Download the ESMO 2012 Abstract Book - Oxford Journals

More documents

Recommendations

Info

Annals of Oncology advanced HCC, tivantinib monotherapy improved time to progression by 56%. However, in that study at the standard phase 2 dose of 360 mg twice daily (BID), tivantinib exposure was increased, and the absolute incidence of severe neutropenia increased approximately 6% compared to pts with solid tumors from previous studies. An exposure-response analysis was conducted to explore the relationship between neutropenia and tivantinib pharmacokinetics (PK). Methods: Tivantinib plasma concentration and incidence of grade ≥ 2 neutropenia were pooled from phase 1/1b and 2 studies. A population PK model (NONMEM v.7.1.0) was used to predict tivantinib exposure in HCC. The relationship between tivantinib exposure and neutropenia was evaluated by logistic regression analysis (S plus v8.0). Results: Data were available from 289 cancer pts, including 73 pts with HCC and mild-to-moderate hepatic impairment. Cases of grade ≥ 3 (n = 28) and grade ≥ 2 (n = 40) neutropenia were included in the analysis. Based on the population PK analysis, tivantinib clearance was reduced approximately 67% in HCC pts, resulting in approximately 3 times higher exposure compared with other cancer pts. There was a significant (P < .001) relationship between tivantinib exposure and incidence of grade ≥ 2/3 neutropenia. By reducing the tivantinib starting dose from 360 to 240 mg BID, the incidence of grade ≥ 3 neutropenia is modeled to decrease from 28% to 16% in HCC pts. Further reduction in the risk of neutropenia (∼6%) was achieved with intensive clinical monitoring and an aggressive dose-reduction schema. Conclusions: Based on the current analysis, the increased incidence of neutropenia in HCC pts compared to pts with other solid tumors resulted from increased tivantinib exposure due to hepatic impairment. Consistent with the model, the risk of neutropenia was successfully managed in HCC pts by implementing dose reduction and tighter clinical monitoring without compromising efficacy. Disclosure: H. Zahir: H Zahir is an employee of Daiichi Sankyo, Inc. H. Kastrissios: H Kastrissios is an employee of Pharsight Corporation and was retained by Daiichi Sankyo to provide scientific consulting services on tivantinib. M. Jansen: M Jansen is an employee of Daiichi Sankyo, Inc. R. Savage: R Savage is currently an employee of ArQule. I participate in the ESPP employee stock purchase plan and receive stock options as part of my compensation package as an employee of ArQule. G. Abbadessa: G Abbadessa is an employee of ArQule, Inc. and owns Arqule stock options. F. Chai: F Chai is an employee of ArQule, Inc., the sponsor of the studies. F Chai holds ArQule stock. B. Schwartz: B Schwartz is currently an employee (Chief Medical officer) of ArQule and own stock in the company. R. Miller: R Miller is a full time employee of Daiichi Sankyo Pharma Development. T. Tokui: T Tokui is an employee of Daiichi Sankyo Co., Ltd. All other authors have declared no conflicts of interest. 739P PHASE 1 EXPERIENCE OF TIVANTINIB IN PATIENTS WITH HEPATOCELLULAR CARCINOMA (HCC) OR BILIARY TRACT CANCER (BTC) F. Chai 1 , G. Abbadessa 2 , R. Savage 3 , H. Zahir 4 , Y. Chen 2 , M. Lamar 5 , J. Kazakin 6 , D. Ferrari 2 , R. von Roemeling 7 , B. Schwartz 2 1 Medical Administration, ArQule, Inc., Woburn, MA, UNITED STATES OF AMERICA, 2 Clinical Development, ArQule, Inc., Woburn, MA, UNITED STATES OF AMERICA, 3 Preclinical Development and Clinical Pharmacology, ArQule, Inc., Woburn, MA, UNITED STATES OF AMERICA, 4 Clinical Pharmacology, Daiichi Sankyo, Inc., Edison, NJ, UNITED STATES OF AMERICA, 5 Clinical Operations, ArQule, Inc., Woburn, MA, UNITED STATES OF AMERICA, 6 Arqule, Inc., ArQule, Inc., Woburn, MA, UNITED STATES OF AMERICA, 7 Clinical Development Oncology, Daiichi Sankyo Pharma Development, Edison, MA, UNITED STATES OF AMERICA Background: Tivantinib is a selective MET inhibitor that is extensively metabolized by the liver. Since 2006, > 700 cancer