Download the ESMO 2012 Abstract Book - Oxford Journals

More documents

Recommendations

Info

Annals of Oncology Methods: The presence and relative quantity of two ALK exon spanning transcript targets located before (ALK-5’) and after (ALK-3’) the translocation breakpoints of this gene were assessed with qRT-PCR in 198 NSCLC RNA samples from paraffin tissues upon stringent intra- and inter-run assay performance validation. ALK mRNA expression was compared with ALK gene status assessed with FISH. Patients had been treated in the adjuvant and/or 1 st line setting. None of them received crizotinib. Results: Four patterns of ALK mRNA expression emerged: tumors negative for both transcripts (85/198, 42.9%) or positive for both (56/198, 28.3%), which were considered as close to normal (ALK-N); and, ALK-5’ positive only (34/198, 17.2%) or ALK-3’ positive only (23/198, 11.6%), which were termed as aberrant (ALK-A). ALK translocation was observed in 9/124 cases (7.3%). ALK copies >2.2 were noticed in 40 cases (32.3%) with >6 copies in 26 cases (21%) and overall complex gene gain patterns. ALK mRNA was unrelated to ALK translocation, but ALK-3’ was associated with increased ALK gene copies (p = 0.017). ALK-A was more common in stage IIIB-IV tumors, while ALK mRNA and gene copy gains were not associated with gender, smoking and histology. ALK gene status was not associated with patient outcome. In comparison to patients with tumors expressing ALK-N, those with ALK-A had a significantly shorter overall survival (OS, median 29.3 vs. 13.1 months, CI95% 19.1-39.6 vs. 5.4-20.9, p = 0.0007). The same unfavorable impact of ALK-N vs. ALK-A was observed on stage IIIB-IV patient OS (median 17.5 vs. 11 months, CI95% 9.1-26.0 vs. 6.6-15.3, p = 0.0050). Conclusions: ALK gene status and mRNA expression seem to suffer a complex pathology in NSCLC. When expressed, ALK mRNA may be fragmented, possibly due to currently unknown genomic alterations. Aberrant ALK mRNA expression appears to have an unfavorable prognostic impact on NSCLC patient outcome; its role on NSCLC biology merits further evaluation. Disclosure: All authors have declared no conflicts of interest. 1313 PROGNOSTIC SIGNIFICANCE OF EGFR, HER-2, CEA ON CIRCULATINGTUMOUR CELLS (CTCS) IN PATIENTS WITH METASTATIC NON-SMALL-CELL LUNG CANCER (MNSCLC) C. Loretelli 1 , E. Galizia 2 , M. Scartozzi 1 , R. Giampieri 1 , D. Gagliardini 1 , C. Brugiati 1 , S. Cascinu 1 , R. Cellerino 1 1 Clinica di Oncologia Medica, AOU Ospedali Riuniti Ancona Università Politecnica delle Marche, Ancona, ITALY, 2 Oncologia Medica, Ospedale “E. Profili”, Fabriano, ITALY Purpose: We aimed to assess the role of CTCs in providing prognostic information of mNSCLC patients receiving chemotherapy. Patients and methods: In this single-center prospective study, blood samples for CTCs analysis were obtained from patients with previously untreated mNSCLC. CTCs were measured using an epithelial cell adhesion molecule-based immunomagnetic technique. Immunomagnetic bead enrichment for cells expressing epithelial cell adhesion molecule (EpCAM) was performed, followed by multi-marker quantitative real-time PCR of a panel of marker genes: EGFR, HER-2, CEA. Results: We analysed 45 patients with mNSCLC: 24 adenocarcinoma, 8 squamous cell carcinoma and 13 poorly differentiated. EGFR, HER-2 and CEA expression were found in CTCs of respectively 12, 5 and 11 patients. Globally, 31 patients (68.9%) progressed during treatment, whereas disease control (i.e. patients with partial/complete response or stable disease) was achieved in 14 patients (31.1%). EGFR expression was detected in 11/31 patients with disease progression (35.5%) and in only 1 out of 14 patients with disease controlled (7.1%) (p 0.07). HER-2 expression was detected in 3/31 patients with disease progression (9.7%) and in 2/ 14 patients with disease controlled (14.3%) (p 0.64). CEA expression was detected in 10/31 patients with disease progression (32.3%) and in 1/14 patients with disease controlled (7.1%) (p 0.13). Only EGFR expression in CTCs showed a correlation with clinical outcome, expressed by progression free survival (PFS). Patients with and without EGFR expression in CTCs were homogeneous for clinical characteristics. PFS was 2.8 v 2.3 months (p 0.03) respectively for patients without and with EGFR expression. Conclusion: CTCs are detectable in patients with mNSCLC and could show novel prognostic factor for this disease. Further validation is warranted before routine clinical application. Disclosure: All authors have declared no conflicts of interest. 