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Annals of Oncology 847P CLINICAL EFFICACY OF SUNITINIB AS POST-OPERATIVE ADJUVANT THERAPY IN PATIENTS WITH HIGH-RISK RENAL CELL CARCINOMA X. Zhang 1 , J.Y. Yuan 2 , L. Wang 2 , L. Chen 3 ,J.Pan 4 ,L.Ye 5 , X. Xiao 6 , J. Qiu 7 , K. Zhang 8 ,G.Ye 9 1 Urology Department, The General Hospital of the People’s Liberation Army, Beijing, CHINA, 2 Urology Department, Xijin Hospital, the Fourth Military Medical University, Xian, CHINA, 3 Urology Department, 307 Hospital of PLA, Beijing, CHINA, 4 Urology Department, Southwest Hospital, the Third Military Medical University, Chongqing, CHINA, 5 Urology Department, 304 Hospital of PLA, Beijing, CHINA, 6 Urology Department, General Hospital of Armed Police Forces, Beijing, CHINA, 7 Urology Department, Bethune International Peace Hospital of PLA, Jilin, CHINA, 8 Urology Department, Daping Hospital, the Third Military Medical University, Chongqing, CHINA, 9 Urology Department, Xinqiao Hospital, the Third Military Medical University, Chongqing, CHINA Objective: To evaluate the efficacy and safety of Sunitinib as post-operative adjuvant therapy in patients with high-risk renal cell carcinoma (RCC). Methods: A total of 60 patients with resected, histologically confirmed clear cell RCC were enrolled in this study. Patients received orally Sunitinib either at a dose of 50mg on treatment schedule 4/2 (once daily for 4 weeks followed by 2 weeks off) or at a dose of 37.5mg once daily for three 6-week cycles from 1 month after surgery. Results: All 60 patients tolerated Sunitinib treatment well and no patient discontinued treatment due to adverse events. Most adverse events were grade I to II. The most frequently reported adverse events were neutropenia (56.7%), thrombocytopenia (53.3%), leucopenia (48.3%), hand-foot syndrome (46.7%) and hypertension (36.7%). The most frequently reported grade 3 or 4 toxicities were thrombocytopenia (25%), neutropenia (15%), hand-foot syndrome (11.7%) and leucopenia (8.3%). The majority of adverse events occurred within the first 1-2 cycles of Sunitinib treatment, and was ameliorated 1 month after 3 cycles finished. No irreversible adverse event was observed. As of April 5, 2012, no recurrence occurred in patients except one death due to cerebrovascular accident unrelated to treatment, with both 6-month and 9-month disease-free survival (DFS) rate of 100%. Conclusion: Myelosuppression occurred less frequently in high-risk RCC patients treated with Sunitinib as operative adjuvant therapy than in advanced RCC patients, with a better benefit trend. However, long-term follow-up data are needed to further confirm the efficacy of Sunitinib in the adjuvant setting. Disclosure: All authors have declared no conflicts of interest. 848P OVERALL SURVIVAL (OS) IN METASTATIC RENAL CELL CARCINOMA (MRCC): A COMPARISON BETWEEN SORAFENIB (SO) AND BEST SUPPORTIVE CARE (BSC) AFTER FIRST LINE TREATMENT WITH SUNITINIB (SU) IN SWEDEN P. Sandström 1 , R. Sandin 2 , J. Kowalski 3 , T. Wahlgren 4 , M. Jakobsson 4 , S. Lundstam 5 , B. Ljungberg 6 , U. Harmenberg 1 1 Department of Oncology-pathology, Karolinska University Hospital and Karolinska Institutet, Stockholm, SWEDEN, 2 Global Health Economics and Outcomes Research, Onology, Pfizer AB, Sollentuna, SWEDEN, 3 Department of Clinical Science, Intervention and Technology, Karolinska University Hospital Huddinge and Karolinska Institutet, Stockholm, SWEDEN, 4 Oncology, Pfizer AB, Sollentuna, SWEDEN, 5 Department of Urology, University Hospital, and the Sahlgrenska Academy, Gothenburg, SWEDEN, 6 Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, SWEDEN Background: There is a paucity of efficacy data after first line treatment with SU in mRCC. This retrospective register study compared OS in patients treated with SO and BSC after first line treatment with SU in Sweden. Methods: Three Swedish national health registers were used: the Swedish Cancer register (diagnosis and death), the National Patient Register (in-/out-patient data), and the Swedish Prescribed Drug Register. 