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Annals of Oncology mono-exponential half-life of ∼15 hours in rats and has a limited volume distribution roughly equivalent to the blood volume. In rat toxicity studies in rats, the MTD of PL-MLP was two to three-fold higher than that of MMC in mg-equivalent doses. Therapeutic studies in BALB/c mice inoculated i.p. with C26 tumor cells show a clear survival advantage for treatment with PL-MLP over free MMC at all dose levels tested, whether treatment was administered by the i.v. or by the i.p. route. In the porcine model, no acute infusion reaction to i.v. administration of PL-MLP was observed. PL-MLP appears to be a stable formulation with minimal prodrug activation and release of MMC in circulation, yet significant antitumor activity, indicating in vivo prodrug activation in tumors. PL-MLP may represent an effective therapeutic tool in a broad spectrum of malignancies, including multi-drug resistant tumors, with improved safety over free MMC, and is due to be tested in a human phase I study in 2012. Disclosure: A.A. Gabizon: I am the founder and Chief Scientist of Lipomedix Inc., a company with a vested interest in the product discussed in this presentation. Y. Amitay: Paid employee of Lipomedix, a product of which is discussed here. All other authors have declared no conflicts of interest. 478P PHASE I SAFETY AND TOLERABILITY OF ONCE DAILY ORAL AFATINIB (A) (BIBW 2992) IN COMBINATION WITH GEMCITABINE (G) IN PATIENTS (PTS) WITH ADVANCED SOLID TUMOURS S. Zanetta 1 , J. Bennouna 2 , N. Isambert 3 , H. De Mont-Serrat 4 , I. Tschoepe 4 , P. Squiban 4 , J. Delord 5 1 Oncology Department, Centre Georges François Leclerc, Dijon, FRANCE, 2 Oncology/ Pneumology, Institut de Cancerologie de l’Ouest-site René Gauducheau, Nantes, FRANCE, 3 Medical Oncology, Centre Georges François Leclerc, Dijon, FRANCE, 4 Medical Affairs, Boehringer Ingelheim, Reims, FRANCE, 5 Clinical Resarch Unit, Institut Claudius Regaud, Toulouse Cedex, FRANCE Background: A is an orally bioavailable, irreversible, ErbB Family Blocker. This open label, Phase I, dose escalation trial investigated the safety, tolerability and pharmacokinetics of A in two parallel dose cohort expansion parts, in combination with either G (Part A) or docetaxel (Part B) in pts with relapsed or refractory solid tumours. Preliminary results from Part A are presented here. Methods: Eligible pts (confirmed diagnosis of advanced solid tumours, Eastern Cooperative Oncology Group Performance Status 0–1) received once-daily, oral dosing of A in combination with G, given intravenously at Day 1 and at Day 8 of every 3 week cycle. Dosing of A started on Day 2 of Cycle 1. The primary objective was to establish the maximum tolerated dose (MTD) based on the occurrence of dose limiting toxicities (DLTs) observed in Cycle 1. Dose escalation was performed with cohorts of 3–6 pts using a 3 + 3 design. Initial starting dose level was A 30 mg/ day and G 1000mg /m 2 , escalating up to A 50 mg/day and G 1250 mg/m 2 , until the MTD was reached, and followed by a pharmacokinetic expansion cohort of 12 pts at the MTD level. Results: Nineteen pts were treated in the escalation part of the study with the following baseline characteristics: mean age (53.7 years), female (63.2%) and number of prior chemotherapies (≤2: 26%; >2: 74%). In Cycle 1, DLTs were experienced by one pt out of six receiving A 30 mg and G 1250 mg/m 2 , and in two pts at a dose level of A 40 mg/day and G 1250 mg/m 2 . Adverse events (AEs) observed in most pts were diarrhoea (89.5%) and rash (63.2%). MTD was exceeded at a dose level of A 40 mg/day and G 1250 mg/m 2 . An intermediate dose level of A 40 mg/day and G 1000 mg/m 2 is currently under evaluation with two pts enrolled to date. Conclusions: In pts with relapsed or refractory advanced solid tumours, the combination of A with G is well tolerated, with manageable AEs. Dose finding is ongoing and MTD, safety profile and preliminary evidence of activity are anticipated to be reported at time of presentation. Disclosure: J. Bennouna: I have received honoraria from roche, boehringer ingelheim, and amgen for advisory board. It is for myself. H. De Mont-Serrat: Employee of Boehringer Ingelheim. I. Tschoepe: Employee of Boehringer Ingelheim. P. Squiban: Employee of Boehringer Ingelheim. All other authors have declared no conflicts of interest. 