patients (pts) have been treated with tivantinib. Herein we summarize safety, pharmacokinetic (PK), and efficacy data for pts with HCC or BTC treated with tivantinib in phase 1 clinical trials. Methods: Adverse events (AEs) were assessed using Common Terminology Criteria for Adverse Events (CTCAE) version 3.0. Tumor responses were assessed via Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1. PK parameters were calculated using blood samples collected on day 1 and on day 2 or day 15 of cycle 1. Results: 53 pts (median age, 63 y) with HCC (n = 42; 79%), cholangiocarcinoma (n = 10; 19%), or gallbladder adenocarcinoma (n = 1; 2%) were included. Of these, 23 pts (43%) received tivantinib monotherapy, and 30 pts (57%) received tivantinib in combination with sorafenib (n = 20; 38%), gemcitabine (n = 8; 15%), or erlotinib (n = 2; 4%). Starting tivantinib BID doses were < 240 mg in 3 (6%), 240 mg in 11 (21%), and 360 mg in 39 (74%) pts. Common treatment-emergent AEs (≥ 15% of pts) were fatigue and anemia (45% each); diarrhea (40%); neutropenia and anorexia (38% each); asthenia (30%); thrombocytopenia, peripheral edema, pyrexia, and nausea (25% each); hyperbilirubinemia (23%); vomiting and alopecia (21% each); rash (19%); leukopenia (17%); and palmar-plantar erythrodysesthesia syndrome, dyspnea, and ascites (15% each). Tivantinib PK analysis indicated peak plasma levels 2 h after oral administration (range, 1-6 h). Tivantinib exposure was higher in pts with HCC vs pts with BTC (12,385 vs 5,992 ng·h/mL). Best responses were complete response in 1 pt (2%), partial response in 2 pts (4%), and stable disease (SD) in 30 pts (57%). Response rate and disease control rate were 6% and 62%, respectively. Conclusions: Tivantinib demonstrated a manageable safety profile and was well tolerated at doses up to 360 mg BID in pts with BTC and up to 240 mg BID in pts with HCC. Only pts with HCC had increased exposure, presumably due to disease-specific hepatic impairment. Encouraging clinical activity (primarily SD) was observed in this pt population. Disclosure: F. Chai: F Chai is an employee of ArQule, Inc., the sponsor of the studies and holds ArQule stock. G. Abbadessa: G Abbadessa is an employee of ArQule, Inc. and owns ArQule stock options. R. Savage: R Savage is currently an employee of ArQule and participates in the ESPP employee stock purchase plan and receives stock options as part of his compensation package as an employee of ArQule. H. Zahir: H Zahir is an employee of Daiichi Sankyo, Inc. Y. Chen: Y Chen is an ArQule employee and own ArQule stocks. M. Lamar: M Lamar is an employee of ArQule, Inc. J. Kazakin: J Kazakin is an employee of ArQule, Inc. and has ArQule’s stock options. D. Ferrari: D Ferrari is an ArQule Inc. employee and currently owns ArQule stock. R. von Roemeling: R von Roemeling is an employee of Daiichi Sankyo Pharma Development. B. Schwartz: B Schwartz is currently an employee of ArQule Inc. and own stock in the company. 740P PHASE I STUDY OF NINTEDANIB (BIBF 1120) IN EUROPEAN PATIENTS WITH ADVANCED HEPATOCELLULAR CARCINOMA D. Palmer 1 , A.B. Loembé 2 , M. Studeny 2 , J. Hocke 3 ,T.Meyer 4 1 Liverpool Cancer Research Uk Centre, University of Liverpool, Liverpool, UNITED KINGDOM, 2 Oncology, Boehringer Ingelheim RCV GmbH & Co KG, Vienna, AUSTRIA, 3 Oncology, Boehringer Ingelheim Pharma GmbH & Co.KG, Biberach an der Riss, GERMANY, 4 UCL Cancer Institute, University College London, London, UNITED KINGDOM Background: Caucasian and Asian patients (pts) with hepatocellular carcinoma (HCC) tolerate anticancer drugs differently. This open-label, multicentre, phase I/ randomised phase II study (NCT01004003; phase II in progress) evaluated the efficacy, safety and pharmacokinetics of nintedanib (a triple angiokinase inhibitor targeting VEGFRs, PDGFRs and FGFRs) versus sorafenib in pts with advanced HCC from Europe. Initial phase I results are reported. Methods: Pts (ECOG performance status ≤2, Child-Pugh [CP] score ≤7) with histologically/cytologically confirmed HCC and no prior systemic