Download the ESMO 2012 Abstract Book - Oxford Journals

More documents

Recommendations

Info

new diagnostics 1173P A HIGHLY SENSITIVE IMMUNOHISTOCHEMICAL ASSAY TO DETECT BRAF V600E MUTATIONS IN PATIENTS WITH COLORECTAL CANCER J. Desai 1 ,F.Day 2 , A. Muranyi 3 , S. Singh 3 , K. Shanmugam 3 , T. Grogan 3 , P. Gibbs 4 , D. Williams 2 , O. Sieber 2 , P. Waring 5 1 Medical Oncology, Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Peter MacCallum Cancer Centre, Parkville, AUSTRALIA, 2 LCCI, Ludwig Institute for Cancer Research, Parkville, AUSTRALIA, 3 Ventana, Ventana Medical Systems, Tucson, AZ, UNITED STATES OF AMERICA, 4 LCCI, Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Parkville, VIC, AUSTRALIA, 5 Pathology, University of Melbourne, Parkville, AUSTRALIA Background: The BRAF V600E mutation is a well-validated negative prognostic biomarker in metastatic colorectal cancer (mCRC), and is a highly attractive drug target. Barriers to the development of agents targeting BRAF V600E in mCRC are the low rate of mutations (approximately 10%) and reliance on to sequencing-based technologies, which are not routinely available outside of large cancer centres. A simple immunohistochemistry (IHC) test, more suited to routine pathology practice, would provide much broader access to patient (pt) identification, and would also enable studies of tumor heterogeneity. Aims: To validate an IHC-based method of detecting the BRAF V600E mutation in a large cohort of community-based CRC patients. Methods: Tissue microarrays, comprising matched normal and tumor paraffin embedded tissue samples obtained from colectomy specimens from a community cohort of 505 pts with stage I–IV CRC, were tested with 2 antibodies (Ab): pBR for total BRAF and VE1 for BRAF V600E, using the Ventana UltraView and OptiView kits, respectively. IHC was assessed independently by 2 blinded pathologists, and results compared to BRAF V600E status determined by Sanger sequencing (SS). pBR negative samples were considered non - evaluable. Nine discordant cases were re-tested with a BRAF V600E SNaPshot assay. Results: Demographic features were evenly matched. SS was evaluable in 504/505; IHC in 477/505; with both evaluable in 476/505 pts. 56/476 (11.8%) pts had V600E mutations detected by SS, 65/476 (13.7%) by IHC. The positive predictive value was 84.6% (55/65). 1 pt was negative by IHC and positive on SS and SNaPshot; resulting in a negative predictive value of 99.8% (410/411 cases). There was 100% concordance between SS and SNaPshot. Further validation is ongoing, and outcome data will be available at the time of presentation. Conclusions: We have conducted a comprehensive analytical and clinical validation and feasibility analysis of an IHC-based method to detect the BRAF V600E mutation in a large community-based population of pts with CRC. Shown to be highly sensitive, we are planning to adopt this approach as our initial screening step in an upcoming prospective combination trial targeting BRAF V600E in pts with mCRC. Disclosure: J. Desai: Research Support: Roche, Ventana Medical Systems, A. Muranyi: Employee: Ventana Medical Systems, K. Shanmugam: Employee and Shareholder, Ventana Medical Systems, T. Grogan: Shareholder and Chief Scientific Officer, Ventana Medical Systems, P. Gibbs: Research Support, Ventana Medical Systems, P. Waring: Research Support: Ventana Medical Systems, All other authors have declared no conflicts of interest. 