1314 ASSESSMENT OF THE PREDICTIVE/ PROGNOSTIC VALUE OF THE MYELOID-DERIVED SUPPRESSOR CELLS (MDSC) AND REGULATORY T CELLS (TREGS) IN NON-SMALL CELL LUNG CANCER (NSCLC). PRELIMINARY RESULTS E.K. Vetsika 1 , E. Skalidaki 1 , A. Koutoulaki 1 , D. Mavroudis 2 , V. Georgoulias 2 , A. Kotsakis 2 1 Laboratory of Tumor Cell Biology, University of Crete, School of Medicine, Heraklion, GREECE, 2 Medical Oncology, University Hospital of Heraklion, Heraklion, GREECE Background: The circulating MDSCs and Tregs in cancer patients suppress immune system. This study is investigating the expression of the MDSCs and Tregs in the peripheral blood of NSCLC patients and their correlation with the clinical outcome of the 1 st line chemotherapy. Methods: 62 chemotherapy naive patients (57 males) with stage IIIB/ IV NSCLC have been enrolled in this study, so far; median age 67. Peripheral blood was collected prior to treatment. 19 healthy, aged-matched donors (12 males) were used as controls. The distinct MDSC subpopulations [A (monocytic): CD11b + CD14 + CD15 − CD33 + CD13 + IL-4R + Lin low/- HLA-DR − ; B (monocytic): CD11b + CD14 + CD15 + CD33 + CD13 + IL-4R + Lin low/- HLA-DR − and C (granulocytic): CD11b + CD14 − CD15 + CD33 + CD13 + IL-4R + )], CD4 + Tregs (CD4 + CD25 +high CD127 low FoxP3 + CD39 + CD13 + ) and CD8 + Tregs (CD3 + CD8 + CD25 + CD45RO + CD13 + CCR7 + FoxP3 + CD39 + ) were determined by using flow cytometry. A comparison of the overall survival (OS) and the progression-free survival (PFS) according to the frequency of the MDSC and Tregs was performed (high expression defined as the percentage of cells above the 75% percentile of the controls). Results: The levels of Tregs prior to treatment did not differ from the controls’. Patients with progression (PD) during the 1 st line treatment had significantly elevated percentage of CD4 + (24.6 ± 8.5) and CD8 + (0.7± 0.2) Tregs at baseline compared to those with no PD (3.7± 1.8, p = 0.04; 0.1± 0.05, p= 0.03, respectively). In contrast, MDSCs were significantly increased (A: 3.8 ±0.7; Β: 2.5 ± 0.5 and C: 10.8 ± 2.3) in patients compared to controls (0.8 ± 0.4, p = 0.001; 0.5 ± 0.2, p= 0.01, and 2.7 ± 1.3, p= 0.05, respectively) but that difference was not associated with response to treatment. Patients with normal CD8 + Tregs levels at baseline had higher OS and PFS compared to those with high levels (13.2 mo vs 7.9 mo, p= 0.02 and 13.1 mo vs 3.7 mo, p= 0.003, respectively). Conclusion: The MDSCs are elevated in NSCLC. The increased expression of CD4 + και CD8 + Tregs negatively correlated with the treatment outcome, indicating that CD4 + and CD8 + Tregs could be a potential predictive/prognostic biomarker. The study is still opened to accrual and more mature data will be presented at the meeting. Disclosure: All authors have declared no conflicts of interest. 1315 CYTOLOGY SAMPLES (S) FOR EGFR AND KRAS MUTATION (MUT) TESTING IN NON-SMALL-CELL LUNG CANCER (NSCLC).EXPERIENCE FROM A SINGLE INSTITUTION T. Moran Bueno1 , E. Castella Fernandez2 , M. Tierno Garcia1 ,C. Buges Sanchez1 , C. Queralt Herrero1 , M. Perez Cano1 , D. Naranjo Hans2 ,F. Andreo Garcia3 , L. Capdevila Riera1 , R. Rosell1 1 Medical Oncology Department, Catalan Institute of Oncology Badalona, Hospital Universitari Germans Trias i Pujol, Badalona, SPAIN, 2 Pathology Department, Hospital Universitari Germans Trias i Pujol, Badalona, SPAIN, 3 Pulmonology Department, Hospital Universitari Germans Trias i Pujol, Badalona, SPAIN Background: Targeted therapy has yielded impressive clinical outcomes in advanced NSCLC. For molecular testing, cytology samples are not commonly used since the tumor content is less likely to be adequate. At ICO-Badalona, Hospital Germans Trias i Pujol we have used cytology specimens when biopsies are not available. We describe the general results when using cytology specimens in NSCLC to detect EGFR and KRAS mut. Methods: From January 2007 to February 2012, 227 cytology samples from patients with NSCLC were collected at the Department of Pathology as cell blocks or fresh specimens extended over an appropriate slide (MembraneSlide 1.0 PEN, Zeiss®). Tumor cells (8-150) were captured by laser microdissection. DNA sequencing for Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds409 | ix431
