appetite (31%), mucosal inflammation (29%), stomatitis and vomiting (both 28%), hand–foot syndrome (HFS; 27%), dysgeusia (25%), hypertension (24%), thrombocytopenia (23%) and asthenia (22%). The most common treatment-related grade 3/4 AEs were fatigue (9%), thrombocytopenia (8%), HFS and asthenia (both 7%), hypertension and neutropenia (both 6%) and diarrhea (5%). In 4,219 evaluable pts, the objective response rate (ORR) was 16% (n = 660) with subgroup ORR as follows: baseline brain metastases (30/324 [9%]), ECOG PS ≥2 (32/587 [5%]), non-clear cell RCC (42/505 [8%]), and age ≥65 yrs (195/1,386 [14%]). Overall median progression-free survival was 9.4 mths (95% CI: 8.8, 10.0) and overall survival was 18.7 mths (95% CI: 17.5, 19.5). Conclusions: Results from this global expanded-access mRCC trial confirm the safety and efficacy of sunitinib in >4,500 pts with wide-ranging disease states in a real-world setting. The sunitinib AE profile in this broad population was manageable and consistent with prior trial results. Disclosure: M.E. Gore: Advisory relationships with Roche, Pfizer, Bristol Myers, Novartis, GSK, Aveo\\Astellas, Bayer. Honoraria to disclose from Roche, Pfizer, Bristol Myers, Novartis.C. Porta: Advisory relationship Pfizer Bayer-Schering Hoffman La Roche GSK Novartis Astellas Boehringer Recordati. Honoraria: Pfizer Bayer-Schering Hoffman La Roche GSK Novartis Astellas Boehringer Recordati Research funding Bayer-Schering Novartis. S. Bracarda: Advisory relationship with Novartis Bayer Schering Pfizer GSK Aveo/Astellas Boheringer-Ingelheim. Honoraria to disclose from Novartis and Pfizer. G.A. Bjarnason: Advisory relationship with Pfizer. Honoraria to disclose from Pfizer. Research funding to disclose from Pfizer.. S. Oudard: Advisory relationships: Pfizer, Bayer-Schering, Hoffman La Roche, Glaxo SmithKline, Novartis Pharma, Sanofi Aventis Honoraria: Pfizer, Bayer-Schering, Hoffman La Roche, Glaxo SmithKline, Novartis Pharma, Sanofi Aventis. S. Lee: Advisory relationships with Pfizer, Novartis, Bayer. Honoraria to disclose from Pfizer, Novartis, Bayer. K. Fly: Employed by Pfizer Inc. as an Oncology Clinician. Hold Pfizer stock as does an immediate family member. C. Szczylik: Advisory relationship with Pfizer, GSK, Bayer. Honoraria from Pfizer, GSK, Bayer. All other authors have declared no conflicts of interest. 821P EVEROLIMUS IN PATIENTS WITH METASTATIC RENAL CELL CARCINOMA WHO PROGRESS AFTER INITIAL VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-TYROSINE KINASE INHIBITOR (VEGFR-TKI) THERAPY: UK RESULTS FROM THE REACT TRIAL ON BEHALF OF THE UK REACT INVESTIGATORS S. Chowdhury 1 , J. Larkin 2 1 Department of Medical Oncology, Guy’s and St. Thomas’ Hospital NHS Trust, London, UNITED KINGDOM, 2 Department of Medicine, Royal Marsden Hospital, London, UNITED KINGDOM Background: The phase III RECORD-1 trial demonstrated clinical benefit of everolimus in patients with metastatic renal cell carcinoma (mRCC) who had failed initial VEGFr-TKI therapy. REACT (RAD001 Expanded Access Clinical Trial in Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds399 | ix271
RCC) was designed to address an unmet medical need by providing everolimus to patients with mRCC prior to regulatory approval. UK results from the REACT trial are reported here. Methods: REACT was an open-label, international, expanded-access program. Eligible patients had measurable or nonmeasurable mRCC of any histology, and had progressed on, or were intolerant of, VEGFr-TKI therapy. Patients received a once-daily oral 10 mg dose of everolimus. The primary objective of REACT was to evaluate long-term safety of everolimus. Tumour response was also assessed according to RECIST. Results: A total of 120 patients were enrolled in the UK, 9% of worldwide enrolment. Prior sunitinib was received by 76% of patients; only 5.8% of patients received more than one VEGFr-TKI. Everolimus was received for a median duration of 21.8 weeks (range, 2.0–59.0), numerically longer than reported overall for REACT (14.0 weeks; range, 0.1–83.7). Safety findings and tumour responses were consistent with those observed in the global patient population. The most commonly reported grade 3/4 AEs were anaemia (20.8%), hyperglycaemia (10%), and lower respiratory tract infection (7.5%). Stomatitis and pneumonitis occurred in 13.3% and 10% of patients, respectively (all grades); grade 3 events were reported in 6.7% and 3.3% of patients (no grade 4 events). Investigator-assessed best overall responses were stable disease in 67 (55.8%) patients and a partial response in 1 patient (0.8%), comparable with the overall population. No complete responses were documented in this trial. Conclusions: The REACT trial provided everolimus in advance of regulatory approval and commercial availability to mRCC patients in the UK who failed initial VEGFr-TKI therapy. Everolimus was well tolerated, and safety findings were consistent with those reported for global REACT. Disclosure: S. Chowdhury: Consultant or Advisory: Novartis, Pfizer, GSK, Sanofi-Aventis, Janssen-Cilag, Dendreon. All other authors have declared no conflicts of interest. 