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Annals of Oncology 717P GEMCITABINE COMBINED WITH THE MTOR INHIBITOR TEMSIROLIMUS(CCI-779) IN PATIENTS WITH INOPERABLE OR METASTATIC PANCREATIC CANCER (HE 3/07). A PHASE I STUDY BY THE HELLENIC COOPERATIVE ONCOLOGY GROUP V. Karavasilis, G. Pentheroudakis, J. Sgouros, S.T. Dimoudis, I. Varthalitis, E. Samantas, G. Fountzilas Data Office, Hellenic Cooperative Oncology Group, Athens, GREECE Aim: To investigate the feasibility of the gemcitabine (G) and mTOR inhibitor temsirolimus (T) combination and define the maximum tolerated dose (MTD) in patients with inoperable or metastatic pancreatic cancer (MPC). Methods: Eligible patients with histologically confirmed inoperable or MPC were entered into the trial. Available biopsy material for subsequent translational research analysis was mandatory for inclusion in the study. G was given bi-weekly and T was administered on a weekly basis. Each cycle consisted of four consecutive weeks of treatment. First dose level was set at G 800 mg/m 2 and T 10 mg. G was escalated in increments of 200 mg/m 2 and T in increments of 5 mg. Results: A total of 30 patients [16M/14F, median age: 63y, PS: 1 (63%)] were enrolled for the pre-planned six dose levels. Up to date, 80 complete cycles of treatment were delivered. Four patients did not complete the first cycle due to rapid disease progression and were therefore replaced. Another patient was found ineligible and was replaced, as well. Ten patients received four or more cycles of treatment. MTD was not achieved and the study was terminated at the sixth dose level of G 1000 mg/m 2 and T 25 mg. Dose-limiting toxicity (DLT) was thrombocytopenia of grade 4, which occurred at the first dose level. Non-DLT grade III toxicities were neutropenia (9 patients), abnormal liver biochemistry (8 patients) and fatigue (1 patient). Toxicities below the grade III level were mild, the most predominant being anemia, neutropenia, raised liver function tests and fatigue. Two patients at the final level of G 1000 mg/m 2 and T 25 mg are still on treatment. This dose is the recommended dose for phase II evaluation. With regard to response, two partial responses were documented and 11 patients had stable disease. Conclusion: Combination of G and T is feasible in patients with inoperable or MPC with manageable side effects. The activity of this combination is currently investigated in a recently initiated phase II study. Disclosure: All authors have declared no conflicts of interest. 718P A THREE-STEP STRATEGY OF INDUCTION CHEMOTHERAPY, CHEMO-RADIOTHERAPY AND SURGERY IN LOCALLY ADVANCED PANCREATIC CANCER (LAPC). A SINGLE INSTITUTIONAL EXPERIENCE O.E. Carranza Rua 1 , E. Arevalo 1 , J.P. Fusco 1 , E. Castanon Alvarez 1 , L. Zubiri 1 ,J. A. Gonzalez 2 , L. Arbea 3 , F. Pardo 4 , S. Martin Algarra 1 , J. Rodriguez 5 1 Medical Oncology, Clinica Universitaria de Navarra, Pamplona, SPAIN, 2 Radiation Oncologist, Clinica Universidad de Navarra, Pamplona, SPAIN, 3 Radiation Oncology, Clinica Universidad de Navarra, Pamplona, SPAIN, 4 Surgical Oncology, Clinica Universidad De Navarra, Pamplona, SPAIN, 5 Medical Oncology, Clinica Universidad de Navarra, Pamplona, SPAIN Background: Pancreatic cancer is one of the most highly fatal cancers. A growing evidence suggests that even potentially resectable patients (pts) benefit from a multidisciplinary approach aimed to improve resectability and reduce recurrence. We report our experience after a long-term follow-up. Methods: From December 2005 to July 2011, 69 histologically confirmed LAPC, endoscopic ultrasound (EUS) staged T3/T4, N0/N1 were scheduled to receive induction gemcitabine-oxaliplatin-based chemotherapy followed by chemo-radiotherapy with weekly oxaliplatin and capecitabine (mean radiotherapy dose of 50.4 Gys) and salvage surgery when feasible. Adjuvant chemotherapy was considered depending on results of the pathologic report. Results: The median age was 63 years (range 35-83 years). Male to female ratio was 37/32. Forty-one pts (59%) completed the whole program (group A), whereas 26 (37%) received chemo and chemo-radiotherapy but were not eligible for surgery (group B). Two patients (3%) progressed after induction chemotherapy (group C). Endoscopic stent placement was performed in thirty-four pts (49%). Toxicity profile was mild, with no grade 4 toxicity being documented. Grade 3 toxicity included: leucopenia (7%), neutropenia (11%), asthenia (13%) and nausea, diarrhea and anorexia (1% each). On an intent to treat basis, the R0 resection rate was 55% (38/ 69). Among resected patients, local and distant failure rates were 5 and 55% respectively. After a median follow up of 43 months (range 9 to 88), median PFS was 17, 9 and 1 month in groups A, B and C respectively. Median overall-survival (mOS) was 13 and 4 months in groups B and C. In group A mOS has not been reached. The 2 and 3-year actuarial overall survival in this group are 71% and 45% respectively. Conclusions: Our data suggest that this three-step strategy is feasible and active in LAPC patients Correlative molecular analysis seem warranted to rule out the subset of pts most likely to benefit from this approach. Disclosure: All authors have declared no conflicts of interest. 