EGFR mut at exons 18, 19, 21, and KRAS mut at codons 12 and 13 and allelic discrimination technique for EGFR mut at exon 20 were performed at Molecular Biology Laboratory (ICO-Badalona). Results: EGFR mut were tested in 227 s. The overall output was 86.3% (15 not evaluable, 8 insufficient tissue, 4 no tumor cells, 4 not done). EGFR mut were detected in 8.81% (20/227). KRAS mut were tested in 41 s with results in 33, 80.5% (2 not evaluable, 3 insufficient tumor cells 1 no tumor and 2 not done). KRAS mut were positive in 14.6% (6/41). The output for cell block was 83.3% (124/148) and testing was not possible in 24 s (11 not evaluable, 6 insufficient tumor cells, 4 not tumor and 3 not done). The output for fresh specimens was 91.1% (72/79) and was not possible in 7 s (4 not evaluable, 2 insufficient tumor cells and 1 not done). Conclusions: Our results support the use of cytology samples for EGFR and KRAS molecular testing in NSCLC when biopsy specimens are not available. Both fresh specimens and cytology blocks have been used and are suitable for molecular testing. Disclosure: All authors have declared no conflicts of interest. 1316 FEASIBILITY AND USEFULNESS OF DETERMINING EGFR AND KRAS MUTATIONS IN CYTOLOGICAL SAMPLES AND CNB OF NSCLC USING AN AUTOMATED REAL-TIME PCR SYSTEM M.D. Lozano 1 , T. Labiano 1 , M. Montañana 1 , J.I. Echeveste 1 , A. Gurpide 2 , J.L. Pérez - Gracia 2 , F. Shieh 3 , T. Ramos 4 , J. Zulueta 5 , S. Martin Algarra 2 1 Pathology, University of Navarra, Pamplona, SPAIN, 2 Clinical Oncology, Clinica Universitaria de Navarra, Pamplona, SPAIN, 3 Roche Molecular System, Roche Molecular System, Pleasanton, UNITED STATES OF AMERICA, 4 Roche Diagnostics, Barcelona, SPAIN, 5 Pulmonary Medicine, Clinica Universidad de Navarra, Pamplona, SPAIN Background: EGFR and KRAS gene mutations guide treatment selection in non-small cell lung cancer (NSCLC) patients. About 70%-80% of these patients are diagnosed at advanced stage, and mutational analysis has to be performed in small samples: core needle biopsy (CNB) and fine needle aspiration (FNA) cytology. Cobas® EGFR Mutation Test has been CE-IVD marked for the detection of 41 mutations in formalin-fixed-paraffin-embedded (FFPE) NSCLC specimens. No validation studies have been performed using cytological samples. Determining the feasibility of cobas® test on such samples is an important step to extend the benefits of molecular targeted therapy. Methods: EGFR and KRAS mutations were studied in 64 non-selected samples from NSCLC patients: 31 CNB and 33 FNA. DNA was extracted directly from stained smears in FNA samples and from 4-micron sections in CNB. All samples contained at least 50% of tumor cells. All cases were studied using the cobas® test, and FNA samples were also analyzed by direct sequencing. DNA was extracted using the cobas® DNA Sample Preparation Kit. DNA concentration and DNA ratio of sample absorbance at 260/280nm (A260/280) were registered. U Mann Whitney test was used. Results: CNB diagnosis was: 23 SqCC, 6 AC, 1 BAC, and 1 NSCLC-NOS. FNA diagnosis was: 26 AC, 3 SqCC, 1 BAC, 1 LCC, and 2 NSCLC-NOS. Mean DNA concentration from CNB was 23.07ng/ul ± 20.99, and from FNA samples 12.41ng/ul ± 20.04 (p < 0.001). However A260/280 was 1.61 ± 0.26 and 1.71 ± 0.55 respectively (p = 0.666). Mutational analysis results from all 31 CNB and from 19 FNA cases are shown in Table 1. Sanger sequencing in all FNA cases rendered concordant results. Updated results will be presented. FNA CNB EGFR WT 6 28 EXON 19 DEL 2 1 EXON 20 INS 0 1 INVALID 1 1 KRAS WT 9 26 12/13 MUTATED 9 4 INVALID 1 1 Conclusions: Assessment of