822P A PHASE I DOSE ESCALATION STUDY INVESTIGATING DOVITINIB AND EVEROLMUS IN COMBINATION IN METASTATIC CLEAR CELL RENAL CANCER PATIENTS WHO HAVE PREVIOUSLY FAILED VEGF TARGETED THERAPY T.B. Powles 1 , R.J. Jones 2 , S. Crabb 3 , S. Sarker 1 , E. Boleti 4 , J. Shamash 1 , N. Sarwar 1 , S. Chowdhury 5 1 QMUL, Barts Cancer Insititute, London, UNITED KINGDOM, 2 Medical Oncology, Beatson West of Scotland Cancer Centre Gartnavel General Hospital, Glasgow, UNITED KINGDOM, 3 Oncology, Southampton University, London, UNITED KINGDOM, 4 Oncology, Royal Free Hospital, London, UNITED KINGDOM, 5 Oncology, Guys and St Thomas Hospital, London, UNITED KINGDOM Introduction: Both dovitinib and everolimus are agents used, or under investigation in patients with renal cancer refractory to VEGF targeted therapy. It is potentially attractive to use these agents in combination in patients with VEGF TKI refractory disease. Together they target mTOR, VEGF and FGF-2. The purpose of this study is to establish a dose for this combination to take forward in randomised trials. Method: This phase I study (EUDRACT 2010-021250-19) followed a classic dose escalation 3 + 3 designed. Sequential patients with metastatic clear cell renal cancer, who had previously failed VEGF tyrosine kinase inhibitors were included. Patients received fixed doses of drug in each escalating cohort (maximum n = 6) until dose limiting toxicity (DLT) was reached. DLT included grade 3 toxicity during the first 6 weeks of therapy. If 2 episodes of grade 3 or more toxicity occurred in a specific cohort the DLT cohort had been reached. The study has appropriate ethical approval. Assement of response and progression free survival was by RECIST v1.1 Results: Patients were entered into 2 cohorts before DLT occurred (cohort 0: dovitinib 200 mg/everolimus 5mg [n = 6]; cohort 1: dovitinib 300 mg/everolimus 5mg [n = 3]) . DLT in cohort 1 included grade 3 fatigue (2/3) after 2 and 3 week of therapy. In cohort 0 the following toxicity was identified: Lethargy grade 2 3/6 and 3 1/6; Diarrhoea Grade 2 2/6 and 3 0/6 mucositis; grade 2 0/6 and 3 0/6; nausea/ vomiting grade 2 0/6 and 3 1/6, pulmonary fibrosis grade 2 1/6 3 0/6 . Grade 3 toxicity after the first 6 weeks of therapy included pulmonary fibrosis 1/6, lipid abnormalities 2/6. Overall 1 patient (11%) had a partial response to therapy. Of the 5 patients who did not stop therapy during the first 6 weeks due to toxicity, 3 continued for 6 months or more without progression. Conclusion: The maximum tolerable dose for this combination was dovitinib 200mg and everolimus 5mg. This dose is being taken forward in an expansion cohort which will explore efficacy. Disclosure: T.B. Powles: Novarits Has supplied an educational grant for this project. Advisroy role for Novratis. S. Chowdhury: Advisory role. All other authors have declared no conflicts of interest. Annals of Oncology 823P SURVIVAL AMONG ADVANCED RENAL CELL CARCINOMA (ARCC) PATIENTS WITH >2 PRIOR TARGETED THERAPIES E. Calvo 1 , R. Casciano 2 , L. Stern 2 , T. Brechenmacher 3 , S. Stergiopoulos 3 , J. Coombs 4 1 Start Madrid, Early Clinical Drug Development Unit, Hospital Madrid Norte San Chinarro Centro Integral Oncologico Clara Campal, Madrid, SPAIN, 2 Global Outcomes Research and Pricing, Analytica LA-SER, New York, NY, UNITED STATES OF AMERICA, 3 Oncology, Novartis Pharmaceuticals, East Hanover, NJ, UNITED STATES OF AMERICA, 4 Global Health Economics and Market Access, Novartis Oncology, East Hanover, NJ, UNITED STATES OF AMERICA Background: Despite the emergence of VEGFR-TKIs and mTORs in aRCC, considerable unmet medical needs remain. There are no published guidelines for 3rd line treatment in aRCC and, despite significant advances, these patients have limited treatment options. This analysis examines the overall survival of patients after discontinuation from a phase III, randomized, double-blind, placebo-controlled trial (RECORD-1), who received at least two targeted therapies. Methods: All patients in RECORD-1 received at least one prior VEGFR-TKI before randomization to everolimus (EVE) or placebo. Demographics, treatment sequence and overall survival were reported for patients who discontinued EVE for reasons other than death and received additional targeted therapy with either sorafenib or sunitinib. Results: Of the 416 patients in RECORD-1, 274 received EVE, 258 discontinued EVE for reasons other than death and approximately one third of those (N = 87) received sunitinib or sorafenib as additional targeted therapy following EVE (49.4% sorafenib only, 40.2% sunitinib only and 10.3% both). Baseline patient demographics at RECORD-1 enrollment are provided in the Table. Median time from EVE discontinuation to additional sunitinib or sorafenib therapy was 0.9 months (mean 1.7, SD 2.5). The median overall survival for patients from start of the additional sunitinib or sorafenib therapy after EVE discontinuation was 13.9 months (95% CI 10.6–17.2 mo). Baseline Characteristics Patients receiving sorafenib or sunitinib post-EVE N=87 Male, n (%) 73 (83.9%) >= 65 years, n (%) 35 (40.2%) MSKCC Intermediate Risk n (%) 52 (59.8%) MSKCC Favorable Risk n (%) 29 (33.3%) KPS— > =90 n (%) 63 (72.4%) KPS—80 n (%) 20 (23.0%) Conclusions: In this heavily pre-treated sub-population, following EVE discontinuation in RECORD-1, some patients experienced meaningful rescue therapy with a TKI, with a median overall survival of more than a year Clinical trials with investigational targeted therapies are ongoing, and may provide additional treatment options. Disclosure: R. Casciano: Roman Casciano is an employee of Analytica LA-SER, which received funding for the research. L. Stern: Lee Stern is an employee of Analytica LA-SER, which received funding for the research. T. Brechenmacher: Thomas Brechenmacher is employed by Novartis Pharmaceuticals, which provided funding for the research. S. Stergiopoulos: Sotirios Stergiopoulos is employed by Novartis Pharmaceuticals, which provided funding for the research. J. Coombs: John Coombs is employed by Novartis Pharmaceuticals, which provided funding for the research. All other authors have declared no conflicts of interest. 