135 patients identified with mRCC, diagnosed no later than 2009, were recorded as having received 1st-line treatment with SU; 59 patients received SO and 76 patients received BSC. Multivariate analysis was performed using the Cox proportional hazards model including estimation of adjusted OS. The regression model included the covariates: age, gender, nephrectomy, time since diagnosis and metastatic disease, time since mRCC diagnoses and start of systemic therapy, geographical region, institutional size, and duration of first line SU treatment. Sensitivity analysis with combinations of explanatory variables, was performed to test the robustness of the results. Results: Patients characteristics differed between the SO and BSC patients, but available information did not indicate a clear advantage in favor of any treatment arm. OS for patients prescribed with SO was improved compared with OS for BSC patients. Including all covariates, median adjusted OS was 9,9 vs. 6,6 months, respectively for patients treated with SO and BSC (HR = 0.652, 95% CI: 0.412, 1.030; P < 0.067). Sensitivity analysis showed a robust and significant reduction in risk of death for patients treated with SO; range of 29-42% (HR: 0,58-0,71). In all models, nephrectomy was independently associated with significantly improved OS. Other individual covariates were generally not statistically significant, likely due to a low number of observations. Conclusion: An improved OS for mRCC patients was seen in patients receiving SO compared to BSC after first line treatment with SU. Some caution should be taken with interpreting the results as confounding due to unmeasured covariates may exist. Disclosure: P. Sandström: Has had an advisory role for Pfizer, Roche, GSK, Novartis, and Bayer, has received honoraria from Pfizer, Roche, bayer, GSK and Novartis and has received research funding from Pfizer and Bayer. R. Sandin: Rickard Sandin is an employee of Pfizer AB and owns Pfizer stock. J. Kowalski: Jan Kowalski is concultant and received compensation from Pfizer for the statistical work for the abstract. T. Wahlgren: Thomas Wahlgren is an employee of Pfizer AB and owns Pfizer stock. M. Jakobsson: Maria Jakobsson is an employee of Pfizer AB and owns Pfizer stock. S. Lundstam: Has had an advisory board role for GSK and Bayer, has received honoraria from Pfizerand GSK, and has received research funding from Pfizer. B. Ljungberg: Has had an advisory role for Pfizer, GSK, Novartis, Astellas and Bayer, and has received honoraria from Pfizer, Novartis, GSK and Bayer. U. Harmenberg: Has had an advisory role for Pfizer, Roche, GSK, Novartis, and Bayer, has received honoraria from Pfizer, Roche, and Novartis and has received research funding from Pfizer, GSK and Novartis. 849P SUNITINIB RECHALLANGE IN METASTATIC RENAL CELL CARCINOMA PATIENTS K. Nagyivanyi1 , K. Bíró2 , F. Gyergyay2 , Z. Küronya2 , H. Nemeth2 , L. Géczi2 1 Chemotherapy C, National Institute of Oncology, Budapest, HUNGARY, 2 Chemotherapy C and Clinical Pharmacology, National Institute of Oncology, Budapest, HUNGARY Background: Sunitinib is an active agent in the first line treatment of metastatic clear cell kidney cancer, based on the result of a global phase III study. However, complete remission is rarely seen and multiply sequential therapies are used in this patient population. Since options in third line setting are limited, we assessed the clinical activity of sunitinib rechallenge after failure on other therapies. Methods: 323 kidney cancer patients were treated with sunitinib from November 2005 to January 2012 in our department. Retrospective data were collected for those 9 patients who we rechallenged with sunitinib failing to at least two previous therapies, including sunitinib. Patient characteristics, objective response based on RECIST criteria and progression-free survival (PFS) were analysed. Tumor assessment was performed every 2nd cycle of sunitinib or every 3 months Results: Data of 8 men and 1 woman of median age (at sunitinib challenge 59 years, at sunitinib rechallenge 63 years) with metastatic clear cell cancer of the kidney were analysed. All patients had nephrectomy prior treatment. Initial treatment with sunitinib