719P DENDRITIC CELL VACCINATION IN COMBINATION WITH OK432, GEMCITABINE AND/OR S-1 IN PATIENTS WITH ADVANCED PANCREATIC OR BILIARY TRACT CANCER M. Ogasawara, S. Ota Internal Medicine, Sapporo Hokuyu Hospital, Sapporo, JAPAN Background: Although dendritic cells (DCs) are potent antigen presenting cells that can generate T cells specific to tumor antigens, efficacy of immunotherapy using DCs is so far limited. To improve the efficacy of this modality, we conducted a clinical trial of DC vaccination in combination with gemcitabine (GEM) and/or S-1 for patients with advanced pancreatic or biliary tract cancer. The advantages of using these drugs are immunomodulatory functions including the inhibition of regulatory T cells (Tregs). OK432, a toll like receptor (TLR) 4 agonist, was employed to enhance activation of DCs both in vitro and in vivo. Methods: 31 patients (17 males, 14 females; aged 27-81 years, median 61 years) with advanced pancreatic (24) or biliary tract (7) cancer refractory to standard treatment were treated with DC vaccination in combination with OK432 and GEM and/or S-1 from 2009 to 2011. Autologous DCs were generated from adherent mononuclear cells using standard protocols. Wilms’ tumor 1 (WT1) and/or MUC1 peptide-loaded mature DCs were administered intradermally every 2 weeks for 7 times. Induction of vaccine-induced T cell responses was monitored using HLA-tetramer assays. Results: The treatment was well tolerated and none of the patients experienced more than grade 3 adverse events during the treatment period. Of 31 patients, 5 patients had partial response (PR), 14 had stable disease (SD), 2 had mixed response and 10 had progressive disease following one course of the treatment. Median overall survival was 289 days for all patients, which was longer than that of the patients treated with GEM and/or S-1.Survival of patients achieving PR or SD (responder) after one course of DC vaccination was longer than those who did not respond to the treatment (p < 0.01). Increased numbers of cancer antigen-specific cytotoxic T cells and decreased numbers of Tregs was observed in responders after one course of treatment. Conclusions: DC vaccine-based immunotherapy combined with a TLR agonist and chemotherapy was demonstrated to be safe and more effective in patients with advanced pancreatic or biliary tract cancer compared with chemotherapy alone. Disclosure: All authors have declared no conflicts of interest. 720P PANCREATIC DUCTAL ADENOCARCINOMA: A HOMOGENEOUS MORPHOLOGICALLY BUT MOLECULARLY HETEROGENEOUS TUMOR. IMPLICATIONS FOR ITS MANAGEMENT L. Faloppi 1 , A. Mandolesi 2 , M. Scartozzi 1 , C. Loretelli 1 , M. Bianconi 1 , A. Bittoni 1 , R. Giampieri 1 , M. Del Prete 1 , I. Bearzi 2 , S. Cascinu 1 1 Clinica di Oncologia Medica, AOU Ospedali Riuniti Ancona Università Politecnica delle Marche, Ancona, ITALY, 2 Anatomia Patologica, AOU Ospedali Riuniti Ancona Università Politecnica delle Marche, Ancona, ITALY Pancreatic cancer has not achieved significant improvements in therapeutic results, probably due to a poor comprehension of the underlying molecular mechanisms. The aim of our study was to classify pancreatic tumors in categories from a molecular point of view, in order to better identify the main pathogenetic molecular alterations potentially useful as targets for new drugs. In 110 histological samples of pancreatic ductal adenocarcinoma were performed immunohistochemical evaluations of K-ras, stromal IL-6 (IL-6s), tumoral IL-6 (IL-6t), Cox-2, EGFR, Her2, Her3, MLH1, MSH2, MSH3 and molecular biology assessment of CD24, MUC6, HGF, MET, SMAD4, CDKN2A, PGF, VEGF-A/B, VEGFR-1/2, PDGFRB, WNT1, BMP4, stemness (ALCAM, PROM1, OCT3/4, CD44, LGR5,), Hedgehog (SHH, DHH, IHH, SMO, PTCH1, PTCH2), SPARC, NOTCH1, BRCA1, BRCA2. A preliminary analysis showed that the positivity of the inflammation mediators stromal IL-6, tumoral IL-6, Cox-2 allowed to differentiate two categories of pancreatic tumors: inflammatory tumors, associated with an intense desmoplastic reaction and alteration of EGFR and MLH1, and on the contrary tumors not associated with inflammation. Within these two groups statistical significant differences were found for EGFR and MLH1. An overexpression of EGFR was found in triple (97%) and double (88%) positive tumors, compared to negative or single positive (52%) (p0.0002). An higher rate of loss of MLH1 expression was found in triple positive tumors (69%), compared to double positive (40%) and negative or single positive (27%) (p0.02). Inflammation has been identified as a significant factor in the development of other malignancies. Mediators of the inflammatory pathway have been shown to be involved in proliferation, loss of tumor suppressor function, oncogene overexpression, all of which may lead to malignancy. Although definitive results concerning all the molecular factors analyzed will be presented during the ESMO 2012 congress, inflammation and its related molecular alterations may be specific targets for novel agents potentially useful for the treatment of these malignancies. Disclosure: All authors have declared no conflicts of interest. Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds398 | ix239
721P FIRST-LINE TREATMENT WITH FOLFIRINOX IN ADVANCED, INOPERABLE PANCREATIC CANCER (APDAC) PATIENTS (PTS): SUPPORTIVE MEASURES OPTIMIZATION FOR A SAFE ADMINISTRATION IN ROUTINE CLINICAL PRACTICE V. Vaccaro 1 , E. Bria 2 , I. Sperduti 3 , F. Massari 2 , M.S. Pino 4 , E. Lucchini 2 , A. Gelibter 1 , F. Cognetti 5 , G. Tortora 2 , M. Milella 1 1 Medical Oncology, Regina Elena National Cancer Institute, Roma, ITALY, 2 Medical Oncology, Azienda Ospedaliera Universitaria Integrata Verona-”Borgo Roma”, Verona, ITALY, 3 Biostatistics, Regina Elena Institute, Roma, ITALY, 4 Medical Oncology, USL 10 Firenze, Firenze, ITALY, 5 Division Medical Oncology A, Istituto Regina Elena, Roma, ITALY Purpose: Although FOLFIRINOX has become one of the standard option for the treatment of aPDAC, tolerability and safety issues, with particular regard to hematologic toxicity and increased risk of AE in pts carrying biliary stents, may represent a barrier for the routinely adoption in clinical practice. Methods: The clinical reports of 36 aPDAC pts undergone 1st-line FOLFIRINOX in 2 different institutions were reviewed. Toxicities, activity and efficacy were determined according to 1) primary G-CSF prophylaxis (dd 7-9-11; yes/no 21/15 pts), and 2) presence/absence biliary stent. Results: Pts characteristics: N°: 36; cycles: 241, M/F: 22/14; median age: 57 yrs [range 37-70]; ECOG PS 0/1: 33/3; stage III/IV: 10/26. G3/4 toxicity occurred in 50% reduction in CA19.9. Conclusions: These data indicate that FOLFIRINOX seems to be well tolerated and easily manageable in young (50%, no PD after 6 months of CT were randomized to O (arm A) or MS at 37.5 mg daily until PD or a maximum of 6 months (arm B). Functional polymorphisms of 6 genes involved in sunitinib activity, metabolism and transport (VEGFA, VEGFR-2, CYP3A5, CYP1A1, ABCB1, ABCG2) were studied in genomic DNA from baseline blood samples, using PCR Taqman®-probes-based assays. Associations of genotypes with overall survival (OS) and progression-free survival (PFS) were evaluated by Log-rank test. Genotyping was successfully performed in all the DNA samples of 43 consenting pts of 55 enrolled in the trial (78%; arm A/B: 83%/73%; p = 0.39). Significantly longer OS was observed in 7 pts harbouring the ABCB1 3435TT genotype (group-1; median OS 20 months) as compared to 36 pts with 3435CC/CT genotype (group-2; median OS 7 months; p = 0.027). Median OS was 26 months in 4 group-1 arm B pts, 7 months in 15 group-2 arm B pts (p = 0.12); 16 months in 3 group-1 arm A pts and 9 months in 21 group-2 arm A pts (p = 0.67). No OS difference was observed in 28 pts harbouring the VEGFA -634GC-CC genotype ix240 | Abstracts Volume 23 | Supplement 9 | September 2012
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Annals of Oncology www.annonc.oxfor
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subscriptions A subscription to Ann
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Annals of Oncology Official Journal
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The European Society for Medical On
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Audit Committee Chair: Fortunato Ci
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Familial cancer Judith Balmaña, Ba
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ESMO 2012 Congress Travel Grants 47
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Exhibitors The following companies
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ESMO Fellowships, 1989-2011 The Eur
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Ondrej Gojis, Czech Republic 2008-2
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abstracts hpv biology and implicati
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abstracts the characterization of l
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abstracts description of intra-tumo
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prevent cell death. It is anticipat
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22IN TARGETING THE HOST IN TNBC G.