EGFR and KRAS mutations in FNA and CNB samples using cobas® EGFR and KRAS test is feasible and reliable. Quality of DNA (A260/ 280) using cobas® DNA Sample Preparation Kit in FNA samples is similar to those from CNB. Molecular results from FNA samples using cobas® test and direct sequencing are concordant, though cobas® tests are simpler, faster and easier to use. Disclosure: All authors have declared no conflicts of interest. Annals of Oncology 1318 FREQUENCY AND SPECTRUM OF EGFR MUTATIONS IN MOROCCAN LUNG ADENOCARCINOMA PATIENTS I. Elghissassi 1 , H. Inrhaoun 2 , A. Boukir 2 , Y. Bensouda 2 , H. Mrabti 1 , H. Errihani 1 1 Medical Oncology, Institut National d’Oncologie Sidi Mohamed Ben Abdellah, Rabat, MOROCCO, 2 Medical Oncology, National Institute of Oncology, Rabat, MOROCCO Background: EGFR mutations reported in lung cancer are potential therapeutic targets leading to improved response with tyrosine kinase inhibitors (TKI). The frequency of EGFR mutations is ethnicity-dependent with a higher proportion in Asian populations (30%) than in Caucasians (10-15%). Furthermore, exon 19 mutation is associated with better response to EGFR-TKI compared to exon 21 mutation. The aim of this study was to report the frequency and spectrum of EGFR mutations in unselected group of Moroccan lung adenocarcinoma patients. Methods: We summarized the result of the EGFR mutation analysis in exons 18-21 for 83 patients performed from November 2010 to march 2012 in three laboratories in Rabat. Mutation detection techniques were PCR amplification and sequencing. Only Moroccan lung adenocarcinoma patients were included. Results: The overall frequency of the EGFR mutation was 22%. It was more frequent in female patients (58%) than in male ones (5%). Mutations were mainly detected in the exon 19 (67%) followed by exon 21 (17%) and exon 20 (11%), while that in the exon 18 was rare (5%). Conclusion: Some one fifth of Moroccan lung adenocarcinoma tumors harbor EGFR mutations. This mutation frequency is higher than that found in Caucasians but lower than in Asian population. The high rate of exon 19 mutation in Moroccan population may result in a higher frequency of response to TKI Disclosure: All authors have declared no conflicts of interest. 1319 THE ROLE OF EPITHELIAL-MESENCHYMAL TRANSITION AND IGF-1R EXPRESSION IN PREDICTION OF GEFITINIB ACTIVITY AS THE SECOND-LINE TREATMENT FOR ADVANCED NON-SMALL CELL LUNG CANCER W. Zhang, B. Chen Oncology, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou, Guangzhou, CHINA We retrospectively analyzed the relationship of EMT, IGF-1R and gefitinib efficacy in 53 NSCLC patients who accepted gefitinib as the second-line treatment. Compared with EMT (+), EMT (-) showed a higher ORR in both EGFR mutation subgroup (50.0% vs. 28.6%) and EGFR wild-type subgroup (20.0% vs. 4.5%), and a longer MST in EGFR wild-type subgroup (6 months vs. 3 months, P = 0.014). IGF-1R (-) showed a higher ORR tendency than IGF-1R (+) in EGFR mutation patients (54.6% vs. 30.0%) and EGFR wild-type patients (18.2% vs. 4.8%). EMT and IGF-1R are correlated with the efficacy of gefitinib as the second-line therapy for NSCLC, especially in patients with wild- type EGFR. (This work is supported by grants from the National Foundation of Natural Science, China. No. 81172225, No. 81101821 and No. 81000819) Disclosure: All authors have declared no conflicts of interest. 1320 PERIODIC MEASUREMENT OF N-TELOPEPTIDES OF TYPE I COLLOGEN IN SERUM (SNTX) FOR EARLY DIAGNOSIS OF BONE METASTASIS IN PATIENTS WITH LUNG CANCER H. Daga 1 , M. Tamiya 2 , S. Tokunaga 3 , K. Taira 3 , H. Okada 3 , H. Suzuki 2 , N. Okamoto 2 , N. Morishita 2 , T. Hirashima 2 , K. Takeda 3 1 Department of Clinical Oncology, Osaka City General Hospital, Osaka, JAPAN, 2 Thoracic Malignancy, Osaka Prefectural Hospital Organization Osaka Prefectural Medical Center for Respiratory and Allergic Diseases, Habikino-City, JAPAN, 3 Clinical Oncology, Osaka City General Hospital, Osaka, JAPAN Background: The bone resorption biomarker sNTx has been previously shown to add value as an aid in the diagnosis of bone metastasis in patients with lung cancer. The objective of this prospective study was to determine if periodic sNTx measurements could lead to early diagnosis of bone metastasis in patients with lung cancer. Methods: Patients with newly diagnosed organ-confined lung cancer were enrolled. sNTx values were determined once each month using the OSTEOMARK TM serum NTx assay (Alere Medical). The presence or absence of bone metastasis was determined by monthly physical examination and by bone scintigraphy every 3 ix432 | Abstracts Volume 23 | Supplement 9 | September 2012