was associated with a median progression free survival (PFS) of 13,7 months. Objective response was partial remissions (PR) as best response. At the time of re-exposure patients again showed clinical benefit which was associated with a median PFS of 6,8 months and consisted of 1 (11%) PR and 5 (55%) disease stabilizations. PD was seen in 3 (33%) patients. Conclusions: In sunitinib-responsive patients, re-challenge with sunitinib has been successful and was well tolerated either after an other TKI or mTOR inhibitor and it seems to be a valid option as a third line treatment. Disclosure: All authors have declared no conflicts of interest. 850P GENETIC POLYMORPHISMS AND SUNITINIB TOXICITY IN METASTATIC RENAL-CELL CARCINOMA J. Sepulveda Sanchez 1 , C. Farfan 2 , F. Villacampa 3 , G. Velasco 4 , J. Benitez 5 , C. Rodriguez 6 , M. Calderon 2 , I. Cañamares 7 , H. Cortes-Funes 1 , D.E. Castellano 1 1 Servicio De Oncologia Medica, University Hosptial 12 De Octubre Medical Oncology, Madrid, SPAIN, 2 Medical Oncology, Hospital Universitario 12 de Octubre, Madrid, SPAIN, 3 Urology- Urooncology Unit, Hospital Universitario 12 de Octubre, Madrid, SPAIN, 4 Medical Oncology, Hopital 12 de Octubre, Madrid, SPAIN, 5 Clinical Pharmacology & Pharmacogenetics, University of Extremadura Medical School & Infanta Cristina University Hospital, Badajoz, SPAIN, 6 Biology, Centro Nacional de Investigaciones Científicas, Madrid, SPAIN, 7 Pharmacy, Hospital Universitario 12 de Octubre, Madrid, SPAIN Background: Sunitinib (SU) is a multi-targeted receptor tyrosine kinase inhibitor that is approved for the treatment of renal cell carcinoma (RCC). However, several patients either do not respond to treatment or they experience significant toxicity. Our study aims to find genetic markers of toxicity and efficacy using a commercially available DNA microarray genotyping system. Methods: 30 patients with newly diagnosed metastatic RCC, from January 2010 to May 2011, were evaluated prospectively at Hospital 12 de Octubre (Madrid, Spain). Pts received SU in repeated 6-wk cycles of 50 mg/day (4 wks on followed by 2 wks off treatment). A total of 92 of single nucleotide polymorphisms (SNPs) in 34 genes in the pharmacokinetic and pharmacodynamic pathways of drugs were analyzed Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds399 | ix281
using Drug inCode ® pharmacogenetic service. SNPs in candidate genes, together with clinical characteristics were tested univariately for association with the number of days of SU treatment until the first reduction of dose, PFS and OS. Results: Complete analysis was possible in 25 pts. Pts with CYP1A2*1/*1. a low metabolizing genotype, had an increased risk of dose reductions due to toxicity compare to allele *1F (Median time to dose reduction: 2.33 months Vs NR; p < 0.006). Pts with CYP2C19*1/*1, wild type genotype, had an increased risk of dose reductions due to toxicity versus other genotypes (Median time to dose reduction: 2.8 months Vs 9.73 months; P < 0.021). No statistically significant associations were observed among drug metabolizing genes and PFS or OS. Catechol-O-methyltransferase (COMT) V158M polymorphism was associated with PFS and OS (Met/Met carriers median PFS and OS NR; Met/Val pts PFS= 15 months; OS = 17.2 months and Val/Val pts PFS = 3.3 months; OS= 4.4 months; p = 0.005 for PFS and P = 0.003 for OS). Conclusions: This preliminary analysis suggests that CYP1A2 and CYP2C19 SNPs may be associated with toxicity in patients with RCC treated with SU. As CYP1A2 and CYP2C19 activity could be affected by a variety of non-genetic factors, if confirmed, these results could lead to the necessity of controlling toxic and dietary habits of pts treated with SU. SNPs associated with toxicity and survival in this preliminary analysis are being validated in an independent cohort of RCC treated with SU (García-Donas J, et al. Lancet Oncol 2011) and will be presented. Disclosure: All authors have declared no conflicts of interest. 