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Annals of Oncology 1491P RESPONSE TO SORAFENIB IN PDGFRA-D842V MUTATED METASTATIC GASTROINTESTINAL STROMAL TUMOR (GIST), SUPPORTED BY BIOMOLECULAR FUNCTIONAL ANALYSES E. Fumagalli1 , S. Pilotti2 , E. Conca2 , R. Bertulli1 , M. Fiore3 , C. Morosi4 , F. Bozzi2 , P.G. Casali1 , E. Tamborini2 1 Adult Mesenchymal Tumour Medical Oncology Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Milan, ITALY, 2 Laboratory of Molecular Pathology, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, ITALY, 3 Department of Surgery, Fondazione IRCCS Istituto Nazionale dei Tumori Milan, Milan, ITALY, 4 Department of Radiology, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Milan, ITALY Background: In GIST, KIT/PDGFRA mutations correlate with response to TKI. The exon 18 PDGFRA-D842V mutation is known to be resistant to imatinib and sunitinib. Activation of PDGFRA involves two main signal transduction pathways, RAS/MEK/ERK, which involves BRAF, and PI3K-AKT. We used sorafenib in three pts with a PDGFRA-D842V mutated metastatic GIST. Methods: Since January 2010, 3 PDGFRA-D842V mutated GIST pts (age: 57, 71, 72 yrs) have been treated with sorafenib 400 mg twice daily, on an individual use basis. Two pts were progressing on imatinib in association to mTOR inhibitors (sirolimus and everolimus), while the third had four previous lines of therapy. Molecular/ biochemical analyses were performed on cryopreserved material taken before sorafenib treatment in two of the three patients (one biopsy and one surgical specimen). A primary cell culture was obtained from one patient. Results: One pt had a Choi’s response 3 mos after starting the treatment; the others a RECIST response at 2 mos. The first pt had a tumor progression after 12 mos from starting therapy and 9 mos from tumor response. The second pt had a partial response lasting 15 mos. Treatment was relatively well tolerated, with G3 skin toxicity in one pt, causing a dose reduction. Biochemical analyses on pretreatment tumors revealed activated S6K and S6, both downstream mTOR, as well as ERK1/2 strong activation. The primary cell culture was treated with sorafenib 0.5 and 1 µM and phosphorylation switch-off of both S6K and S6 (Ser 240/244), associated with a retained ERK1/2 expression/activation, was observed. Further analyses are ongoing to verify which pathways converging on mTOR are inhibited by sorafenib. Conclusions: In the unresponsive PDGFRA-D842V mutated GIST we saw clinical signs of antitumor activity of sorafenib in 3 pts. This was consistent with biochemical analyses, which showed an inhibitory effect downstream mTOR. This clinical setting constitutes a high-priority unmet medical need, since very few clinical data are known and no functional analyses on sorafenib activity have been reported so far. Disclosure: P.G. Casali: Advisory role and honoraria for lectures: Novartis Pharma, Pfizer. Advisory role: Bayer. All other authors have declared no conflicts of interest. 1492P MONITORING OF PATIENTS WITH GASTROINTESTINAL STROMAL TUMOUR: SHOULD THE CHEST BE SCANNED? A. Findlay 1 , T. Ishfaq 1 , A. Raja 1 , A. Thacoor 1 , P. Hall 2 , M. Marples 3 1 School of Medicine, University of Leeds, Leeds, UNITED KINGDOM, 2 Leeds Institute of Health Sciences, University of Leeds, Leeds, UNITED KINGDOM, 3 St James’s Institute of Oncology, St James’s University Hospital, Leeds, UNITED KINGDOM Introduction: Thoracic CT scanning is often used for monitoring patients with sarcoma and upper gastrointestinal carcinoma, but its role in monitoring gastrointestinal stromal tumour (GIST) is variably defined in guidelines. In line with study protocols, it has been our practice to include chest CT for monitoring patients with GIST, and we now report the role of these scans. Method: We reviewed the electronic records of all patients diagnosed with GIST at St James’s Institute of Oncology, Leeds, UK, between 1 January 2001 and 1 January 2011. Primary site, stage at diagnosis, pattern of metastatic disease and frequency of CT scans were recorded. Results: We identified 176 patients diagnosed with GIST. All patients had CT scans of the chest, abdomen and pelvis performed at intervals agreed by the Yorkshire Sarcoma Network. Primary site was stomach in 96 patients (55%), small bowel in 27 (15%), rectum in 5 (3%), other sites in 38 (22%), and unknown in 10 (6%). Median follow-up was 34.3 months. Of the 139 patients who had no metastases at presentation, five developed local recurrence and 11 developed metastases. 