479P THE IMPACT OF PATIENT SOCIO-ECONONOMIC STATUS ON ACCESS TO EARLY PHASE CANCER TRIALS A. Mohd Noor 1 , S. Vizor 2 , B. McLennan 2 , D. Sarker 2 , H. Moller 1 , J. Spicer 1 , S. Papa 1 1 School of Medicine, Cancer Research Division, King’s College London, London, UNITED KINGDOM, 2 Medical Oncology, Guy’s and St Thomas NHS Foundation Trust, London, UNITED KINGDOM Background: Little is known about the influence of sociodemographic factors on patient access to early phase cancer trials. The toxicity and efficacy of cancer drugs can vary according to sociodemographic factors, and these differences should be considered to ensure generalisability of results and equality of access. Method: We conducted a review of patients referred to the early phase trials unit at our centre in the five years to 2012. Electronic records were studied for demographic and cancer-specific data. Socio-economic status was defined by the Index of Multiple Deprivation (IMD; 1 - least deprived, 5 - most deprived) recorded for the regional Cancer Registry population according to postal code. Multivariate analysis (adjusting for gender, age and tumour type) was performed comparing 10,784 incident cancer cases in south east London with the patients referred to our unit, and with those enrolled in a trial. Results: 430 patients (195 female) were referred for consideration of an early phase trial, with a median age of 62 years (range: 22-86). Ethnicity was 74% white. Univariate analysis of ethnicity suggested the non-white population was less likely to be recruited (OR 0.48, 95% CI 0.26-0.88), but this relationship was lost with adjustment for age, gender, cancer type and IMD. Multivariate analysis showed that referral was less likely for patients in the more deprived quintiles (IMD-5: OR 0.53, 95% CI 0.38-0.74). However, once referred to the unit, enrollment in a trial was not affected by IMD (IMD-5: OR 0.81, 95% CI 0.40-1.63). Conclusion: We show for the first time that social deprivation affects referral to an early phase cancer trials unit. The least deprived patients are almost twice as likely to be referred to the trial unit compared with the most deprived. This may be because patients in the higher deprivation quintiles are less suitable for a trial, for example due to comorbidities, or because of inequalities that could be addressed with patient or referrer education. Disclosure: All authors have declared no conflicts of interest. 480P SINGLE INSTITUTION PHASE I TRIAL OF THE NOVEL COMPOUND FIRST-IN-CLASS PDM08 IN REFRACTORY SOLID TUMORS (NCT01380249) J. Barriuso 1 , I. Soria 2 , V. Moreno 1 , M. Coronado 3 , I. Galicia 4 , M.A. Figueredo 2 , J. Frias 5 , J. Feliu 6 , A. Carcas 5 , J.L. Subiza 2 1 Oncology Phase I Unit, La Paz University Hospital, Madrid, SPAIN, 2 Inmunology Department, San Carlos Hospital, Madrid, SPAIN, 3 Nuclear Medicine, La Paz University Hospital, Madrid, SPAIN, 4 UCICEC, La Paz University Hospital, Madrid, SPAIN, 5 Pharmacology, La Paz University Hospital, Madrid, SPAIN, 6 Medical Oncology, La Paz University Hospital, Madrid, SPAIN Background: PDM08 is a synthetic derivative of the pyroglutamic acid with anti tumor effect in different murine cancer models. The absence of direct effect on tumour cells and the antitumor activity found in immunocompetent models indicates an immune response mediated mechanism. The aim was to assess the tolerability and safety profile of PDM08. Methods: PDM08 was administered twice a week for four-week cycles. An accelerate escalation phase was chosen with cohorts of 2 patients (pts) that had the possibility of escalate once to the next dose level if no grade ≥2 toxicity and no progressive disease were observed. An expansion cohort was planned at the MTD or the optimal biological dose (OBD). Extensive pharmacokinetic and pharmacodynamic (PD) data were collected. Preliminary efficacy was evaluated by PET-CT. Results: Since July 2011, 17 patients (pts) were recruited into 8 different dose levels (4pts were escalated) ranged from 0.560 mg to 56 mg. Pt characteristics were: males 52.9%. Median age: 68 (28-76). ECOG 0: 64.7%. Median of previous treatments was 3 ranged 2 to 5. 3 pts presented G1 headache. No DLTs were found. The best outcome was stable disease (SD) for 5 pts (4 colorectal and 1 endometrial), one being stable for 12 weeks, one 14 weeks and one remains stable after 21 weeks. 