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Annals of Oncology 1137P IMMUNO-CHEMOABLATION OF METASTATIC MELANOMA WITH INTRALESIONAL ROSE BENGAL S.S. Agarwala 1 , J.F. Thompson 2 , B.M. Smithers 3 , M. Ross 4 , B.J. Coventry 5 , D.R. Minor 6 , C.R. Scoggins 7 , E. Wachter 8 1 Cancer Center, St. Luke’s Hospital & Health Network, Bethlehem, UNITED STATES OF AMERICA, 2 Surgery, Melanoma Institute, Sydney, AUSTRALIA, 3 Surgery, Princess Alexandra Hospital, Woolloongabba, AUSTRALIA, 4 Surgery, MD Anderson, Houston, UNITED STATES OF AMERICA, 5 Surgery, Royal Adelaide Hospital, Adelaide, AUSTRALIA, 6 Medical Oncology, California Pacific Medical Center, San Francisco, UNITED STATES OF AMERICA, 7 Surgery, University of Louisville, Louisville, UNITED STATES OF AMERICA, 8 Drug Development, Provectus Pharmaceuticals, Knoxville, UNITED STATES OF AMERICA Intralesional rose bengal (PV-10) is being investigated for treatment of solid tumors, where it may elicit selective chemoablation of injected lesions and a tumor-specific, immune-mediated bystander response in untreated bystander lesions. In phase 1 testing in 20 subjects with AJCC Stage III-IV melanoma, single-dose treatment with PV-10 was well tolerated, producing a durable objective response (OR) at 12-24 weeks in 40% of subjects (20% CR + 20% PR by modified RECIST) and locoregional disease control (CR + PR + SD) in 75% of subjects; 15% of subjects achieved an OR in bystander lesions, which strongly correlated with response of their injected lesions. Phase 2 testing in 80 subjects with Stage III-IV metastatic melanoma (median age 70.0 yrs, range 33-97) commenced at 7 centers in Australia and the USA in October 2007 with final clinical evaluation completed in May 2010 (Clinical Trials ID NCT00521053). In this study, subjects could receive up to four courses of PV-10 to up to 20 cutaneous or subcutaneous lesions (median 2 courses, range 1-4). Preliminary study data was presented at SMR 2010 in Sydney, Australia, and showed that treatments were well tolerated, with adverse events predominantly mild to moderate, locoregional and transient, with no grade 4 or 5 AEs attributed to PV-10. Preliminary evaluation also showed robust response, with 24% of subjects achieving a CR, 25% PR and 22% SD of their target lesions. Additionally, 24% of 38 subjects with evaluable, untreated bystander lesions achieved CR in their bystander lesions, along with 13% PR and 18% SD. As observed in phase 1, response of bystander lesions strongly correlated with response of injected lesions. Final efficacy data will be presented, including response rate and time-to-event (progression free survival and overall survival). These data demonstrate that the safety and efficacy profile of PV-10 compares favorably with available and emerging treatment options for this patient population, and serve as the basis for phase 3 testing of PV-10 in Stage III patients with recurrent, in-transit or satellite metastases. A randomized controlled trial to assess PFS against standard care is expected to commence in the second half of 2012 at centers in Australia, the USA and the EU. Disclosure: S.S. Agarwala: Provectus Pharmaceuticals: advisory board, corporate-sponsored research. J.F. Thompson: Provectus Pharmaceuticals: advisory board, corporate-sponsored research. B.M. Smithers: Provectus Pharmaceuticals: corporate-sponsored research. M. Ross: Provectus Pharmaceuticals: advisory board, corporate-sponsored research. B.J. Coventry: Provectus Pharmaceuticals: corporate-sponsored research. D.R. Minor: Provectus Pharmaceuticals: corporate-sponsored research. C.R. Scoggins: Provectus Pharmaceuticals: advisory board, corporate-sponsored research. E. Wachter: Employee of sponsoring company, stock holder 1138P CHEMOTHERPAY AND DENDRITIC CELL VACCINE IN PATIENT WITH METASTATIC MELANOMA: PHASE II PROSPECTIVE RANDOMIZED TRIAL I.V. Samoylenko 1 , T.N. Zabotina 2 , I.N. Mikhaylova 1 , G.Z. Chkadua 3 ,O. V. Korotkova 2 , K. Baryshnikov 1 , L.V. Demidov 1 1 Tumor Biotherapy, N.N Blokhin Russian Cancer Research Center, Moscow, RUSSIAN FEDERATION, 2 Laboratory of Clinical Immunology, N.N Blokhin Russian Cancer Research Center, Moscow, RUSSIAN FEDERATION, 3 Laboratory of Experimental Diagnostics and Tumor Biotherapy, N.N Blokhin Russian Cancer Research Center, Moscow, RUSSIAN FEDERATION Introduction: We performed a vaccine trial in metastatic melanoma patients with a stable disease course. Aim: Primary end point was 6-month progression-free survival; secondary end points included overall survival, progression free survival, immunological parameters. Patients and methods: Inclusion criteria were morphologically proven metastatic melanoma, ECOG status 0-2, LDH level