Page 1 and 2:
Annals of Oncology www.annonc.oxfor
Page 3 and 4:
subscriptions A subscription to Ann
Page 6 and 7:
Annals of Oncology Official Journal
Page 8 and 9:
The European Society for Medical On
Page 10 and 11:
Audit Committee Chair: Fortunato Ci
Page 12 and 13:
Familial cancer Judith Balmaña, Ba
Page 14 and 15:
ESMO 2012 Congress Travel Grants 47
Page 16 and 17:
Exhibitors The following companies
Page 18 and 19:
ESMO Fellowships, 1989-2011 The Eur
Page 20:
Ondrej Gojis, Czech Republic 2008-2
Page 23 and 24:
abstracts hpv biology and implicati
Page 25 and 26:
abstracts the characterization of l
Page 27 and 28:
abstracts description of intra-tumo
Page 29 and 30:
prevent cell death. It is anticipat
Page 31 and 32:
22IN TARGETING THE HOST IN TNBC G.
Page 33 and 34:
abstracts a paradigm shift in early
Page 35 and 36:
abstracts how can medical oncologis
Page 37 and 38:
feasibility), but by how high the c
Page 39 and 40:
abstracts re-inventing the medical
Page 41 and 42:
abstracts emerging diagnostic and t
Page 43 and 44:
abstracts biologically based treatm
Page 45 and 46:
abstracts molecular targets in mali
Page 47 and 48:
abstracts melanoma therapy: from fr
Page 49 and 50:
diagnosis and can also be used for
Page 51 and 52:
analysis at 11 months median follow
Page 53 and 54:
mouse model of Kras mutant NSCLC. I
Page 55 and 56:
abstracts subtyping soft tissue sar
Page 57 and 58:
abstracts key topics in supportive
Page 59 and 60:
ESMO-CSCO Joint Symposium: Building
Page 61 and 62:
ESMO-EANM-ESR Joint Symposium: Imag
Page 63 and 64:
ESMO-ESTRO Joint Symposium: Innovat
Page 65 and 66:
ESMO-MASCC Joint Symposium: Integra
Page 67 and 68:
ESO Society Symposium: Celebrating
Page 69 and 70:
Results: TIMP-1 expression was incr
Page 71 and 72:
will benefit from this targeted the
Page 73 and 74:
cytomegalovirus (CMV). Analysis of
Page 75 and 76:
functional consequences of Endoglin
Page 77 and 78:
elationship between the ROR score,
Page 79 and 80:
183P EPIDERMAL GROWTH FACTOR RECEPT
Page 81 and 82:
Plasma adiponectin level on the pre
Page 83 and 84:
Table: 198P PFS OS Median, mo HR Me
Page 85 and 86:
204P EVALUATION OF PTEN AND PIK3CA
Page 87 and 88:
Material and methods: We searched P
Page 89 and 90:
Results: The median concentration o
Page 91 and 92:
Table: 226P Methods: Pts were rando
Page 93 and 94:
However, additional analysis sugges
Page 95 and 96:
number of biomarkers have been trie
Page 97 and 98:
Table: 248O 249PD PROTEOMIC PREDICT
Page 99 and 100:
Conclusions: BW and serum Ctrough o
Page 101 and 102:
261P BREAST CANCER SUBTYPES AND OUT
Page 103 and 104:
90 mg/m2-cyclophophamide 600 mg/m2
Page 105 and 106:
to 9 weeks after dosing. Trastuzuma
Page 107 and 108:
Patients and methods: We reviewed d
Page 109 and 110:
sector patients. The aim of this st
Page 111 and 112:
Linear Logistic Model with Relaxed
Page 113 and 114:
Results: The median CTC fold change
Page 115 and 116:
312: Table: Chemotherapy uptake wit
Page 117 and 118:
abstracts breast cancer, locally ad
Page 119 and 120:
Results: 8 trials (2092 pts) with 1
Page 121 and 122:
absolute difference of median value
Page 123 and 124:
Novartis, Genentech, and sanofi-ave
Page 125 and 126:
Results: Three RCTs with 1023 patie
Page 127 and 128:
collected from all patients for det
Page 129 and 130:
355P FIRST REPORT OF LONG-TERM RESP
Page 131 and 132:
361P A RETROSPECTIVE ANALYSIS OF PL
Page 133 and 134:
publications and aggregated in a me
Page 135 and 136:
Thus the primary aim to target BCSC
Page 137 and 138:
383 WHY DO WOMEN WITH BREAST CANCER
Page 139 and 140:
Results: We evaluated 76 pts with M
Page 141 and 142:
more than 6 cycles of capecitabine.