1174P DIAGNOSTIC AND PROGNOSTIC SIGNIFICANCE OF THE ALTERNATIVELY SPLICED ACTN4 VARIANT IN HIGH-GRADE NEUROENDOCRINE PULMONARY TUMOURS A. Miyanaga 1 , K. Honda 1 , K. Tsuta 1 , M. Masuda 1 , H. Tsuda 2 , H. Asamura 3 , A. Gemma 4 , T. Yamada 1 1 Division of Chemotherapy and Clinical Research, National Cancer Center Research Institute, Tokyo, JAPAN, 2 Pathology and Clinical Laboratory Division, National Cancer Center Hospital, Tokyo, JAPAN, 3 Division of Thoracic Surgery, National Cancer Center Hospital, Tokyo, JAPAN, 4 Internal Medicine, Nippon Medical School, Tokyo, JAPAN Background: High-grade neuroendocrine tumours (HGNTs) of the lung manifest a wide spectrum of clinical behaviour, but no method of predicting their outcome has been established. Materials and methods: We newly established a monoclonal antibody specifically recognizing the product of the alternatively spliced ACTN4 transcript (namely, variant actinin-4), and used it to examine the expression of variant actinin-4 Annals of Oncology 23 (Supplement 9): ix383–ix384, 2012 doi:10.1093/annonc/mds406 immunohistochemically in a total of 609 surgical specimens of various histological subtypes of lung cancer. Results: Variant actinin-4 was expressed in 55% (96/176) of HGNTs, but in only 0.8% (3/378) of non-neuroendocrine lung cancers. Expression of variant actinin-4 was significantly associated with unfavorable overall survival in HGNT patients (P = 0.00021, log-rank test). Multivariate analysis using the Cox proportional hazards model showed that expression of variant actinin-4 was the most significant independent negative predictor of survival in HGNT patients (hazard ratio, 2.18; P = 0.000714) after the presence of lymph node metastasis (hazard ratio, 2.30; P = 0.00012). Conclusions: Expression of variant actinin-4 is an independent prognostic factor for patients with HGNTs. This protein has high affinity for filamentous actin polymers and likely promotes aggressive behaviour of cancer cells. The present clinical findings clearly support this notion. Disclosure: All authors have declared no conflicts of interest. 1175P CLINICAL FEASIBILITY STUDY OF A NOVEL CYTOMETRY-BASED SYSTEM FOR THE DETECTION OF CIRCULATING TUMOR CELLS IN PATIENTS WITH LUNG CANCER Y. Koh 1 , M. Watanabe 1 , T. Sawada 2 , Y. Uehara 2 , Y. Fujimura 3 , T. Tamura 4 , F. Koizumi 2 1 Division of Drug Discovery and Development, Shizuoka Cancer Center, Sunto-gun, JAPAN, 2 Shien-Lab, National Cancer Center Hospital, Tokyo, JAPAN, 3 R&D, On-Chip Biotechnologies Co., Ltd, Koganei, JAPAN, 4 Division of Thoracic Oncology, National Cancer Center Hospital, Tokyo, JAPAN Background: The presence and number of circulating tumor cells (CTCs) in the peripheral blood of solid tumor patients are predictive of clinical outcome. To date the CellSearch system has been the only FDA-cleared CTCs enumeration system for advanced breast, prostate and colon cancers. However, low prevalence of CTCs and lack of capability as an application platform for molecular analysis have limited the use of CTCs in the clinic. To overcome these shortcomings, innovative and emerging technologies with easier access to further molecular analysis are under development worldwide. Methods: We have developed a flow cytometry-based CTCs detection system independent of EpCAM expression level of tumor cells with cytokeratin and vimentin-staining after the depletion of CD45-expressing cells. In a preclinical study, various cancer cell lines were spiked into blood from healthy donors and the sensitivity in detection was evaluated at two different sites (Shizuoka Cancer Center and National Cancer Center Tokyo). Then clinical feasibility study was conducted in patients with lung cancer. Results: Enumeration of the spiked cancer cells (10 to 1000 cells in 4 ml of blood) was linear, with a recovery rate of over 90%. A