or cutaneous melanoma. A survival update was performed on 31 March 2011. CS-PHP melphalan 3.0 mg/kg ideal body weight was infused into the hepatic artery over 30 min with concurrent extracorporeal filtration for 60 min. Up to 6 treatments were given every 4–8 wks. In the BAC group, crossover to CS-PHP melphalan was permitted after hepatic disease progression. The primary endpoint was investigator-assessed hepatic progression-free survival (hPFS). An exploratory post-hoc analysis of pts who crossed from BAC to CS-PHP vs. BAC-only pts was also performed. Results: 93 pts were randomized to CS-PHP (n = 44) or BAC (n = 49). After hepatic disease progression, 28 pts crossed over to CS-PHP. Results are shown in the Table. The most common grade 3/4 toxicities in CS-PHP pts (n = 40) were hematological peri-procedural thrombocytopenia (73%) and anemia (55%) and post-procedural (beyond day 4 post-treatment) neutropenia (93%) or thrombocytopenia (83%). The safety profile in crossover pts was similar to that in pts randomized to CS-PHP melphalan. Conclusions: CS-PHP melphalan significantly prolonged hPFS compared with BAC in pts with liver-dominant metastatic melanoma, thereby meeting the primary study objective. Efficacy was similar after hepatic disease progression in BAC-CS-PHP crossover pts as in those randomized initially to CS-PHP. Median hPFS, Hazard ratio Median Hazard ratio Treatment group n mo (95% CI) OS, mo (95% CI) CS-PHP 44 8.0 0.35 (0.23-0.54) 9.8 1.08 (0.69-1.68) BAC 49 1.6 P < 0.0001 9.9 NS BAC only 21 1.6 0.32 4.1 0.33 BAC → CS-PHP crossover 28 8.8 15.3 Disclosure: All authors have declared no conflicts of interest. 1142P THE CONCORDANCE OF HER2 STATUS IN PRIMARY AND METASTATIC SITES OF EXTRAMAMMARY PAGET’S DISEASE R. Tanaka 1 , Y. Sasajima 2 , H. Tsuda 2 , K. Namikawa 1 , A. Tsutsumida 1 , N. Yamazaki 1 1 Division of Dermatologic Oncology, National Cancer Center Hospital, Tokyo, JAPAN, 2 Pathology and Clinical Laboratory Division, National Cancer Center Hospital, Tokyo, JAPAN Background: HER2-targeted therapies have been introduced to treat breast and stomach cancers that show HER2 protein overexpression and/or HER2 gene amplification. However, the HER2 status of primary tumors and their corresponding metastatic sites is shown to be heterogeneous in less than 20% of cases. In extramammary Paget’s disease (EMPD), HER2 protein overexpression and gene amplification has been shown to occur in 5-80% of cases; however, knowledge regarding the concordance of HER2 status in primary and metastatic sites of EMPD is limited. The aim of this study was to clarify the concordance rate of HER2 status in the primary tumors and metastatic sites of EMPD. Methods: Twenty-six tissue blocks of primary tumors and corresponding lymph node metastases were subjected to an immunohistochemistry (IHC) analysis. The IHC scores were classified into four groups (0 to 3+) according to the American Society of Clinical Oncology/College of American Pathologists Guidelines (2007). When the primary tumors and lymph node metastases showed IHC scores of either 2+ or 3 + , the presence of HER2 gene amplification was examined using fluorescence in situ hybridization (FISH) and dual-colored in situ hybridization (DISH). Results: mmunohistochemically, 27% (7/26) of the primary tumors and 38% (10/26) of the lymph node metastases showed IHC scores of either 2+ or 3+. When HER2 protein overexpression was classified as being either positive (2 + , 3+) or negative (0, 1+), the concordance rate of the HER2 status of the primary tumors and corresponding lymph node metastases was 85% (22/26). The presence of HER2 gene amplification was examined in six primary tumors and 10 metastatic sites. HER2 gene was amplified in a total of seven cases (27%): four cases in both the primary and metastatic sites, two cases in the metastatic sites only and one case in the primary site only. Conclusion: Good concordance of HER2 protein overexpression and gene amplification status was seen in the primary tumors and corresponding lymph node metastases of patients with EMPD. Furthermore, the HER2 gene was found to be always amplified in cases with an IHC score of 3+ and in two cases with an IHC score of 2+ in the lymph node metastases, which is suitable to be targeted for therapy. Disclosure: All authors have declared no conflicts of interest. Annals of Oncology 1143P A COMPARISON OF GENERAL POPULATION AND PATIENT UTILITY VALUES FOR ADVANCED MELANOMA A. Batty 1 , B. Winn 1 , L. Pericleous 2 ,D.Rowen 