12.9% of the lesions evaluated by PET-CT showed a reduction in the maximum Standard Uptake Value (SUV) of 18-FDG. A pooled analysis of PD data from patients with the best response showed a statistically significant increased in serum levels of IL-17A, IL-13, IL-4, IL-5, TNFα, IL-22 and IL-1β (p < 0.05) from baseline. Interestingly patients without benefit showed higher basal levels of these cytokines. The analysis of blood cell populations in pts with SD found a trend to increase the absolute numbers of NKT (CD56, CD4), neutrophils (CD45, CD15, CD16b) and some specific markers of Myeloid-derived suppressor cells (CD11b, CD33). The OBD derived from PD changes was 56 mg. Conclusions: PDM08 is the first compound of a new class of drugs that can be dose-escalated safely in an accelerated manner and has promising activity. PD results suggest that PDM08 is boosting the innate immune response against cancer cells confirming preclinical data. Disclosure: All authors have declared no conflicts of interest. 481P TESETAXEL: ANALYSIS OF TWO DOSING SCHEDULES (ONCE WEEKLY VS. EVERY 3 WEEKS) USING A NOVEL ORAL TAXANE M. Beeram 1 , K. Papadopoulos 1 , A.W. Tolcher 1 , D. Rasco 1 , T. Cousin 2 , L. Itri 2 , A. Patnaik 1 1 Developmental Therapeutics, The START Center for Cancer Care, San Antonio, TX, UNITED STATES OF AMERICA, 2 Developmental Therapeutics, Genta Incorporated, Berkeley Heights, NJ, UNITED STATES OF AMERICA Background: Tesetaxel (TST) is a novel oral taxane that is active in taxane-resistant models, is not a substrate for p-glycoprotein, and has limited preclinical neuropathy. Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds395 | ix165
TST is active in breast and gastric cancers when administered orally once every 3 weeks (Q3W). Taxanes may have schedule-related activity and adverse reactions. We conducted a dose-ranging study comparing the safety, efficacy, and pharmacokinetics (PK) using two schedules. Methods: Patients (pts) had solid tumors, ECOG PS ≤ 2, and adequate organ function. In Schedule 1, TST was given once every 3 weeks from 18 to 27 mg/m2, escalated in increments of 3 mg/m2 to determine the MTD. In Schedule 2, TST was given once weekly for 3 weeks every 28 days, beginning at a total flat dose of 25 mg/ cycle with increases up to 75 mg/cycle. Dosing was then converted to a weight-based regimen at weekly doses of 12.5, 15, and 17.5 mg/m2 (i.e. total per cycle dose up to 52.5 mg/m2). 3 pts were treated at each dose level until the MTD. Results: 27 pts were treated on Schedule 1. The MTD was 27 mg/m2 and neutropenia was dose-limiting. One pt with nasopharyngeal carcinoma had a PR and 11 pts had stable disease, including several with taxane-resistant breast cancer. Cmax and AUC increased with increasing dose; however, the differences across the dose range examined were modest. No dose-related differences were apparent for other PK parameters. On schedule 2, 26 pts were treated in 8 dose cohorts. The MTD was 15 mg/m2 (total cycle dose, 45 mg/m2). Constitutional symptoms (fatigue and anorexia) proved dose-limiting at 17.5 mg/m2/wk. Only 1 pt had Grade 3 neutropenia. One pt with MBC (who had progressed after 2 prior taxane regimens) had a PR; 1 pt with prostate cancer had prolonged PSA reduction. PK analyses showed low but progressive increases in trough TST concentrations (0.4–4.6 nmol/mL) 7 days after each succeeding dose, consistent with the prolonged T½ of this drug (∼180 hrs). There was no substantial drug accumulation over multiple cycles. Conclusions: Tesetaxel administered once every 3 weeks is active in pts with advanced gastric, breast and other solid tumors, including pts who have received prior taxanes. The weekly regimen is currently being evaluated in Phase 2. Disclosure: A.W. Tolcher: Corporate sponsored research. T. Cousin: Employee of Genta Inc. L. Itri: Employee of Genta Inc. All other authors have declared no conflicts of interest. 482P PHASE 1 STUDY OF BPM 31510 (UBIDECARANONE) IN ADVANCED SOLID TUMORS: UPDATED ANALYSIS OF A NOVEL TREATMENT WITH PROMISING ACTIVITY S.P. Chawla 1 , A. Hendifar 1 , V.S. Chua 1 , D. Quon 1 , V. Narasimhan 1 , Y. Lavinski 2 , J. McCook 3 , R. Sarangarajan 3 , P. Song 3 , N. Narain 3 1 Clinical Research, Sarcoma Oncology Center, Los Angeles, CA, UNITED STATES OF AMERICA, 2 Research, MutualHealth LLC, Newport Beach, CA, UNITED STATES OF AMERICA, 3 Clinical Research, Berg Pharma, Natick, CA, UNITED STATES OF AMERICA Background: BPM is a novel small molecule that targets aerobic glycolytic pathway, re-capitulates BCL-2 mediated apoptosis and disrupts tumor angiogenesis. Methods: A standard 3 + 3, dose-escalation study was designed with primary objectives of dose finding (MTD), toxicity and pharmacokinetic correlates (PK). Secondary objectives included response, response duration and clinical benefit. Results: 42 patients with advanced solid tumors (refractory to standard therapy) were enrolled in 8 dose cohorts (5.6 mg/kg to 104.3 mg/kg). The trial is still ongoing as the MTD has yet to be reached. 