27 patients had metastases at presentation, and the status of 10 was unknown. All patients with metastases had disease below the diaphragm, and only two had lung involvement as well (one at recurrence, one at initial presentation). Thirty-seven patients with metastatic disease were treated with imatinib. Of the 31 patients who progressed on imatinib, all had progression below the diaphragm; the patient with lung and abdominal metastases progressed in both areas. Four of these patients also developed lung metastases at the time of progression elsewhere. Conclusions: We observed synchronous progression in lungs and abdomen in 5/31 patients progressing on imatinib (16%), but no patients in our cohort relapsed or progressed in the lungs alone. We conclude that progression confined to the lungs is rare in GIST. Patients being monitored for recurrence or progression should have CT scans of the abdomen and pelvis only, with completion CT of the thorax being reserved for baseline and progression of disease. Disclosure: M. Marples: Dr Marples has accepted sponsorship to research meetings from Novartis. Novartis support mutation testing for GIST at Dr Marples’ institution. All other authors have declared no conflicts of interest. 1493P RESULTS OF HRQOL DATA FROM PALETTE: A RANDOMIZED DOUBLE BLIND PHASE III TRIAL OF PAZOPANIB VERSUS PLACEBO IN METASTATIC SOFT TISSUE SARCOMA (STS) PATIENTS. AN EORTC STBSG GLOBAL NETWORK STUDY (EORTC 62072) C. Coens 1 , W.T.A. van der Graaf 2 , J. Blay 3 , S.P. Chawla 4 , D. Kim 5 , R. Sanfilippo 6 , S. Manson 7 , M. Ouali 8 , S. Marreaud 9 , A. Bottomley 1 1 Quality of Life Department, EORTC HQ, Brussels, BELGIUM, 2 Medical Oncology /452, Radboud University Medical Centre NijmegenUniversity Medical Center St. Radboud, Nijmegen, NETHERLANDS, 3 University Claude Bernard Lyon I, Centre L, Lyon Cedex, FRANCE, 4 Clinical Research, Sarcoma Oncology Center, Los Angeles, CA, UNITED STATES OF AMERICA, 5 Internal Medicine, Seoul National University Hospital, Seoul, KOREA, 6 Cancer Medicine Department, Istituto Nazionale dei Tumori, Milano, ITALY, 7 R&D, GlaxoSmithKline, Uxbridge, UNITED KINGDOM, 8 Statistical Department, EORTC HQ, Brussels, BELGIUM, 9 Medical Department, EORTC HQ, Brussels, BELGIUM Background: HRQoL was an important secondary endpoint in this global double-blind, randomised phase III trial of pazopanib 800 mg QD versus placebo as second or later line treatment for advanced STS patients (N = 369) where progression free survival was significantly improved in the pazopanib arm (median: 4.6 versus 1.6 months; hazard ratio = 0.31; P < 0.001), but no statistically significant difference was observed in overall survival. Toxicity of pazopanib consisted mainly of fatigue, diarrhea, nausea weight loss and hypertension. Methods: HRQoL was assessed using EORTC QLQ-C30 at baseline, week 4, 8 and 12 in patients who were progression free. The primary HRQoL endpont was the QLQ-C30 global health scale, analyzed using linear mixed modeling supplemented with sensitivity analyses using alternative scales, methods and imputation of missing data. Results: Compliance of HRQoL was good in this trial, ranging from 94% at baseline to 81% at week 12. Placebo patients completed fewer questionnaires, largely due to a higher progression rate (median number of completed questionnaires- pazopanib: 3 vs placebo: 2). Differences in the global health scale between the two treatment arms assessed at weeks 4, 8 and 12 were not significant and did not exceed the pre-determined minimally important difference of 10 points (P = 0.291; average difference = 2.6 points). The EQ-5D data and sensitivity analyses mainly confirmed this finding. Among the other scales, the pazopanib arm reported significantly worse symptom scores for diarrhea (P < 0.001), loss of appetite (P < 0.001), nausea/vomiting (P < 0.001) and fatigue (P = 0.012). On the pazopanib arm, 74.8% of patients reported at least one minimally important worsening in any of those four symptom scales, compared to 51.2% on the placebo arm. In general, HRQoL scores tended to decline over time in both arms, indicative of the underlying disease. Exploratory factor analysis revealed that global health was associated mainly with functioning