Page 143 and 144:
406TiP PHASE II TRIAL OF PRIMARY SY
Page 145 and 146:
abstracts CNS tumors 410O CONDITION
Page 147 and 148:
Conclusions: Our data suggested tha
Page 149 and 150:
Conclusions: As in other cancer typ
Page 151 and 152:
432 GAMMA KNIFE RADIOSURGERY AS A M
Page 153 and 154:
abstracts developmental therapeutic
Page 155 and 156:
1PR), but no responses were seen in
Page 157 and 158:
RO and Cd, as well as PD data for c
Page 159 and 160:
and vulvar Ca), and 11 SDs were obs
Page 161 and 162:
knowing HLA-A status double-blindly
Page 163 and 164:
Acquired-resistance to EGFR inhibit
Page 165 and 166:
474P PHASE 1 STUDY OF THE SELECTIVE
Page 167 and 168:
TST is active in breast and gastric
Page 169 and 170:
Treatment-induced shedding of circu
Page 171 and 172:
Methods: Either co-cultures of peri
Page 173 and 174:
501 PRECLINICAL DATA INVESTIGATING
Page 175 and 176:
509TiP LUX-LUNG 8: A RANDOMIZED, OP
Page 177 and 178:
(P = 0.64). Synchronous BBC was sig
Page 179 and 180:
abstracts gastrointestinal tumors,
Page 181 and 182:
Disclosure: M. Lee: I am an employe
Page 183 and 184:
plus intravenous Bev(7.5mg/kg q 21d
Page 185 and 186:
anti-EGFR treatment. The present st
Page 187 and 188:
patients harboring a T/T genotype t
Page 189 and 190:
551P ADJUVANT CHEMOTHERAPY (AC) USE
Page 191 and 192:
experienced significantly more ≥
Page 193 and 194:
functioning scales. Exploratory ana
Page 195 and 196:
oxaliplatin (100 mg/m 2 )/raltitrex
Page 197 and 198:
572P PANERB STUDY: WHICH CATEGORY O
Page 199 and 200:
Results: 92/114 patients were preop
Page 201 and 202:
585P CHANGES IN THE INTESTINAL ENVI
Page 203 and 204:
592P PHASE II TRIAL OF COMBINED CHE
Page 205 and 206:
minutes. In a previous study, 30-mi
Page 207 and 208:
Patients and methods: Chemotherapy-
Page 209 and 210:
612P ARE PATIENTS WITH RESECTABLE R
Page 211 and 212:
Conclusions: AMPK and ACC activatio
Page 213 and 214:
of surgical monotherapy in patients
Page 215 and 216:
Table: 632 633 AFLIBERCEPT/FOLFIRI
Page 217 and 218:
factors play the determining role i
Page 219 and 220:
Abstract withdrawn in exceptional c
Page 221 and 222:
were respectively 10.6 vs 8.5 vs 3.