31 (74%) patients completed at least one cycle and are considered evaluable for efficacy and toxicity. Median number of treatment cycles administered were 2 (range, 1-7) with median duration of 14 weeks (4-52 weeks). Of the 31 evaluable patients, 23 had grade I and 14 patients grade II elevation of INR without any significant clinical bleeding. Normalization of INR was observed in all the patients with vitamin K supplementation. Nine patients (29.0%) experienced mild headache during the first week of therapy, relieved with acetaminophen. There was no grade 3/4 treatment related toxicity. The pharmacokinetics of BPM was noted to be linear. The values for t1/2 ranged from 2.18 to 13.3 hr, with little or no dependence of t1/2 on dose. Objective tumor responses were noted at the dose of 58.6mg/kg with 1 complete response (myxoid liposarcoma) and 1 minor response (fibrosarcoma). With a median follow up of 14 weeks (4-52 weeks) clinical stabilization was observed in 61% of the patients. Conclusions: Interim data from this phase I study indicate that BPM is well tolerated with no dose limiting toxicity to date. There was no grade III/IV toxicity. Grade I/II toxicity included elevation of INR (without significant clinical bleeding) and mild headache. One patient had partial and one patient had minor response with stabilization of the disease in the majority. The current trial is in progress and there is strong rationale for further development of this unique compound which lacks the toxicity associated with chemotherapy. Disclosure: S.P. Chawla: I am an adviser to Berg Pharma LLC, Natick, MA; USA. A. Hendifar: I am an adviser to Berg Pharma LLC, Natick, MA; USA. V.S. Chua: I am an adviser to Berg Pharma LLC, Natick, MA; USA. D. Quon: I am an adviser to Berg Pharma LLC, Natick, MA; USA. Y. Lavinski: I am an employee of Berg Pharma LLC, Natick, MA; USA. J. McCook: I am an employee of Berg Pharma LLC, Natick, MA; USA. R. Sarangarajan: I am an employee of Berg Pharma LLC, Natick, MA; USA. P. Song: I am an employee of Berg Pharma LLC, Natick, MA; USA. N. Narain: I am an employee of Berg Pharma LLC, Natick, MA; USA. All other authors have declared no conflicts of interest. Annals of Oncology 483P DESIGNER PEPTIDE ANTAGONIST OF THE LEPTIN RECEPTOR WITH PERIPHERAL ANTINEOPLASTIC ACTIVITY S. Beccari1 , L.J. Otvos2 , G.L. Cetto3 , E. Surmacz2 1 Medical Oncology, Azienda Ospedaliera Universitaria Integrata Verona-"Borgo Roma", Verona, ITALY, 2 Sbarro Institute for Cancer Research and Molecular Medicine, Temple University, Philadelphia, PA, UNITED STATES OF AMERICA, 3 Medicine, Azienda Ospedaliera Universitaria Integrata Verona-"Borgo Roma", Verona, ITALY Background: Obesity-related hormone leptin has been implicated in the development and progression of different cancer types. Studies in vitro and animal models documented that leptin promotes cancer cell proliferation and neoangiogenesis. Targeting leptin signaling could become a new therapeutic option for the treatment of cancer, especially in obese patients. In order to inhibit pro-neoplastic leptin activity, we developed peptidomimetics that are analogs of leptin/leptin receptor (ObR) interaction site, able to compete with leptin binding and capable of blocking leptin effects in vitro and in vivo. The lead compound (Allo-aca), however, crosses the blood-brain-barrier (BBB), inducing undesirable orexigenic effects and consequent weight gain. Redesign of Allo-aca to decouple its Central Nervous System (CNS) and peripheral activity should produce superior compound for cancer treatment. Objective: The aim of this study was to design and test Allo-aca derivatives for their biodistribution, BBB penetration and in vitro anti-neoplastic activity against breast and colorectal cancer cells. Results: Examination of several Allo-aca derivatives resulted in identification of the peptidomimetic D-Ser. D-Ser did not distribute across BBB but was present in the periphery of experimantal animals. D-Ser was shown to bind ObR, and inhibit