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ESMO-JSMO Joint Symposium: Recent advances in the treatment of GI tract and liver cancer in the EU and Japan 124IN HEPATOCELLULAR CARCINOMA: PRESENT TREATMENT STRATEGY IN JAPAN J. Furuse Department of Medical Oncology, Kyorin University School of Medicine, Tokyo, JAPAN Hepatocellular carcinoma (HCC) develops mainly from liver cirrhosis due to hepatitis B or C virus infection. A screening system in patients with cirrhosis is important to diagnose HCC at as earlier a stage as possible. As a result, in Japan, approximately 90% of HCC patients successfully undergo local therapies including hepatectomy, local ablation, and transcatheter arterial chemoembolization (TACE). However, many patients develop recurrences or progression after these treatments, and an effective systemic therapy is needed to improve the survival. Sorafenib is the first agent which demonstrated survival benefits in patients with unresectable advanced HCC that was approved for HCC in Japan in May, 2009, and more than 13,000 patients have received systemic therapy using sorafenib. In a survey by the Study Group on New Liver Cancer under the auspices of the Health and Labour Sciences Research Grant in Japan, 264 patients treated with sorafenib were analyzed and 90% of these patients treated with sorafenib received prior treatments including hepatectomy, local ablation and/or TACE. Common adverse events were hand-foot skin reaction, rash and diarrhea. The median overall survival was 11.0 months. These results were comparable with those of a large phase III trial of sorafenib, the SHARP trial. Following sorafenib, several targeted agents are currently under investigation in the treatment of HCC at various stages. Large randomized control trials are needed to establish new standard treatments, and most trials have been conducted in international collaboration including Japan. On the other hand, some trials are conducted only in Japan, for example combination of hepatic arterial infusion chemotherapy with sorafenib. In this presentation, the outcomes of sorafenib treatment in Japan and recent clinical trials in chemotherapy are summarized and discussed. Disclosure: J. Furuse: I received honoraria and consulting fee from Bayer, Eli Lilly, Taiho, Chugai and Eisai. 125IN HEPATOCELLULAR CARCINOMA IN THE EU J. Bruix Liver Unit, Hospital Clinic y Provincial de Barcelona, University of Barcelona, Barcelona, SPAIN The incidence of liver cancer varies across Europe. However, while figures have stabilised in Italy and Spain, Northern countries present a slight increase in recent years. In most cases, liver cancer appears in the background of chronic liver disease related to hepatitis C or B, infection and alcoholism, among other risk factors. Current data show that hepatocellular carcinoma is the leading cause of death in patients with cirrhosis and that the incidence of intrahepatic cholangiocarcinoma is on the rise. Because of its clinical relevance all scientific associations have developed practice guidelines to inform patients, physicians and regulatory agents about the established diagnostic and therapeutic procedures. Non-invassive diagnostic criteria have been accepted and in almost all documents the recommended strategy for staging and treatment indication is the BCLC model. Following it, patients diagnosed with HCC are stratified into stages for which different treatment options are to be considered. References 1. Jelic S, Sotiropoulos GC; ESMO Guidelines Working GroupHepatocellular carcinoma: ESMO Clinical Practice Guidelines for diagnosis, treatment and followup. Ann Oncol. 2010 ;21 Suppl 5:v59–64 2. Bruix J, Sherman M. Management of hepatocellular carcinoma: An update. Hepatology. 2011 Mar 1;53 (3):1020–2. 3. EASL-EORTC Clinical Practice Guidelines: Management of hepatocellular carcinoma. J Hepatol. 2012 Apr;56 (4):908–43. 4. Forner A, Llovet JM, Bruix J. Hepatocellular carcinoma. Lancet. 2012;379 (9822):1245–55. Disclosure: The author has declared no conflicts of interest. Annals of Oncology 23 (Supplement 9): ix63, 2012 doi:10.1093/annonc/mds487 126IN COLORECTAL CANCER: A NEW ORAL CYTOTOXIC AGENT REAPPEARS T. Yoshino Department of Gastroenterology & Gi Oncology, National Cancer Center Hospital East, Kashiwa, JAPAN Cytotoxic agents, such as fluoropyrimidine, irinotecan, and oxaliplatin and antibodies such as bevacizumab, and cetuximab and panitumumab have been shown to significantly improve the survival of patients with unresectable metastatic colorectal cancer (mCRC). Although many patients have a good long-term performance status, a standard therapy for patients refractory to or unable to tolerate these agents does not currently exist. TAS-102 is a novel oral nucleoside antitumor agent consisting of trifluorothymidine (FTD) and 5-chloro-6-(2-iminopyrrolidin-1-yl) methyl-2,4 (1H,3H)-pyrimidinedione hydrochloride (TPI) at a molar ratio of 1 to 0.5. TAS-102 possesses a mechanism of action different from that of other antitumor agents, including fluoropyrimidine, irinotecan and oxaliplatin. Based on a phase I clinical trial in Japan, the recommended dose of TAS-102 (35 mg/m 2 /b.i.d) twice daily administered orally in days 