significantly higher recovery rate was observed with our system (90 to 102%) than that with CellSearch system (0%) particularly when EpCAM-negative PC-14 non-small lung cancer cells were spiked in, suggesting a superior sensitivity of our system in capturing EpCAM-negative tumor cells. In 22 blood samples from lung cancer patients, CTCs were detected with numbers ranging from 0 to 16 CTCs (median, 6.5) per 4 ml of blood with our system and in 72.7% (17/23) of the patients, 4 CTCs or more per 4 ml of blood were detected. On the other hand with CellSearch system, 2 CTCs or more per 7.5 ml of blood were detected in only 27% of the patients. Conclusions: The preclinical study and the results of the clinical feasibility study suggested superior sensitivity of our flow cytometry-based detection method than CellSearch system. Cell sorting device under development will be combined with this system for isolation and collection of CTCs for molecular analysis with next-generation sequencing. Disclosure: All authors have declared no conflicts of interest. 1176P EBUS-TBNA GIVES ADEQUATE TISSUE INFORMATION ON CELL TYPE IN LUNG CANCER M.K. Wong, M.S. Ip, D.C. Lam, J.C.M. Ho Medicine, Queen Mary Hospital, Hong Kong, HONG KONG Introduction: In formulating systemic treatment in patients with advanced stage lung cancer, it is now considered imperative to know the cell type such as squamous carcinoma, adenocarcinoma and large cell carcinoma as chemotherapeutic agents would be tailored to treat different cell type. © European Society for Medical Oncology 2012. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com abstracts
Method: Endobronchial ultrasound guided transbronchial needle aspiration (EBUS-TBNA)was performed under local anaesthesia in patients presented with mediastinal abnormality suspected of or confirmed lung cancer for diagnosis and staging purpose. Once malignancy was confirmed from the pathological materials, exact cell type, origin of tumour, differentiation were recorded. In the later phase of the study period, molecular profiling was also deployed to confirm the EGFR mutation and ALK translocation status. Results: Over the study period of 4 years and 4 months, there were 269 EBUS-TBNA performed in 258 patients. Of the 209 patients confirmed having malignancy as their final diagnosis, EBUS-TBNA was able to detect extrathoracic malignancy in 23 (11.0%) and primary lung cancer in 133 (63.6%). Among those 133 patients confirmed having primary lung cancer, 116 (87.2%) had exact cell type delineated. For those 40 patients who had molecular profiling performed, patients with adequate tissue for EGFR mutation and/or ALK translocation were obtained in 38 (95.0%). Of the 157 patients confirmed to have malignancy by EBUS-TBNA, only 22 (14%) had revealed NSCLC without knowing the exact cell type, differentiation of the tumour, EGFR status or primary origin of the tumour. In the 220 patients with final diagnosis of malignancy, the sensitivity was 89.0% and negative predictive value was 65.0% Conclusion: EBUS-TBNA is effective in subtyping of tumour cells and molecular profiling in patients with lung cancer. Disclosure: All authors have declared no conflicts of interest. 