3 , D. Lee 1 , T. Nikoglou 2 1 Health Economics, BresMed, Sheffield, UNITED KINGDOM, 2 Health Economics and Outcomes, Bristol Myers Squibb, Uxbridge, UNITED KINGDOM, 3 School of Health and Related Research, University of Sheffield, Sheffield, UNITED KINGDOM Background: Health-related quality of life (HRQL) is a fundamental part of health technology assessment. Utility values are vital because they can be used as preference weights and allow the calculation of HRQL benefits. The objective of this study was to compare utilities calculated for patients with advanced melanoma in the Phase III clinical trial for ipilimumab (MDX010-20) using a generic and a condition-specific preference-based measure to utilities produced by vignettes for advanced melanoma. A secondary objective was to determine how different analyses might be used most appropriately within cost-effectiveness modelling. Methods: The trial utilities were generated using the condition-specific EORTC-8D (1,190 observations) and generic SF-6D (1,157 observations) preference-based measures. Progression-status and time-to-death analyses were conducted on the patient-level data and the predictive abilities were compared. Patient-level results were compared to the utilities derived for progression status using vignettes valued by the general population. Results: On disease progression, vignette-generated utilities showed a greater decrease (0.77 to 0.59) than either the generic SF-6D (0.64 to 0.619) or condition-specific EORTC-8D (0.801 to 0.763). SF-6D and EORTC-8D showed a large decrease in utility in the 180 days prior to death (from 0.826 to 0.628 and from 0.655 to 0.505, respectively). Compared to progression status, time to death showed a lower Root Mean Squared Error and higher R2 when used to predict patient utility. Conclusion: Practitioners should carefully analyse patient level utility data prior to constructing economic models as standard measures, such as progression status, may not fully capture the patient experience. Similarly, where vignettes are valued to represent health states in an economic model, their applicability to the disease and patient population should be carefully scrutinised. The use of standard progression based cost-effectiveness modelling techniques may not be appropriate for this disease. Consequently, there are implications for the analysis of utility information in future studies and the methods of cost-effectiveness modelling used for cancer treatments. Disclosure: A. Batty: BresMed were funded by BMS to conduct the analysis presented within this paper. Other than this I have not received any personal funding and do not have any personal interest in BMS or any competitor products. B. Winn: BresMed were funded by BMS to conduct the analysis presented within this paper. Other than this I have not received any personal funding and do not have any personal interest in BMS or any competitor products. L. Pericleous: I have worked for BMS. Other than this I have not received any personal funding and do not have any personal interest in BMS or any competitor products. D. Lee: BresMed were funded by BMS to conduct the analysis presented within this paper. Other than this I have not received any personal funding and do not have any personal interest in BMS or any competitor products. T. Nikoglou: I work for BMS. Other than this I have not received any personal funding and do not have any personal interest in BMS or any competitor products. All other authors have declared no conflicts of interest. 1144 CETUXIMAB IN METASTATIC SQUAMOUS CELL CANCER OF THE SKIN: A CASE SERIES K. Conen 1 , N. Fischer 2 , G.F. Hofbauer 3 , B. Shafaeddin-Schreve 3 , R. Wintherhalder 4 , C. Rochlitz 5 , A. Zippelius 1 1 Medical Oncology, University Hospital Basel, Basel, SWITZERLAND, 2 Medical Oncology, Kantonsspital Winterthur, Winterthur, SWITZERLAND, 3 Dermatologische Klinik, Universitätsspital Zürich, Zürich, SWITZERLAND, 4 Medical Oncology, Kantonsspital Luzern, Luzern, SWITZERLAND, 5 Medical Onkology, University Hospital Basel, Basel, SWITZERLAND Background: Treatment of metastatic squamous cell cancer of the skin (SCCS) is challenging. Only few therapeutic options including cisplatin-based combinations are currently available. In a recently published phase II trial, cetuximab, a monoclonal antibody against the epidermal growth factor receptor (EGRF), has demonstrated a promising clinical activity with an overall 69% disease control rate (DCR) and 28% response rate (RR) in patients with unresectable SCCS. Whether this treatment is also effective in metastatic SCCS is unclear. Purpose: To summarize the efficacy of cetuximab at any line in a series of patients with metastatic SCCS. Patients and methods: We performed a retrospective analysis of six patients from four centres in Switzerland. We collected standard baseline data by reviewing the ix372 | 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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feasibility), but by how high the c