therapy were enrolled in the phase I trial and stratified into two groups: (I) AST and ALT ≤2 x upper limit of normal (ULN), and CP 5–6; (II) AST or ALT >2 to ≤5 x ULN, or CP 7. Utilising a 3 + 3 design, cohorts received oral nintedanib continuously in 28-day courses, starting at 50mg bid (group II) or 100mg bid (group I) and escalating up to 200mg bid in 50mg bid intervals. Therapy was continued until no clinical benefit or undue toxicity. The phase I primary endpoint was the maximum tolerated dose (MTD) of nintedanib in Course 1. Results: A total of 28 pts (71% Caucasian) have been treated: 13 in group I (median [range] days: 345 [2–757]; 100/150/200mg bid, n = 6/3/4) and 15 in group II (median [range] days: 74 [17–428]; 50/100/150/200mg bid, n = 3/4/4/4). No dose-limiting toxicities (DLTs) were seen in group I or II during Course 1 at doses up to 200mg bid, which was the MTD of nintedanib. After the dose-escalation phase and determination of MTD, seven pts reported DLTs at various dose levels (CTCAE Grade [G]3 bilirubin increase, G3 AST increase, G4 amylase increase, G3 hypertension/ALP increase, G3 amylase increase, G5 multi-organ failure, G3 bilirubin increase). The most frequent adverse events (AEs) in both groups, by system organ class, were gastrointestinal (89%) and general/administration site (39%) disorders. Class-related AEs (any grade) were uncommon (hypertension [n = 2], rash [n = 3]). Hepatic enzyme data will be presented. Conclusions: Nintedanib has an acceptable safety profile in pts with advanced HCC at the same dose used in other cancers (200 mg bid). Disclosure: D. Palmer: Daniel Palmer: research funding from Boehringer Ingelheim. A.B. Loembé: Arsene-Bienvenu Loembé: employee of Boehringer Ingelheim. M. Studeny: Matus Studeny: employee of Boehringer Ingelheim. J. Hocke: Julia Hocke: employee of Boehringer Ingelheim. T. Meyer: Tim Meyer: research funding from Boehringer Ingelheim 741P VALIDATION OF PROGNOSTIC VALUE OF AJCC 7TH STAGING SYSTEM IN PATIENTS WITH RESECTED HEPATOCELLULAR CARCINOMA (HCC) S.F. Ang1 ,H.Li2 , S. Choo1 , I.B. Tan1 , M.H. Tan1 , H.C. Toh1 1 Medical Onocology, National Cancer Center Singapore, SINGAPORE, 2 Department of Clinical Research, Singapore General Hospital, Singapore, SINGAPORE Background: Accurate cancer staging is essential to determine prognosis and appropriate treatment. The American Joint Committee on Cancer (AJCC) Staging Manual 7th edition for HCC released in 2010 subdivided stage III HCC to IIIA (multiple tumors of which any are greater than five centimeters, but lack major vessel invasion, T3A) and IIIB (invasion of major vessels, T3B). Both were previously classified as stage IIIA in the AJCC 6th. T4N0M0 and patients with node-positive disease (N1) are upstaged to stage IIIC and IVA respectively. The aim of our study is Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds398 | ix245
validate the revised AJCC 7th staging system based on outcomes of patients undergoing liver resection for HCC from a single institution. Methods: Records for all patients undergoing potentially curative surgery for localized HCC between 1992 – 2007 were retrospectively reviewed. Pathological staging were determined post-operatively. Survival curves were plotted with the Kaplan–Meier method and were compared by using a log-rank test for various disease stages based on AJCC 7th staging system. Results: 543 patients were included (439 male) and 80% were Chinese ethnicity. 303 patients were chronic hepatitis B carriers. The median follow up was 1.78 years with 282 relapsed patients (51.9%) and 189 deaths (34.8%). Median survival (MS) and time-to-relapse (TTR) were 4.83 years and 2.00 years respectively. MS for AJCC 7 stage I, II, III and IV were 6.35, 4.44, 2.41 and 0.49 years respectively (p
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: 735P RADIOGRAPHIC PARAMETERS IN PRE
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 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

Create successful ePaper yourself

Delete template?

Save as template?