scales (Physical, Role and Social) and less with symptom scales except for fatigue. Conclusion: The toxicity profile of pazopanib is reflected in the patients’ self-reported symptoms but did not translate into worse overall global health while on-treatment, as patients maintained continued good functioning. Disclosure: J. Blay: research support and honoraria from GSK, Novartis, Roche, MSD, PharmaMar. S.P. Chawla: consultant GSK. D. Kim: consultant GSK, MEK Advisory Board. R. Sanfilippo: Honoraria from GSK. S. Manson: employee of GSK, holds GSK shares. A. Bottomley: Funding for EORTC research projects from Roche, Genentech, BMS. All other authors have declared no conflicts of interest. 1494P IMATINIB MESYLATE IN DESMOPLASTIC SMALL ROUND CELL TUMOUR A.F. Bertuzzi 1 , G. Bisogno 2 , M. Carli 2 , A. Ferrari 3 , A. Comandone 4 , M. Gasco 1 , R. De Sanctis 1 , C. Gnocchi 5 , A. Santoro 1 1 Medical Oncology and Hematology, Humanitas Cancer Center, IRCCS, Rozzano, ITALY, 2 Pediatric Medical Oncology and Hematology, Clinica di Onco-Ematologia Pediatrica, Padova, ITALY, 3 Pediatric Oncology Unit, Fondazione IRCCS - Istituto Nazionale dei Tumori, Milano, ITALY, 4 Medical Oncology, Ospedale Gradenigo, Torino, ITALY, 5 Novartis Farma, Novartis, Origgio, ITALY Introduction: Desmoplastic small round cell tumor (DSRCT) is a very rare and aggressive mesenchymal neoplasia with an extremely poor prognosis. The typical translocation t(11;22) determines the overexpression of PDGF-Rα and β, responsible of clinical stromal fibrosis reaction constantly detected in abdominal lesions. We investigated the role of imatinib, as tyrosine kinase inhibitor of PDGF-R, in DSRCT. Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds414 | ix483
Patients and methods: From August 2005 to June 2009 we enrolled patients (pts) with histologically proven diagnosis of DSRCT, refractory to conventional treatment. Inclusion criteria comprised immunohistochemical positivity of imatinib targets (PDGF-Rα and β). Treatment consisted of imatinib 400 mg p.o. daily. Primary endpoint of the study was objective response rate. Secondary endpoint was safety and tolerability assessment. Results: Of the 13 enrolled patients, 8 pts were evaluable for response (4 screening failure and 1 never treated). Median age was 20 years (range, 9-32). M/F ratio was 7/ 1. ECOG PS was 0 in 6 pts. Median time from diagnosis was 24.5 months (range, 6-148). 75% of pts had metastatic disease. The primary site was abdominal-pelvic for all pts. PDGFRα and β were expressed with an heterogeneous intensity pattern. Objective responses at first radiological evaluation at 3 months were: stable disease in one pt (12.5%) and progressive disease in 7 (87.5%) pts. Treatment-related adverse events were G1-2 nausea/vomiting, fatigue and periorbital oedema. Conclusions: In our limited case series, imatinib showed no efficacy in the treatment of DSRCT pts unresponsive to conventional therapy, despite molecular-based selection of pts. Probably to identify responder pts, it is necessary a more complex evaluation comprehensive of both levels of expression and activation of PDGFRα and β. Furthermore, enrolled pts were affected by advanced refractory disease, probably less responsive to target therapies. It would be hopeful a global effort to define a new combined approach based on the association of conventional chemotherapy and biological drugs. Disclosure: C. Gnocchi: Novartis Patient Advocacy Manager. All other authors have declared no conflicts of interest. 1495P SUNITINIB THERAPY IN ADVANCED ALVEOLAR SOFT PART SARCOMAS H.M. Kosela, K. Wiater, T. Switaj, A. Klimczak, S. Falkowski, P. Rutkowski Soft Tissue/bone Sarcoma and Melanoma, MSC Memorial Cancer Centre and Institute Maria Sklodowska-Curie, Warsaw, POLAND Background: Alveolar soft part sarcoma (ASPS) is a rare entity making up < 1% of soft tissue sarcomas (STS). It is characterized by slow, indolent growth but with a high frequency of metastatic disease especially to lungs. Chemotherapeutic regimens used for the treatment of other soft tissue sarcomas lack efficacy in ASPS. The purpose of our analysis was to assess sunitinib activity in ASPS. Methods: Since July 2009, 7 patients with metastatic ASPS have been treated with sunitinib continuous daily dosing 37,5mg (1 pts started treatment at 50mg/d on a 4/2 week schedule). All patients’ initial performance status according to ECOG was 0-1. Median age at time of diagnosis was 23 yrs (range 18-57), gender distribution M/F was 1/ 6. Primary localization of the tumor was: lower extremity (3), trunk (2), retroperitoneum (1), pelvis (1). Primary tumor size ranged from 5 to 12 cm (median 7cm). All patient had unresectable metastases to the lungs. 