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abstracts a paradigm shift in early
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abstracts how can medical oncologis
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feasibility), but by how high the c
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abstracts re-inventing the medical
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abstracts emerging diagnostic and t
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abstracts biologically based treatm
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abstracts molecular targets in mali
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abstracts melanoma therapy: from fr
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diagnosis and can also be used for
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analysis at 11 months median follow
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mouse model of Kras mutant NSCLC. I
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abstracts subtyping soft tissue sar
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abstracts key topics in supportive
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ESMO-CSCO Joint Symposium: Building
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ESMO-EANM-ESR Joint Symposium: Imag
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ESMO-ESTRO Joint Symposium: Innovat
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ESMO-MASCC Joint Symposium: Integra
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ESO Society Symposium: Celebrating
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Results: TIMP-1 expression was incr
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will benefit from this targeted the
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cytomegalovirus (CMV). Analysis of
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functional consequences of Endoglin
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elationship between the ROR score,
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183P EPIDERMAL GROWTH FACTOR RECEPT
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Plasma adiponectin level on the pre
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Table: 198P PFS OS Median, mo HR Me
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204P EVALUATION OF PTEN AND PIK3CA
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Material and methods: We searched P
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Results: The median concentration o
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Table: 226P Methods: Pts were rando
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However, additional analysis sugges
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number of biomarkers have been trie
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Table: 248O 249PD PROTEOMIC PREDICT
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Conclusions: BW and serum Ctrough o
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261P BREAST CANCER SUBTYPES AND OUT
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90 mg/m2-cyclophophamide 600 mg/m2
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to 9 weeks after dosing. Trastuzuma
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Patients and methods: We reviewed d
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sector patients. The aim of this st
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Linear Logistic Model with Relaxed
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Results: The median CTC fold change
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312: Table: Chemotherapy uptake wit
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abstracts breast cancer, locally ad
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Results: 8 trials (2092 pts) with 1
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absolute difference of median value
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Novartis, Genentech, and sanofi-ave
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Results: Three RCTs with 1023 patie
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collected from all patients for det
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355P FIRST REPORT OF LONG-TERM RESP
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361P A RETROSPECTIVE ANALYSIS OF PL
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publications and aggregated in a me
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Thus the primary aim to target BCSC
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383 WHY DO WOMEN WITH BREAST CANCER
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Results: We evaluated 76 pts with M
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more than 6 cycles of capecitabine.