Page 223 and 224:
Results: 20 gastrointestinal cancer
Page 225 and 226:
abstracts gastrointestinal tumors,
Page 227 and 228:
Day 8. A second identical course wa
Page 229 and 230:
proven in stage I GC. The aim of th
Page 231 and 232:
Conclusions: Longer OS to FOLFOX wa
Page 233 and 234:
692P PRELIMINARY SAFETY DATA FROM A
Page 235 and 236:
subgroup. Taking into consideration
Page 237 and 238:
Results: Three years of adjuvant im
Page 239 and 240:
considered sufficient to give an 80
Page 241 and 242:
721P FIRST-LINE TREATMENT WITH FOLF
Page 243 and 244:
after Gem-based therapy. The additi
Page 245 and 246:
735P RADIOGRAPHIC PARAMETERS IN PRE
Page 247 and 248:
validate the revised AJCC 7th stagi
Page 249 and 250:
Results: Among 862 MM we identified
Page 251 and 252:
Results: Frequently reported advers
Page 253 and 254:
gastric cancer patients with CNS me
Page 255 and 256:
discriminate the prognosis of HCC p
Page 257 and 258:
prospective, non-interventional stu
Page 259 and 260:
abstracts genitourinary tumors, non
Page 261 and 262:
787O EXTERNAL VALIDATION OF THE ASS
Page 263 and 264:
patient preference for P over S, an
Page 265 and 266:
798PD OPEN-LABEL PHASE II TRIAL OF
Page 267 and 268:
Hb, PS and LM. Median PFS for patie
Page 269 and 270:
may have led to reduced dose and sh
Page 271 and 272:
Results: 1,622 patients were identi
Page 273 and 274:
RCC) was designed to address an unm
Page 275 and 276:
Patients and methods: This is a sin
Page 277 and 278:
treatment at week 4, and week 12 by
Page 279 and 280:
effective in second or further line
Page 281 and 282:
Conclusions: In pts with RCC treate
Page 283 and 284:
using Drug inCode ® pharmacogeneti
Page 285 and 286:
Table: 857P standard, but is not av
Page 287 and 288:
efused HDCT. Of 23 patients, 20 com
Page 289 and 290:
we identified 49 and 220 patients w
Page 291 and 292:
879 TREATMENT OF PATIENTS WITH META
Page 293 and 294:
Median overall survival (OS) was 26
Page 295 and 296:
abstracts Genitourinary tumors, pro
Page 297 and 298:
and week 13 BPI-SF Q3 scores), 28%
Page 299 and 300:
Working Group (PCWG)-2 guidelines r
Page 301 and 302:
atio HR 0.39; CI 0.18, 0.83, p = 0.
Page 303 and 304:
We observed tumor responses and pro
Page 305 and 306:
Here we report emerging data from t
Page 307 and 308:
928P LHRH AGONIST-INDUCED SUPPRESSI
Page 309 and 310:
Disclosure: S. Oudard: Has acted as
Page 311 and 312:
939P NEOADJUVANT SIPULEUCEL-T IN LO
Page 313 and 314:
945 BONE TURNOVER MARKERS AND POTEN
Page 315 and 316:
952 SEQUENTIAL ANDROGEN DEPRIVATION
Page 317 and 318:
managed in a multidisciplinary (MD)
Page 319 and 320:
or hypercalcemia at screening; prio
Page 321 and 322:
meeting. The prevalence of LGSC is
Page 323 and 324:
Table: 975PD Continued AMG 386 + pa
Page 325 and 326:
physicians in the U.S. and Europe.
Page 327 and 328:
989P PHASE II STUDY OF COMBINATION
Page 329 and 330:
elated with stage, nodal involvemen
Page 331 and 332:
1004P CASE CONTROL STUDY ON TWO DIF
Page 333 and 334:
eight patients who had infertility
Page 335 and 336:
abstracts head and neck cancer 1016
Page 337 and 338:
same CT/RT; Arm B2: 3 cycles of ind
Page 339 and 340:
induction chemotherapy in the treat
Page 341 and 342:
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: Results: The patients’ characteri
Page 435 and 436: Methods: EML4-ALK fusion was screen
Page 437 and 438: Results: The median survival time (
Page 439 and 440: enefit from sustained EGFR blockade
Page 441 and 442: epresented by 19 pts (32%) female,
Page 443 and 444: and at least one prior course of ch
Page 445 and 446: Methods: NSCLC patients with radiog
Page 447 and 448: 1367TiP LONG-TERM ERLOTINIB THERAPY
Page 449 and 450: Austria, Czech Republic, Finland, G
Page 451 and 452: were every 6 weeks (wk) (S1), every
Page 453 and 454: Advantage enrollees (83% vs. 25%) [
Page 455 and 456: Results: Based on 10,000 simulation
Page 457 and 458: cancer tumors 12%, Germ cell tumor
Page 459 and 460: Material and methods: 50 lung cance
Page 461 and 462: 1414TiP IMPLEMENTATION OF CANCER RE