leptin-dependent-proliferation of ObR-positive breast and colorectal cancer cells in vitro at the concentration of 1 nM. Its efficacy was demonstrated both in adhesion and in three-dimensional cultures, without showing any partial agonistic activity. Antiproliferative D-Ser action was associated with the inhibition of several leptin-induced pathways, including JAK/STAT3, MAPK/ERK1/2 and PI3K/AKT, Cyclin D1 and E-cadherin. Conclusions: D-Ser is the first novel leptin-based peptidomimetic featuring peripheral ObR antagonistic activity. D-Ser inhibits leptin-dependent growth of breast and colorectal cancer cells through downregulation of several key mitogenic/ survival pathways. The novel peptide may serve as a prototype to develop new oncotherapeutics, useful for the management of obesity-related cancers. Disclosure: All authors have declared no conflicts of interest. 484P LURBINECTEDIN (PM01183) IN COMBINATION WITH GEMCITABINE (GEM). PRELIMINARY RESULTS OF AN ONGOING PHASE IB STUDY E. Calvo 1 ,L.Ares 2 , M. Foster 3 , I. López Calderero 2 , A. Cubillo 1 , A. Velasco 4 , V. Boni 1 , D. Wilkins 3 , A. Soto-Matos 5 , S. Szyldergemajn 4 1 Oncology, Hospital Sanchinarro/START, Madrid, SPAIN, 2 Oncology Service, Hospital Virgen del Rocio, Seville, SPAIN, 3 Oncology, University College of London Hospital, London, UNITED KINGDOM, 4 Clinical Operations, PharmaMar, Colmenat Viejo, Madrid, SPAIN, 5 Clinical, PharmaMar, Colmenat Viejo, Madrid, SPAIN Background: PM01183 is a new anticancer agent. It exerts a wide anti-tumour activity through minor groove DNA-binding. Pre-clinical evidence of synergism has been observed in combination with GEM. Single agent PM01183 has clinical activity in pancreatic and platinum-resistant ovarian cancer. Reversible neutropenia and high emetogenic potential are the main single agent toxicity. Methods: Informed and consented adult patients (pts) were included. The starting dose was PM01183 2.5 mg + GEM 800 mg/m 2 , on Days 1 and 8 q3wk. The dose was escalated in cohorts of 3-6 pts aiming to define the maximum tolerated dose (MTD). The highest dose reached with less than 1/3 of at least 9 pts having dose-limiting toxicities (DLTs) in Cycle 1 will be the recommended dose (RD). Age was restricted up to 75 years, PS-ECOG 0-1, have adequate major organ function and no more than 2 prior chemotherapy lines. Prior adjuvant GEM was allowed if relapse occurred >6 months. Results: As of MAY 2012, 23 pts were treated across 4 dose levels (DL), 8 (35%) were female, median age was 60 (37–72). NSCLC (n = 12; 52%), pancreatic/biliary tract (n = 5; 22%) and gynaecological (n = 4; 17%) were the most frequent tumour types. Dose escalation proceeded until the MTD was reached: DL 4 PM01183 3.5 mg + GEM 1000 mg/m 2 . Three pts experienced DLTs: Day 8 omission (neutropenia), febrile neutropenia, neutropenic infection/sepsis and grade 4 thrombocytopenia. One fatal sepsis occurred at the MTD. DL 3 (PM01183 3.5 mg + GEM 800 mg/m 2 ) expansion as possible RD is ongoing. PM01183/GEM seems well tolerated at doses below the MTD. Other toxicities in addition to reversible myelosuppression were mild nausea/vomiting, asymptomatic LFTs increases, pneumonia, anaemia or fatigue. Evidence of activity includes: 2/12 partial (PR) + 1/12 complete response (CR) in NSCLC (2 pts are ongoing after 13+ and 10+ cycles) and 1/4 PR in gynecological. No pharmacokinetic interaction was observed. ix166 | Abstracts Volume 23 | Supplement 9 | September 2012
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Annals of Oncology www.annonc.oxfor
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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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ESMO 2012 Congress Travel Grants 47
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Exhibitors The following companies
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ESMO Fellowships, 1989-2011 The Eur
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Ondrej Gojis, Czech Republic 2008-2
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abstracts hpv biology and implicati
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abstracts the characterization of l
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abstracts description of intra-tumo
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prevent cell death. It is anticipat
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22IN TARGETING THE HOST IN TNBC G.