57% of thepatientswerepreviouslytreatedwith standard chemotherapy. Median time from diagnosis to start of sunitinib therapy was 6 months (range: 2-156). Responses were evaluated after 2 months from baseline, then every 3 months by CT scan and/or MRI, according to RECIST criteria. Results: At the time of present analysis 3 of the patient continue therapy. After 2 months of treatment 2 patients had RECIST PR, 5 SD. Median PFS was 15 months with 86% patients free of progression of the disease at 6 months. Median therapy duration was 18 months (range: 5-31). Median OS was 15 months; 3 patients died due to disease progression at the time of analysis. One of the patients had SD after 4 months of treatment, interrupted treatment for 3 months and experienced progression of the disease, after restarting therapy she again gained SD lasting 12 months. Toxicity was rather moderate. All the patients experienced some side effects, 4 patients (57%) had toxicity grade 3/4 CTC. The common treatment toxicity was neutropenia, hypothyroidism, arterial hypertension, hand and foot syndrome. 2 patients required dose reduction. There was one death related to the treatment (sepsis). Conclusion: Our analysis shows efficacy of sunitinib in patients with advanced ASPS. Disclosure: P. Rutkowski: honoraria: Pfizer and Novartis. All other authors have declared no conflicts of interest. 1496P SUNITINIB MALATE IN CLEAR CELL SARCOMA S. Stacchiotti 1 , E. Palassini 1 , T. Negri 2 , C. Morosi 3 , A. Messina 3 , R. Patuzzo 4 , A. Gronchi 4 , S. Pilotti 2 , P.G. Casali 1 1 Cancer Medicine, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, ITALY, 2 Pathology and Molecular Biology, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, ITALY, 3 Radiology, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, ITALY, 4 Surgery, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, ITALY Background: Clear cell sarcoma (CCS) is a rare soft tissue sarcoma, characterized in most cases by the t(12;22), resulting in the EWS-ATFE1 fusion protein. It has a high Annals of Oncology metastatic potential. CCS is poorly sensitive to chemotherapy. We already reported on the activity of sunitinib (SM) in one case of CCS. Methods: Since September 2009, 9 patients with progressive, metastatic CCS (M/ F 3/6; median age 36 yrs; translocated/ non translocated: 6/3; site of primary: extremities 6, other 3; pretreated: 9) have been treated with continuous SM 37.5 mg/day, on a named basis. PET response was assessed in 6 cases. Responses were evaluated after 2 months from baseline, then every 3 months by CT scan and/or MRI, according to RECIST. Pre-treatment PDGFRB and VEGFR status analysis by immunohistochemistry, western/blotting and phospho-RTK array is ongoing in evaluable cases. Results: At the time of the present analysis, 6/9 pts are evaluable for response (1 early interruption; 2 just started), and 4 patients are still on treatment. After 3 months of SM, 3 patient had a RECIST partial response (PR) (50%), along with subjective improvement in symptoms, 1 stable disease (SD), 2 progressive disease (PD). PET was consistent. One patient had a complicated major response characterized by an ulcer to the site of previous surgery; thus she underwent surgery with evidence of pathologic partial response, marked by extensive necrosis. The median PFS is 5 months (range 2-7). Conclusions: SM is active in a proportion of CCS. Prospective studies are needed. Disclosure: S. Stacchiotti: Pfizer: reseach grant for studies in which my Institution is involved; honoraria. E. Palassini: Pfizer: research grant for studies in which my Institution is involved. P.G. Casali: Pfizer: research funds for studies in which my Institution is involved; Compensated Advisory; Honoraria. All other authors have declared no conflicts of interest. 