1177P VARIATIONS OF DISCORDANCE OF THE CLINICAL TNM STAGE WITH THE PATHOLOGICAL TNM STAGE BETWEEN JAPANESE DESIGNATED CANCER HOSPITALS F. Nakamura 1 , T. Higashi 2 , Y. Emori 3 , H. Nishimoto 3 1 Healthcare Epidemiology, Kyoto University Graduate School of Medicine and Public Health, Kyoto, JAPAN, 2 Department of Public Health/Health Policy, The University of Tokyo Graduate School of Medicine, Tokyo, JAPAN, 3 Cancer Surveillance Division, National Cancer Center, Tokyo, JAPAN Introduction: Previous studies showed that TNM stages that were clinically determined before surgery were not often concordant with pathological TNM stages. However, no previous studies have examined variations of discordance of the clinical TNM stage with the pathological TNM stage among hospitals. We aimed to examine the discordance of the clinical and pathological stages among Japanese designated cancer hospitals using compiled data from the hospital-based cancer registry submitted from 286 designated cancer care hospitals in Japan. Methods: The registry data had UICC TNM stages before and after surgery for stomach, colorectal, lung and breast cancer patients treated in these hospitals. We excluded patients who received adjuvant chemotherapy or radiotherapy, patients who received care from facilities with less than 10 patients, male breast cancer and patients whose stages were unknown from the analysis. We also calculated discordance of stages that could have theoretically resulted in changes in surgical procedures or treatment choice. Discordance was also calculated after excluding stage IV patients as sensitivity analysis. Results: In total, 145,726 patients (38,692 stomach, 47,304 colorectal, 19,643 lung and 40,096 breast cancer patients) were included in the analysis. Patients’ mean age and clinical TNM stage varied across hospitals. The facility-level discordance between clinical and pathological stages ranged from 4% to 52% in stomach cancer, 3% to Annals of Oncology 57% in colorectal cancer, 0% to 50% in lung cancer and 1% to 45% in breast cancer. TNM stages before surgery were lower than after surgery in more than half of the cases. The multi-level logistic regression model showed that variance in facilities existed after adjustment for age, sex and clinical TNM stage. Discordance of stages that could lead to changes in the surgical procedures or treatment choice ranged from 4% to 58% in stomach cancer, 4% to 63% in colorectal cancer, 0% to 5% in lung cancer, and 5% to 52% in breast cancer. Sensitivity analysis yielded similar results. Conclusion: We can confirm variations of discordance of TNM stages before and after surgery. Disclosure: All authors have declared no conflicts of interest. 1178TiP PROSPECTIVE EVALUATION OF PLANAR BONE SCINTIGRAPHY, SPECT/CT, 18F NAF PET/CT AND WHOLE BODY 1.5T MRI FOR DETECTION OF BONE METASTASES IN HIGH RISK BREAST AND PROSTATE CANCER PATIENTS A.K. Kuisma 1 , I. Jambor 2 , R. Huovinen 1 , M. Sandell 2 1 Oncology and Radiotherapy, University Hospital of Turku, Turku, FINLAND, 2 Radiology, University Hospital of Turku, Turku, FINLAND Purpose: The aim of the study was to compare the diagnostic accuracy of 99mTc methylene-diphosphonate planar bone scintigraphy (99mTc-MDP BS), 99mTc methylene-diphosphonate single photon emission tomography/computed tomography (99mTc-MDP SPECT/CT), 18F NaF positron emission tomography/ computed tomography (PET/CT) and whole body 1.5 Tesla magnetic resonance imaging (1.5T MRI) for the detection of bone metastases in high risk breast and prostate cancer patients. Materials and methods: Twenty breast cancer patients and eight prostate cancer patients at high risk of bone metastases prospectively underwent 99mTc-MDP BS, 99mTc-MDP SPECT/CT, 18F NaF PET/CT and whole body 1.5T MRI using spine and surface coils. Four independent reviewers interpreted each individual modality without the knowledge of other imaging findings. The final metastatic status was based on the consensus reading of all imaging modalities. The findings were compared on patient and region basis. In the region based analysis, the skeleton was divided into five regions. Results: Based on the consensus reading, 13 (46%) patients and 42 (30%) regions had presence of bone metastases while 15 patients and 98 regions were free of bone metastases. 