851P A PHASE IV MULTICENTER STUDY OF THE EFFICACY AND SAFETY OF SUNITINIB AS FIRST-LINE THERAPY IN CHINESE PATIENTS WITH METASTATIC RENAL CELL CARCINOMA (MRCC) S. Qin 1 , J. Jin 2 , J. Guo 3 , J. Wang 4 , F. Zhou 5 , Y. Huang 6 ,X.Ren 7 ,D.Ye 8 , Q. Wang 9 ,S.Pan 10 1 Pla Cancer Center, Nanjing Bayi Hospital, Nanjing, CHINA, 2 Urology, Peking University First Hospital, Beijing, CHINA, 3 Department of Renal Cancer and Melanoma, Peking University Cancer Hospital and Institute, Beijing, CHINA, 4 Chinese Academy of Medical Sciences and Peking Union Medical College, Cancer Hospital/Institute, Beijing, CHINA, 5 Cancer Center, Sun Yat-sen University, Guangzhou, CHINA, 6 Urology, Shanghai Renji Hospital, Shanghai, CHINA, 7 Biotherapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin, CHINA, 8 Urology, Fudan University Shanghai Cancer Center, Shanghai, CHINA, 9 Global Research and Development, Pfizer, Shanghai, CHINA, 10 Clinical Statistics, Pfizer, New York, NY, UNITED STATES OF AMERICA Background: Based on the effectiveness and safety profile established in two single-arm phase II trials and a pivotal phase III trial versus interferon-alfa, sunitinib is approved worldwide for advanced RCC. Here we report a single-arm, open-label phase IV study to assess use of sunitinib as first-line therapy in Chinese patients with mRCC. Methods: Treatment-naïve patients aged ≥18 yr with ECOG performance status 0/1 and histologically confirmed mRCC received oral sunitinib 50 mg/d on the approved 4-wk-on-2-wk-off schedule. Treatment continued until disease progression, unacceptable toxicity, or consent withdrawal. The primary endpoint was progression-free survival (PFS). Tumor measurements were performed at screening, regular intervals, suspected disease progression, to confirm response, and end of treatment/withdrawal. Safety was assessed regularly using NCI CTCAE version 3.0. Results: 105 patients received treatment. Mean age was 54.6 yr, 75% were male, and mean BMI was 23.9 kg/m 2 . The most common site of baseline metastases was the lungs (76%). Median (range) number of treatment cycles completed was 8 (0–27). All patients discontinued treatment; reasons included disease progression/relapse (63%) and treatment-related AEs (8%). In 105 treated patients, median PFS was 61.7 wk (14.2 mo; 95% CI: 45.1–106.3 wk) and median overall survival (OS) was 133.4 wk (30.7 mo; lower bound of 95% CI: 94.1 wk). In 103 evaluable patients, objective response rate (ORR) was 31.1% (95% CI: 22.3–40.9%). Most treatment-emergent AEs were grade 1/2 severity and the most common were hand-foot syndrome (64%), decreased white blood cell count (52%), fatigue (51%), decreased platelet count (51%), diarrhea (49%), and decreased appetite (43%). There were no occurrences of treatment-emergent congestive heart failure, left ventricular dysfunction, or cardiomyopathy. Conclusions: With median PFS of 61.7 wk (14.2 mo) and OS of 133.4 wk (30.7 mo), these results compare favorably with those of the phase III trial, while ORR of 31.1% is comparable. The AE profile is acceptable and generally similar to that in other single-agent sunitinib studies and/or in patients with advanced RCC. Disclosure: Q. Wang: Employed by Pfizer Inc. as a clinician.S. Pan: Employed by Pfizer Inc. as a Director of Clinical Statistics and holds Pfizer stock. All other authors have declared no conflicts of interest. Annals of Oncology 852P PREDICTIVE VALUE OF TIME TO BEST RESPONSE FOR EFFICACY MTOR INHIBITORS (MTORI) IN METASTATIC RENAL CELL CARCINOMA (MRCC) PATIENTS (PTS) R.T. Elaidi 1 , C. Teghom 2 , A. Comte 2 , M. Jebali 2 , J. Fouque 3 , J. Medioni 4 , S. Oudard 5 1 Oncology, Hospital G.Pompidou, Paris, FRANCE, 2 Medical Oncology Service, Hopital European George Pompidou, Paris, FRANCE, 3 Pharmacy, Hopital Europeen Georges-Pompidou, Paris, FRANCE, 4 Medical Oncology, Georges Pompidou Hospital and Rene Descartes University, Paris, FRANCE, 5 Medical Oncology Department, Georges Pompidou Hospital and Rene Descartes University, Paris, FRANCE Background: mTORi usually induce stable disease but some patients present with a rapid objective response. In order to predict early those patients susceptible to respond to mTORi, we investigated the relationship between time to best response and time to progression. Methods: Data were retrospectively collected in patients treated with mTORi (Ev: everolimus, Tem:temsirolimus) for mRCC in 1 st to 4th line setting at the European G. Pompidou Hospital in Paris between 2007 and 2011. Time to best response was obtained from CT-scan and objective response assessed according to RECIST 2.0. Efficacy was assessed by time to progression (TTP) from initiation of 1 st mTORi until disease progression/death. Overall survival (OS) was defined as the time from 1 st mTOR to death/last contact. Kaplan-Meier estimates with Log-Rank test were used for categorical data. Cox model was used for continuous data and hazard ratios calculation. Only pts having received at least 1 cycle of mTORi were included. Results: Among the 75 pts, 63 presented with a documented response: PR = 6, SD = 40, PD = 17. 12 pts were excluded for mTORi discontinuation due to toxicity before any response assessment or uncertain date of best response. The 63 eligible pts had a median age = 61 (range: 28-86), sex ratio = 51/12, Ev/Tem = 37/26. Line setting: 1 st =7, 2 nd =17, 3 rd =19, 4 th = 17, 5 th = 3. Median follow-up time = 22.8m. Time to progression= 7.3m (95%CI: [4.3–9.1]). Time to best response: SD = 2.3 (0.7–8.2), PR = 7.6 (0.7–18.8), PD = 2.1 (0.9–5.0). Time to best response was significantly associated with TTP (N = 46, 35 events, HR = 0.86, 95% CI [0.76–0.97], p = 0.014), but also OS (N = 46, 31 events, HR = 0.83, 95% CI [0.70-0.98], p = 0.03]), an early response leading both to a more rapid progression and being of poor prognosis. Conclusions: Time to best response was significantly associated to time to progression and overall survival in pts treated with mTORi for mRCC. Given the small sample and the rough assessment of RECIST criteria, further study is needed to investigate the real value of percentage in tumor decrease at each evaluation and velocity of response as a more precise predictive marker of efficacy for these drugs. Disclosure: S. Oudard: Advisory board to disclose: Sanofi Aventis, Bayer, Novartis, Roche, Pfizer Compensated consultant relatioship to disclose: Novartis, Roche Honoraria to disclose: Sanofi Aventis, Bayer, Novartis, Roche, PfizerAll other authors have declared no conflicts of interest. 853P PRELIMINARY RESULTS OF EARLY ASSESSMENT OF RESPONSE WITH PERFUSION-CT IN PATIENT WITH METASTATIC RENAL CELL CARCINOMA TREATED WITH SUNITINIB O. Reig Torras 1 , M.C. Sebastia 2 , I. Victoria 1 , B. Paño 3 , M. Campayo 1 , C. Nicolau 3 , B. Mellado 1 1 Medical Oncology, Hospital Clinic y Provincial de Barcelona, Barcelona, SPAIN, 2 Radiodiagnóstico, Hospital Clínic de Barcelona, Barcelona, SPAIN, 3 Radiology, Hospital Clínic de Barcelona, Barcelona, SPAIN Introduction: The fact that renal cell carcinoma (RCC) is highly dependent of angiogenesis has allowed the development of antiangiogenic drugs (e.g. sunitinib). The assessment of response was based on Response Evaluation Criteria in Solid Tumors (RECIST) but in RCC there is no good correlation between response rate and survival data. So, it is necessary to adopt new image methods that allow a more accurate assessment of response. Objectives: To evaluate the pattern of response with perfusion-CT one month after the beginning of the antiangiogenic treatment and correlate with the radiologic evolution. Material and methods: Patients (pts) with metastatic RCC and candidates for sunitinib treatment were selected. A volumetric study (21 cm) with perfusion-CT (Flash Definition, Siemens, Erlangen, Germany) was done in these patients before starting the treatment, 1 and 4 months after the antiangiogenic initiation. We defined 6 types of response patterns based on changes in density (D), perfusion (P) and size (S) of the metastases. ix282 | Abstracts Volume 23 | Supplement 9 | September 2012
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Familial cancer Judith Balmaña, Ba
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patients. We have developed a rando
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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

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