1497P SIMULTANEOUS TARGETING OF THE INSULIN-LIKE GROWTH FACTOR 1 RECEPTOR (IGF-1R) AND ANAPLASTIC LYMPHOMA KINASE (ALK) IN EMBRYONAL AND ALVEOLAR RHABDOMYOSARCOMA J.C. van Gaal 1 , Y.M.H. Versleijen-Jonkers 1 , M.H.S. Roeffen 1 , U.E. Flucke 1 , G. van der Heijden 1 , A.J.H. Suurmeijer 2 , E.S.J.M. De Bont 3 , W.T.A. van der Graaf 4 1 Department of Medical Oncology, Radboud University Nijmegen Medical Centre, Nijmegen, NETHERLANDS, 2 Pathology, University Medical Center Groningen, Groningen, NETHERLANDS, 3 Pediatric Oncology, University Medical Center Groningen, Groningen, NETHERLANDS, 4 Medical Oncology /452, Radboud University Medical Centre MijmegenUniversity Medical Center St. Radboud, Nijmegen, NETHERLANDS Introduction: Rhabdomyosarcoma (RMS) is an aggressive soft tissue tumour that occurs predominantly in children and adolescents. Its two most common forms are embryonal (eRMS) and alveolar RMS (aRMS). Although survival has increased over the past decades after the introduction of multi-agent chemotherapy, the survival for the high-risk subpopulation remains poor (not exceeding 50%). Therefore, there is an urgent need for new systemic treatment options. The aim of the current study is to investigate the insulin-like growth factor-1 receptor (IGF-1R) and anaplastic lymphoma kinase (ALK) pathway as potential targets in RMS. Methods: A total of 112 paraffin-embedded RMS tumor specimens (eRMS n = 86; aRMS n = 26) were collected on a tissue microarray. IGF-1R and ALK expression was evaluated by immunohistochemistry. A binary scoring system was used in which staining was scored positive when present in at least 10% of the tumour cells. The effect of the ALK small molecule inhibitor NVP-TAE684 (Novartis), the IGF-1R monoclonal antibody R1507 (Roche) and combined treatment was investigated by cytotoxicity assay MTT in four RMS cell lines (aRMS Rh30 and Rh41; eRMS Rh18 and RD). Results: Expression of IGF-1R was seen in 72% of aRMS and 62% of eRMS, respectively. ALK expression was observed in 92% of aRMS and 39% of eRMS. Co-expression of IGF-1R and ALK was observed in 68% of aRMS and 32% of eRMS. In vitro, inhibition of the IGF-1R by R1507 resulted in diminished cell growth only in aRMS cell line Rh41 (IC50 11 ng/ml). NVP-TAE-684 resulted in diminished cell growth in aRMS cell lines Rh41 (IC50 103 nM) and Rh30 (IC50 211 nM), and to a lesser extent in eRMS cell lines Rh18 (IC50 585 nM) and RD (IC50 734nM). Simultaneous treatment could be assessed in aRMS cell line Rh41 by using different concentrations of R1507 and NVP-TAE684, and revealed a synergistic effect (combination index
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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-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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abstracts breast cancer, locally ad
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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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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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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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functioning scales. Exploratory ana
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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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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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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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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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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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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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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
Page 343 and 344:
evaluated by the screening instrume
Page 345 and 346:
morbidities that radiation would le
Page 347 and 348:
Conclusions: Through adequate selec
Page 349 and 350:
abstracts hematological malignancie
Page 351 and 352:
anthracyclines in vitro. A favorabl
Page 353 and 354:
1076P RITUXIMAB PLUS SUBCUTANEOUS C
Page 355 and 356:
than the standard target of ≥2.5
Page 357 and 358:
Patients: From November 2002 to May
Page 359 and 360:
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: 1488P ORGANISATION OF SARCOMA PATIE
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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