824P OVERALL SURVIVAL (OS) IN METASTATIC RENAL CELL CARCINOMA (MRCC) SEQUENTIALLY TREATED WITH DIFFERENT TARGETED THERAPIES (TTS): RESULTS FROM A LARGE COHORT OF PATIENTS G. Procopio 1 , E. Verzoni 1 , I. Testa 1 , R. Iacovelli 2 , E. Garanzini 1 , F.G.M. De Braud 1 1 Medical Oncology, Fondazione IRCCS - Istituto Nazionale dei Tumori, Milano, ITALY, 2 Dipartimento di Medicina Sperimentale, Policlinico Umberto I, Roma, ITALY Introduction: Targeted Therapies (TTs) have improved survival in patients with mRCC. However expert opinion on the optimal therapeutic strategy is not entirely shared. This study was performed to assess the overall survival (OS) in a consecutive series of mRCC patients receiving TTs. ix272 | 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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abstracts a paradigm shift in early
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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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ESMO-CSCO Joint Symposium: Building
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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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Table: 198P PFS OS Median, mo HR Me
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However, additional analysis sugges
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number of biomarkers have been trie
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90 mg/m2-cyclophophamide 600 mg/m2
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sector patients. The aim of this st
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Linear Logistic Model with Relaxed
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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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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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abstracts CNS tumors 410O CONDITION
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Conclusions: Our data suggested tha
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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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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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TST is active in breast and gastric
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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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experienced significantly more ≥
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functioning scales. Exploratory ana
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minutes. In a previous study, 30-mi
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Patients and methods: Chemotherapy-
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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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Table: 975PD Continued AMG 386 + pa
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physicians in the U.S. and Europe.
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elated with stage, nodal involvemen
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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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morbidities that radiation would le
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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
Page 361 and 362:
prospective non-interventional stud
Page 363 and 364:
Funding: GSK Biologicals Disclosure
Page 365 and 366:
survival rates of 13-25% (Prieto et
Page 367 and 368:
high response rates and prolonged p
Page 369 and 370:
GlaxoSmithKline, Merck Sharp & Dohm
Page 371 and 372:
advisor for Merck Sharp & Dohme, an
Page 373 and 374:
or cutaneous melanoma. A survival u
Page 375 and 376:
systemic therapy or were intolerant
Page 377 and 378:
abstracts neuroendocrine tumors and
Page 379 and 380:
morbidity, with G3 tumors behaving
Page 381 and 382:
pts. Poorly differentiated endocrin
Page 383 and 384:
Adenocarcinoma was present in 25 pa
Page 385 and 386:
Method: Endobronchial ultrasound gu
Page 387 and 388:
widely used by single agent or plat
Page 389 and 390:
disease after surgery were treated
Page 391 and 392:
stage IIIA NSCLC, EML4-ALK fusion-p
Page 393 and 394:
1200P CONCOMITANT CHEMORADIATION GI
Page 395 and 396:
Patients and methods: The study was
Page 397 and 398:
months (95% CI:13-25). The PFS and
Page 399 and 400:
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 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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