1-5 and 8-12 of a 28-day cycle was determined. These results indicated that TAS-102 was expected to further improve the outcomes of patients with unresectable mCRC. We conducted randomized, double-blind phase II trial as a placebo-controlled study to evaluate the efficacy of TAS-102. A total of 172 colorectal cancer patients who were refractory or intolerable to 2 or more regimens of standard chemotherapy with a fluoropyrimidine, irinotecan, and oxaliplatin underwent either TAS-102 plus best supportive care (BSC) (114 patients) or placebo plus BSC (58 patients) with the primary endpoint of overall survival. TAS-102 significantly decreased death risk compared to placebo (hazard ratio, 0.56; 95% confidential interval [CI], 0.39-0.81; P = 0.0011). The median overall survival was 9.0 months in the TAS-102 group and 6.6 months in the placebo group. TAS-102 significantly improved progression-free survival (median, 2.0 months vs 1.0 month; hazard ratio, 0.41; 95% CI, 0.28-0.59; P < 0.0001). TAS-102 was effective regardless of KRAS mutational status. Grade 3 or higher adverse events observed in the TAS-102 group were neutropenia (50.4%), leucopenia (28.3%), and anemia (16.8%). There were no treatment-related deaths. An international phase III trial is ongoing to confirm the clinical benefits of TAS-102 worldwide. Disclosure: T. Yoshino: I have honoraria with Chugai, Takeda, Bristol-Myers Squibb, Yakult and Merck Serono. I have research funding from Bayer, Taiho, Daiichi-sankyo and Quintiles. I have received consulting fee from Takeda. 127IN CAN PET IMAGING HELP INDIVIDUALIZE THE TREATMENT OF COLORECTAL CANCER PATIENTS? A. Hendlisz Medicine Department, Institut Jules Bordet, Brussels, BELGIUM While the science of medicine tries to understand the rules and hidden laws behind diseases and their management, the art of medicine aims to treat individual patients by matching clinical observations and existing knowledge. The ambiguity between the art and the science of medicine has never been so obvious than in our attempts to tailor cancer treatment to individual patients: the growing evidence of tumor heterogeneity makes understanding a patient’s disease increasingly complex, especially when one considers the inadequacy of current assessment tools, which is becoming more apparent each day. In the setting of advanced colorectal cancer (aCRC), three main clinical situations coexist: metastasis that is immediately resectable with curative intent, borderline resectable disease and definitively non-resectable disease. Despite broad parameters within which to treat disease, clinicians lack tools that can rapidly and reliably point out treatment inefficiency in order to allow a therapeutic strategy to be quickly stopped or adapted. The usual endpoints of prospective randomized trials, which form the basis of the science of medicine, are seldom usable at the bedside to exercise the art of medicine. Death (overall survival) and progression (progression-free survival) both occur too long after the beginning of a treatment, and quality of life is much too subjective. The RECIST-based response rate is more readily available and relatively well standardized, but careful analysis reveals a definite but only small correlation with survival outcome in the aCRC setting. Several alternates for tumor response assessment have been studied: plasma tumor markers, circulating tumor cells, and functional imaging, notably the FDG-PET scan. However, few data from well-structured studies are available, and they are sometimes discordant. Among these alternatives, metabolic imaging by FDG-PET appears to be the most promising, bearing the highest and the most reproducible negative predictive value. This means that it could become useful both in the daily clinic and to develop new concepts for clinical trials. The aim of this review is to present the available evidence, point out areas of weakness, and consider how current findings might shape the future development of both FDG-PET techniques and study designs. Disclosure: The author has declared no conflicts of interest. Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds487 | ix63
ESMO-MASCC Joint Symposium: Integration between medical oncology and supportive care: Two sides of the same coin 128IN SUPPORTIVE AND PALLIATIVE CARE: CORE ELEMENTS OF QUALITY CANCER CARE N.I. Cherny Dept Medical Oncology, Shaare Zedek Medical Centre Oncology Institute, Jerusalem, ISRAEL There has been much confusion regarding the definitions of supportive care (SC) and palliative care (PC) and many authorities use the terms interchangeably. Both MASCC and ESMO are among the minority of professional organizations that distinguish between the two. SC is defined as care that facilitate safe and effective anti cancer care, minimizing toxicity and optimizing physical, psychological and social function of patients undergoing disease management strategies. SC facilitates the ability to deliver optimal anti cancer care and it has a particular focus on side effect prevention and management. All cancer patients undergoing treatment need SC and this is equally true for those undergoing curative treatments as it is for those undergoing treatment to mitigate