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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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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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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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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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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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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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NSCLC diagnosis and time of BM diag
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1291P PHASE I/II DOSE-FINDING STUDY
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Network utilization of WBCGF in the
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1303P COST EFFECTIVENESS OF PEMETRE
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Results: The patients’ characteri
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EGFR mut at exons 18, 19, 21, and K
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Methods: EML4-ALK fusion was screen
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Results: The median survival time (
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enefit from sustained EGFR blockade
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epresented by 19 pts (32%) female,
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and at least one prior course of ch
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Methods: NSCLC patients with radiog
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1367TiP LONG-TERM ERLOTINIB THERAPY
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Austria, Czech Republic, Finland, G
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were every 6 weeks (wk) (S1), every
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Advantage enrollees (83% vs. 25%) [
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Results: Based on 10,000 simulation
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cancer tumors 12%, Germ cell tumor
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Material and methods: 50 lung cance
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1414TiP IMPLEMENTATION OF CANCER RE
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abstracts palliative care 1422O EFF
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Method and results: A total of 317
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1436P SURVEY ON MODELS OF INTEGRATI
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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
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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
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author index author index A Aamdal
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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
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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)
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author index Trypaki M. ix429 (1308
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author index Whitmore J.B. ix310 (9
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subject index subject index A AAV-H
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subject index ix115 (316TiP), ix116
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subject index diffuse large B-cell
Page 593 and 594:
subject index (1033P), ix340 (1036P
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subject index medical information,
Page 597 and 598:
subject index (612P), ix214 (633),
Page 599 and 600:
subject index RCC, ix274 (830P) re-
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subject index TR-FRET, ix84 (206P)
Page 603 and 604:
drug index drug index 1248P, 1250P,
Page 605 and 606:
translational research index transl
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Page 609:
show all

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