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406TiP PHASE II TRIAL OF PRIMARY SY
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abstracts CNS tumors 410O CONDITION
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Conclusions: Our data suggested tha
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Conclusions: As in other cancer typ
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432 GAMMA KNIFE RADIOSURGERY AS A M
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abstracts developmental therapeutic
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1PR), but no responses were seen in
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RO and Cd, as well as PD data for c
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and vulvar Ca), and 11 SDs were obs
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knowing HLA-A status double-blindly
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Acquired-resistance to EGFR inhibit
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474P PHASE 1 STUDY OF THE SELECTIVE
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TST is active in breast and gastric
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Treatment-induced shedding of circu
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Methods: Either co-cultures of peri
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501 PRECLINICAL DATA INVESTIGATING
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509TiP LUX-LUNG 8: A RANDOMIZED, OP
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(P = 0.64). Synchronous BBC was sig
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abstracts gastrointestinal tumors,
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Disclosure: M. Lee: I am an employe
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plus intravenous Bev(7.5mg/kg q 21d
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anti-EGFR treatment. The present st
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patients harboring a T/T genotype t
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Page 235 and 236: subgroup. Taking into consideration
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879 TREATMENT OF PATIENTS WITH META
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Median overall survival (OS) was 26
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abstracts Genitourinary tumors, pro
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and week 13 BPI-SF Q3 scores), 28%
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Working Group (PCWG)-2 guidelines r
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atio HR 0.39; CI 0.18, 0.83, p = 0.
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We observed tumor responses and pro
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Here we report emerging data from t
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928P LHRH AGONIST-INDUCED SUPPRESSI
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Disclosure: S. Oudard: Has acted as
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939P NEOADJUVANT SIPULEUCEL-T IN LO
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945 BONE TURNOVER MARKERS AND POTEN
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952 SEQUENTIAL ANDROGEN DEPRIVATION
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managed in a multidisciplinary (MD)
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or hypercalcemia at screening; prio
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meeting. The prevalence of LGSC is
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Table: 975PD Continued AMG 386 + pa
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physicians in the U.S. and Europe.
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989P PHASE II STUDY OF COMBINATION
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elated with stage, nodal involvemen
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1004P CASE CONTROL STUDY ON TWO DIF
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eight patients who had infertility
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abstracts head and neck cancer 1016
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same CT/RT; Arm B2: 3 cycles of ind
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induction chemotherapy in the treat
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patients. We have developed a rando
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evaluated by the screening instrume
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morbidities that radiation would le
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Conclusions: Through adequate selec
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abstracts hematological malignancie
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anthracyclines in vitro. A favorabl
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1076P RITUXIMAB PLUS SUBCUTANEOUS C
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than the standard target of ≥2.5
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Patients: From November 2002 to May
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lymphadenopathy and multiple cutane
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prospective non-interventional stud
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Funding: GSK Biologicals Disclosure
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survival rates of 13-25% (Prieto et
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high response rates and prolonged p
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GlaxoSmithKline, Merck Sharp & Dohm
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advisor for Merck Sharp & Dohme, an
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or cutaneous melanoma. A survival u
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systemic therapy or were intolerant
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abstracts neuroendocrine tumors and
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morbidity, with G3 tumors behaving
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pts. Poorly differentiated endocrin
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Adenocarcinoma was present in 25 pa
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Method: Endobronchial ultrasound gu
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widely used by single agent or plat
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disease after surgery were treated
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stage IIIA NSCLC, EML4-ALK fusion-p
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1200P CONCOMITANT CHEMORADIATION GI
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Patients and methods: The study was
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months (95% CI:13-25). The PFS and
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maintenance therapy had favourable
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abstracts non-small cell lung cance
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Ingelheim, GSK Biologicals (compens
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1234PD RANDOMIZED PHASE III TRIAL O
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GlaxoSmithKline (myself, compensate
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1243P IDENTIFICATION OF MICRORNA (M
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N-arm n=34 P-arm n=32 All n=66 Male
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1255P POPULATION BASED EVALUATION O
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1262P DISTINCT SPREAD OF EGFR MUTAT
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1268P VISUAL DISTURBANCES IN PATIEN
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MERCK SERONO: Advisor, speaker in s
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Conclusions: These data from SAiL a
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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.
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:
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