the trajectory and consequences of advanced and incurable cancer. PC optimizes the comfort, function and social support of the patient and their family when cure is not possible. The context of incurability, with all of its implications for the patent and family, that grounds palliative care as a special entity. “End of life care” or “terminal care” is defined as PC when death is imminent. End-of-life care acknowledges that the intensity of physical, psychological, existential, spiritual and family issues may be magnified by the patient’s approaching death. Patients with incurable cancer receiving antitumor therapies will often need both S + PC. Conclusion: The delivery of high quality S + PC are core elements of quality oncological service and it is incumbent upon clinicians to be adequately skilled, to tend to these needs with due diligence and to promote the development of effective service delivery frameworks to ensure that patients receive these vita elements of quality care. Disclosure: The author has declared no conflicts of interest. 129IN ANTIEMETICS: A WINDOW TO TRANSLATIONAL MEDICINE S. Grunberg Hematology/Oncology, University of Vermont, Burlington, VT, UNITED STATES OF AMERICA The concepts of targeted therapy, molecular pharmacology, and population genetics are not new to the field of clinical antiemetic care. The most basic principle of antiemetic care is to identify and target neurotransmitter/neurotransmitter receptor pairs within the emetic reflex arc that can be suppressed without causing severe disruption of physiologic function. Early research focused on dopamine (D2) receptors led to effective antiemetics but also resulted in significant antidopaminergic toxicity. Identification of serotonin (5HT3) receptor pathways with similar emetogenic activity provided a target that could be effectively suppressed without antidopaminergic toxicity. Appreciation of the role of neurokinin (NK-1) receptors in delayed emesis complements previous knowledge and allows for more effective suppression of emesis throughout the period of emetic risk. More recently genetic mutations that alter these neural pathways as well as the metabolic pathways of antiemetic agents have been appreciated. Over-expression of the CYP 2D6 pathway increases metabolism of some serotonin antagonist antiemetics and has been shown to decrease the efficacy of these agents. A mutation in the 5-HT3B subunit of the serotonin (5HT3) receptor itself can also alter sensitivity to emetogenic chemotherapy and to antiemetic agents. Appreciation of the role of genotype and phenotype in the response of different ethnic groups to therapy has now allowed correlation of lessons from population science with clinical treatment. A study from Malaysia comparing Chinese, Malay, and Indian populations receiving similar chemotherapy and similar antiemetics has demonstrated an increased emetic response in the Chinese population. A study from the United States similarly demonstrated increased emetic response in a Chines population compared to a Caucasian population. Whole genome analysis to identify differences between these ethnic groups may therefore lead back to genetic foci of interest that will in turn affect the clinical science of antiemetic protection. Such translational and multidisciplinary efforts increase knowledge of the basic mechanisms of disease and treatment while simultaneously improving patient quality of life. Disclosure: S. Grunberg: I have served as a consultant to Helsinn, Merck, Tesaro, AP Pharma, and Prostrakan. I also am a stockholder in and have received honoraria from Merck. Annals of Oncology 23 (Supplement 9): ix64, 2012 doi:10.1093/annonc/mds488 130IN GASTROINTESTINAL TOXICITY IN ONCOLOGY: EVOLUTIONARY SCIENCE D. Keefe Medicine, University of Adelaide, Adelaide, SA, AUSTRALIA Proper practice of Medical Oncology requires an understanding of the science of regimen-related toxicity (RRT); and as treatment regimens evolve, so too does that science. Mouth ulcers, pain, diarrhea and constipation are among the common side effects of chemotherapy and hinder our ability to give adequate, perhaps curative, doses. As we increase our understanding of toxicity mechanism, so we slowly improve its prevention and treatment. However, this must not come at the cost of tumour-response, thus requiring understanding of the interaction between mechanism of action and of toxicity. Animal models have become increasingly sophisticated, and are used to screen for interventions that reduce toxicity without affecting tumour response. The introduction of the targeted anti-cancer (TAT) agents has further complicated the picture, with GI toxicity being a major, and not always predicted effect. The mechanism of toxicity is often the same as the mechanism of action, making successful management difficult. Each new class of TAT has a new mechanism, epidemiology and presentation of toxicity, so we constantly need to update our understanding of the science. A mouth ulcer caused by methotrexate is not the same as one caused by an mTOR inhibitor. There has been a corresponding evolution in the doctor-patient relationship surrounding toxicity, as we have moved from the paternalistic relationship