99mTc-MDP BS was false negative in four patients. In the patient/region based analysis, the sensitivity for 99mTc-MDP BS, 99mTc-MDP SPECT/CT, 18F NaF PET/CT and whole body 1.5T MRI was 69%/44%, 77%/76%, 92%/90% and 77%/71%, respectively, while the accuracy was 86%/82%, 89%/92%, 96%/97% and 86%/91%, respectively. Conclusions: 99mTc-MDP SPECT/CT, 18F NaF PET/CT and whole body MRI including diffusion weighted imaging demonstrated higher sensitivity and accuracy in detection of bone metastasis compared to planar bone scintigraphy. Observed difference between imaging modalities might potentially affect the patient management. Clinical relevance statement: 99mTc-MDP SPECT/CT, 18F NaF PET/ CT and whole body MRI including diffusion weighted imaging showed higher sensitivity for detecting bone metastases in high risk breast and prostate cancer patients to planar bone scintigraphy. Disclosure: All authors have declared no conflicts of interest. ix384 | 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: Adenocarcinoma was present in 25 pa
Page 387 and 388: widely used by single agent or plat
Page 389 and 390: disease after surgery were treated
Page 391 and 392: stage IIIA NSCLC, EML4-ALK fusion-p
Page 393 and 394: 1200P CONCOMITANT CHEMORADIATION GI
Page 395 and 396: Patients and methods: The study was
Page 397 and 398: months (95% CI:13-25). The PFS and
Page 399 and 400: maintenance therapy had favourable
Page 401 and 402: abstracts non-small cell lung cance
Page 403 and 404: Ingelheim, GSK Biologicals (compens
Page 405 and 406: 1234PD RANDOMIZED PHASE III TRIAL O
Page 407 and 408: GlaxoSmithKline (myself, compensate
Page 409 and 410: 1243P IDENTIFICATION OF MICRORNA (M
Page 411 and 412: N-arm n=34 P-arm n=32 All n=66 Male
Page 413 and 414: 1255P POPULATION BASED EVALUATION O
Page 415 and 416: 1262P DISTINCT SPREAD OF EGFR MUTAT
Page 417 and 418: 1268P VISUAL DISTURBANCES IN PATIEN
Page 419 and 420: MERCK SERONO: Advisor, speaker in s
Page 421 and 422: Conclusions: These data from SAiL a
Page 423 and 424: NSCLC diagnosis and time of BM diag
Page 425 and 426: 1291P PHASE I/II DOSE-FINDING STUDY
Page 427 and 428: Network utilization of WBCGF in the
Page 429 and 430: 1303P COST EFFECTIVENESS OF PEMETRE
Page 431 and 432: Results: The patients’ characteri
Page 433 and 434: EGFR mut at exons 18, 19, 21, and K
Page 435 and 436:
Methods: EML4-ALK fusion was screen
Page 437 and 438:
Results: The median survival time (
Page 439 and 440:
enefit from sustained EGFR blockade
Page 441 and 442:
epresented by 19 pts (32%) female,
Page 443 and 444:
and at least one prior course of ch
Page 445 and 446:
Methods: NSCLC patients with radiog
Page 447 and 448:
1367TiP LONG-TERM ERLOTINIB THERAPY
Page 449 and 450:
Austria, Czech Republic, Finland, G
Page 451 and 452:
were every 6 weeks (wk) (S1), every
Page 453 and 454:
Advantage enrollees (83% vs. 25%) [
Page 455 and 456:
Results: Based on 10,000 simulation
Page 457 and 458:
cancer tumors 12%, Germ cell tumor
Page 459 and 460:
Material and methods: 50 lung cance
Page 461 and 462:
1414TiP IMPLEMENTATION OF CANCER RE
Page 463 and 464:
abstracts palliative care 1422O EFF
Page 465 and 466:
Method and results: A total of 317
Page 467 and 468:
1436P SURVEY ON MODELS OF INTEGRATI
Page 469 and 470:
care unit (PCU) at the National Can
Page 471 and 472:
Characteristic No. % Total 63 1 st
Page 473 and 474:
hysterectomised-9.10% and cervix ca
Page 475 and 476:
abstracts psycho-oncology 1462PD IN
Page 477 and 478:
events, tumour response, and surviv
Page 479 and 480:
abstracts sarcoma 1477O ADHESION TO
Page 481 and 482:
1481PD A PHASE II STUDY OF DOVITINI
Page 483 and 484:
1488P ORGANISATION OF SARCOMA PATIE
Page 485 and 486:
Patients and methods: From August 2
Page 487 and 488:
chemotherapy respectively. At a med
Page 489 and 490:
of this group Those with relapsed d
Page 491 and 492:
1515 PREDICTORS OF SURVIVAL IN ADOL
Page 493 and 494:
abstracts small cell lung cancer an
Page 495 and 496:
emaining receiving either CAV or to
Page 497 and 498:
1533P EXPRESSION OF WILM⍰TUMOUR G
Page 499 and 500:
more than 3 months after first line
Page 501 and 502:
lower recurrence rate of NE. Pegfil
Page 503 and 504:
egimens (HR = 2.5, p < 0.001). Phys
Page 505 and 506:
1561P PREDICTIVE DIAGNOSTICS FOR RE
Page 507 and 508:
Methods: A prospective multicentre
Page 509 and 510:
Table: 1574P Pharmacokinetic parame
Page 511 and 512:
Novartis and unrestricted research
Page 513 and 514:
studies have shown that chemotherap
Page 515 and 516:
(Grade 1) and moderate to severe (G
Page 517 and 518:
declined to relatively lower level
Page 519 and 520:
1609P PHYSICAL ACTIVITY (PA) AND PH
Page 521 and 522:
patients were admitted to the oncol
Page 523 and 524:
Dicarbamin 100 mg/day on day 5 befo
Page 525 and 526:
Results: Anemia was detected in 83.
Page 527 and 528:
important to carry out randomized s
Page 529 and 530:
abstracts translational research 16
Page 531 and 532:
expression. Then, we analyzed PB sa
Page 533 and 534:
Table: 1657P TH BV + TH HR (95% CI)
Page 535 and 536:
BRAF mutations. Circulating free DN
Page 537 and 538:
1671P PHASE I CLINICAL TRIAL OF CAN
Page 539 and 540:
1678P PREDICTIVE VALUE OF TWO PHENO
Page 541 and 542:
theorized that the PI3K/AKT pathway
Page 543 and 544:
Material and methods: 101 patients
Page 545 and 546:
overexpressing and 232 had triple n
Page 547 and 548:
author index author index A Aamdal
Page 549 and 550:
author index Badran A. ix288 (874)
Page 551 and 552:
author index Bösmüller H. ix209 (
Page 553 and 554:
author index Chen A. ix319 (966O) C
Page 555 and 556:
author index De Droogh E. ix452 (13
Page 557 and 558:
author index Esposito G. ix209 (618
Page 559 and 560:
author index Geiges G. ix306 (930P)
Page 561 and 562:
author index Hartono S. ix70 (155P)
Page 563 and 564:
author index Iwasaki H. ix542 (1694
Page 565 and 566:
author index Kodaira M. ix90 (228P)
Page 567 and 568:
author index Lichtensztejn D. ix350
Page 569 and 570:
author index Martinez A. ix496 (153
Page 571 and 572:
author index Morishita N. ix432 (13
Page 573 and 574:
author index Okamoto N. ix432 (1320
Page 575 and 576:
author index Piau S. ix456 (1401P)
Page 577 and 578:
author index Rodríguez Rodríguez
Page 579 and 580:
author index Scoggins C.R. ix371 (1
Page 581 and 582:
author index Stern L. ix272 (823P)
Page 583 and 584:
author index Trypaki M. ix429 (1308
Page 585 and 586:
author index Whitmore J.B. ix310 (9
Page 587 and 588:
subject index subject index A AAV-H
Page 589 and 590:
subject index ix115 (316TiP), ix116
Page 591 and 592:
subject index diffuse large B-cell
Page 593 and 594:
subject index (1033P), ix340 (1036P
Page 595 and 596:
subject index medical information,
Page 597 and 598:
subject index (612P), ix214 (633),
Page 599 and 600:
subject index RCC, ix274 (830P) re-
Page 601 and 602:
subject index TR-FRET, ix84 (206P)
Page 603 and 604:
drug index drug index 1248P, 1250P,
Page 605 and 606:
translational research index transl
Page 607 and 608:
Page 609:
show all

Download the ESMO 2012 Abstract Book - Oxford Journals

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?