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abstracts a paradigm shift in early
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abstracts how can medical oncologis
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feasibility), but by how high the c
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abstracts re-inventing the medical
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abstracts emerging diagnostic and t
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abstracts biologically based treatm
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abstracts molecular targets in mali
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abstracts melanoma therapy: from fr
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diagnosis and can also be used for
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analysis at 11 months median follow
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mouse model of Kras mutant NSCLC. I
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abstracts key topics in supportive
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ESMO-CSCO Joint Symposium: Building
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ESMO-EANM-ESR Joint Symposium: Imag
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ESMO-ESTRO Joint Symposium: Innovat
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ESMO-MASCC Joint Symposium: Integra
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ESO Society Symposium: Celebrating
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Results: TIMP-1 expression was incr
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will benefit from this targeted the
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cytomegalovirus (CMV). Analysis of
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functional consequences of Endoglin
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elationship between the ROR score,
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183P EPIDERMAL GROWTH FACTOR RECEPT
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Plasma adiponectin level on the pre
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Table: 198P PFS OS Median, mo HR Me
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Table: 226P Methods: Pts were rando
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number of biomarkers have been trie
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Table: 248O 249PD PROTEOMIC PREDICT
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Conclusions: BW and serum Ctrough o
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90 mg/m2-cyclophophamide 600 mg/m2
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sector patients. The aim of this st
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Linear Logistic Model with Relaxed
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Results: The median CTC fold change
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factors play the determining role i
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Abstract withdrawn in exceptional c
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were respectively 10.6 vs 8.5 vs 3.
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Results: 20 gastrointestinal cancer
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abstracts gastrointestinal tumors,
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Day 8. A second identical course wa
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proven in stage I GC. The aim of th
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Conclusions: Longer OS to FOLFOX wa
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692P PRELIMINARY SAFETY DATA FROM A
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subgroup. Taking into consideration
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Results: Three years of adjuvant im
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considered sufficient to give an 80
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721P FIRST-LINE TREATMENT WITH FOLF
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after Gem-based therapy. The additi
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735P RADIOGRAPHIC PARAMETERS IN PRE
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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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gastric cancer patients with CNS me
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discriminate the prognosis of HCC p
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prospective, non-interventional stu
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abstracts genitourinary tumors, non
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787O EXTERNAL VALIDATION OF THE ASS
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patient preference for P over S, an
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798PD OPEN-LABEL PHASE II TRIAL OF
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Hb, PS and LM. Median PFS for patie
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may have led to reduced dose and sh
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Results: 1,622 patients were identi
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RCC) was designed to address an unm
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Patients and methods: This is a sin
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treatment at week 4, and week 12 by
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Conclusions: In pts with RCC treate
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Table: 857P standard, but is not av
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efused HDCT. Of 23 patients, 20 com
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879 TREATMENT OF PATIENTS WITH META
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Median overall survival (OS) was 26
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abstracts Genitourinary tumors, pro
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and week 13 BPI-SF Q3 scores), 28%
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Working Group (PCWG)-2 guidelines r
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atio HR 0.39; CI 0.18, 0.83, p = 0.
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We observed tumor responses and pro
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Here we report emerging data from t
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Disclosure: S. Oudard: Has acted as
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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

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