to a partnership, with Patient Reported Outcomes (PROs) increasingly important. Clinicians will usually rate a given toxicity less severely than will the patient; the message being that we need to listen to the patient. Risk prediction is receiving more attention, with Oncologists now talking about response prediction and risk prediction as two sides of the same coin, aiming to offer treatment to non-toxic responders, treatment with toxicity interventions to toxic responders, and completely avoid ineffective treatment for non-responders. We have moved from the simplistic risk prediction of age, sex, comorbidity and drugs, to complex gene and SNP analysis using modern bioinformatics. However, given the common lag between drug development and successful toxicity interventions, toxicity specialists should be involved earlier in drug development. The science will continue to evolve as long as cancer treatment evolves. Disclosure: D. Keefe: Prof Keefe works with many companies in the development of agents in the field of GI toxicity. These include: Helsinn, Entera Health, Pfizer, GSK and Merck. 131IN DEVELOPMENT OF RATIONAL THERAPEUTIC STRATEGIES FOR PATIENTS WITH PRE-CACHEXIA AND CACHEXIA THROUGH THE INTEGRATION OF ONCOLOGY AND PALLIATIVE CARE AND COLLABORATIVE CLINICAL TRIALS (EAPC-RESEARCH NETWORK) F. Strasser Oncological Palliative Medicine, Cantonal Hospital, St.Gallen, SWITZERLAND Nutritional issues are frequent but underestimated in advanced, incurable cancer patients (pts), impacting patients’ tolerability of anticancer treatment, quality of life, physical (and social) function, effective health services use and family members. The new cancer cachexia framework (Fearon & Strasser, Lancet Oncology 2011) separating simple starvation from cachexia, facilitates the development of both effective nutritional, multimodal and tailored treatments. Collaborative, international efforts and EU-funding made this framework possible. Cachexia is defined by muscle loss relevantly impacting physical function, which is not reversible by nutrition only, and is caused by a combination of dysregulated eating ability and a dysbalanced catabolic and anabolic metabolism. To identify such pts in clinical practice, monitoring of % weight loss in the last 6 months and asking pts about appetite and eating shall become a standard procedure. The clinical assessment will diagnose cachexia, then classify pts for the phase (pre-cachexia, cachexia, refractory cachexia), main domains (stores, intake, potential, performance), and severity. Currently a consensual cachexia assessment is developed involving various professional groups. For pre-cachexia and cachexia there is currently no established therapeutic intervention. Clinical trials investigating increase of nutritional intake (oral, enteral, parenteral) focus on patient populations having simple starvation. For cachexia treatment a multimodal approach is mandatory, tackling in a combined strategy its main causes of decreased eating ability, catabolism, decreased anabolism, and impaired neuro-muscular function. Preclinical studies and several clinical trials document the potential of such interventions. A sentinel next step however, is the conduct of well powered, multimodal phase III trials in pre-cachexia and cachexia. For refractory cachexia, efforts concentrate to characterize these pts and develop psychosocial and other symptom alleviating interventions. Currently guidelines on treatment are updated, applying the procedures of ESPEN. Educational initiatives emerge. All these efforts mandate collaboration of professionals and working groups of involved societies (e.g., EAPC-RN, ESPEN, MASCC, ESMO PCWG, SCWD). Disclosure: F. Strasser: Unrestricted grants: Celgene (NCT01127386), Fresenius (http://www.surveymonkey.com/s/XBT6HQW.). Participation BYM338 trial (NCT01433263). Occasional Advisor: Baxter, Danone, Fresenius, Helsinn, Novartis, X-Biotech. ix64 | Abstracts Volume 23 | Supplement 9 | September 2012
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subscriptions A subscription to Ann
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Annals of Oncology Official Journal
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The European Society for Medical On
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Audit Committee Chair: Fortunato Ci
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Familial cancer Judith Balmaña, Ba
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publications and aggregated in a me
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383 WHY DO WOMEN WITH BREAST CANCER
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more than 6 cycles of capecitabine.
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abstracts CNS tumors 410O CONDITION
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Conclusions: Our data suggested tha
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Conclusions: As in other cancer typ
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knowing HLA-A status double-blindly
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Acquired-resistance to EGFR inhibit
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TST is active in breast and gastric