Page 463 and 464: abstracts palliative care 1422O EFF
Page 465 and 466: Method and results: A total of 317
Page 467 and 468: 1436P SURVEY ON MODELS OF INTEGRATI
Page 469 and 470: care unit (PCU) at the National Can
Page 471 and 472: Characteristic No. % Total 63 1 st
Page 473 and 474: hysterectomised-9.10% and cervix ca
Page 475 and 476: abstracts psycho-oncology 1462PD IN
Page 477 and 478: events, tumour response, and surviv
Page 479 and 480: abstracts sarcoma 1477O ADHESION TO
Page 481 and 482: 1481PD A PHASE II STUDY OF DOVITINI
Page 483 and 484:
1488P ORGANISATION OF SARCOMA PATIE
Page 485 and 486:
Patients and methods: From August 2
Page 487 and 488:
chemotherapy respectively. At a med
Page 489 and 490:
of this group Those with relapsed d
Page 491 and 492:
1515 PREDICTORS OF SURVIVAL IN ADOL
Page 493 and 494:
abstracts small cell lung cancer an
Page 495 and 496:
emaining receiving either CAV or to
Page 497 and 498:
1533P EXPRESSION OF WILM⍰TUMOUR G
Page 499 and 500:
more than 3 months after first line
Page 501 and 502:
lower recurrence rate of NE. Pegfil
Page 503 and 504:
egimens (HR = 2.5, p < 0.001). Phys
Page 505 and 506:
1561P PREDICTIVE DIAGNOSTICS FOR RE
Page 507 and 508:
Methods: A prospective multicentre
Page 509 and 510:
Table: 1574P Pharmacokinetic parame
Page 511 and 512:
Novartis and unrestricted research
Page 513 and 514:
studies have shown that chemotherap
Page 515 and 516:
(Grade 1) and moderate to severe (G
Page 517 and 518:
declined to relatively lower level
Page 519 and 520:
1609P PHYSICAL ACTIVITY (PA) AND PH
Page 521 and 522:
patients were admitted to the oncol
Page 523 and 524:
Dicarbamin 100 mg/day on day 5 befo
Page 525 and 526:
Results: Anemia was detected in 83.
Page 527 and 528:
important to carry out randomized s
Page 529 and 530:
abstracts translational research 16
Page 531 and 532:
expression. Then, we analyzed PB sa
Page 533 and 534:
Table: 1657P TH BV + TH HR (95% CI)
Page 535 and 536:
BRAF mutations. Circulating free DN
Page 537 and 538:
1671P PHASE I CLINICAL TRIAL OF CAN
Page 539 and 540:
1678P PREDICTIVE VALUE OF TWO PHENO
Page 541 and 542:
theorized that the PI3K/AKT pathway
Page 543 and 544:
Material and methods: 101 patients
Page 545 and 546:
overexpressing and 232 had triple n
Page 547 and 548:
author index author index A Aamdal
Page 549 and 550:
author index Badran A. ix288 (874)
Page 551 and 552:
author index Bösmüller H. ix209 (
Page 553 and 554:
author index Chen A. ix319 (966O) C
Page 555 and 556:
author index De Droogh E. ix452 (13
Page 557 and 558:
author index Esposito G. ix209 (618
Page 559 and 560:
author index Geiges G. ix306 (930P)
Page 561 and 562:
author index Hartono S. ix70 (155P)
Page 563 and 564:
author index Iwasaki H. ix542 (1694
Page 565 and 566:
author index Kodaira M. ix90 (228P)
Page 567 and 568:
author index Lichtensztejn D. ix350
Page 569 and 570:
author index Martinez A. ix496 (153
Page 571 and 572:
author index Morishita N. ix432 (13
Page 573 and 574:
author index Okamoto N. ix432 (1320
Page 575 and 576:
author index Piau S. ix456 (1401P)
Page 577 and 578:
author index Rodríguez Rodríguez
Page 579 and 580:
author index Scoggins C.R. ix371 (1
Page 581 and 582:
author index Stern L. ix272 (823P)
Page 583 and 584:
author index Trypaki M. ix429 (1308
Page 585 and 586:
author index Whitmore J.B. ix310 (9
Page 587 and 588:
subject index subject index A AAV-H
Page 589 and 590:
subject index ix115 (316TiP), ix116
Page 591 and 592:
subject index diffuse large B-cell
Page 593 and 594:
subject index (1033P), ix340 (1036P
Page 595 and 596:
subject index medical information,
Page 597 and 598:
subject index (612P), ix214 (633),
Page 599 and 600:
subject index RCC, ix274 (830P) re-
Page 601 and 602:
subject index TR-FRET, ix84 (206P)
Page 603 and 604:
drug index drug index 1248P, 1250P,
Page 605 and 606:
translational research index transl
Page 607 and 608:
Page 609:
show all

Download the ESMO 2012 Abstract Book - Oxford Journals

Create successful ePaper yourself

Delete template?

Save as template?