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Treatment-induced shedding of circu
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(P = 0.64). Synchronous BBC was sig
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abstracts gastrointestinal tumors,
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Disclosure: M. Lee: I am an employe
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anti-EGFR treatment. The present st
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patients harboring a T/T genotype t
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experienced significantly more ≥
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Results: 92/114 patients were preop
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minutes. In a previous study, 30-mi
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Patients and methods: Chemotherapy-
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Conclusions: AMPK and ACC activatio
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of surgical monotherapy in patients
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factors play the determining role i
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considered sufficient to give an 80
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validate the revised AJCC 7th stagi
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Results: Among 862 MM we identified
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Results: Frequently reported advers
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discriminate the prognosis of HCC p
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abstracts genitourinary tumors, non
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patient preference for P over S, an
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Hb, PS and LM. Median PFS for patie
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Results: 1,622 patients were identi
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Conclusions: In pts with RCC treate
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physicians in the U.S. and Europe.
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eight patients who had infertility
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patients. We have developed a rando
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morbidities that radiation would le
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anthracyclines in vitro. A favorabl
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survival rates of 13-25% (Prieto et
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advisor for Merck Sharp & Dohme, an
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or cutaneous melanoma. A survival u
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systemic therapy or were intolerant
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abstracts neuroendocrine tumors and
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morbidity, with G3 tumors behaving
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pts. Poorly differentiated endocrin
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Adenocarcinoma was present in 25 pa
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Method: Endobronchial ultrasound gu
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widely used by single agent or plat
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disease after surgery were treated
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stage IIIA NSCLC, EML4-ALK fusion-p
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months (95% CI:13-25). The PFS and
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maintenance therapy had favourable
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abstracts non-small cell lung cance
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Ingelheim, GSK Biologicals (compens
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GlaxoSmithKline (myself, compensate
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N-arm n=34 P-arm n=32 All n=66 Male
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MERCK SERONO: Advisor, speaker in s
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Conclusions: These data from SAiL a
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NSCLC diagnosis and time of BM diag
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1291P PHASE I/II DOSE-FINDING STUDY
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Network utilization of WBCGF in the
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1303P COST EFFECTIVENESS OF PEMETRE
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Results: The patients’ characteri
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EGFR mut at exons 18, 19, 21, and K
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Methods: EML4-ALK fusion was screen
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Results: The median survival time (
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epresented by 19 pts (32%) female,
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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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