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Annals of Oncology Results: The frequencies of ERP29 c.293AA + PTCH1 g.79755CC (95.0 vs 80.1%, P= 0.006; PA= 86%), ERP29 c.293AA + PTCH1 g.79456CC (94.9 vs 79.4%, P= 0.005; PA= 88%), ERP29 c.293AA + ZNF415 c.443GG (56.2 vs 31.6%, P= 0.01; PA= 84%) combined genotypes were more common in patients than in controls. Individuals with the referred genotypes were under a 4.3 (95%CI: 1.61-13.43), 4.3 (95%CI: 1.63-13.49), and 3.05 (95%CI: 1.29-7.53) fold increased risk for CM than others. In addition, the frequencies of ERP29 c.293AA + PTCH1 g.79456CC + IKBKAP p.1072CysCys (98.5 vs 83.3%, P= 0.01; PA= 86%), ERP29 c.293AA + PTCH1 g.79456CC + ZNF415 c.443GG (85.7 vs 44.1%, P= 0.004; PA= 96%) combined genotypes were also higher in patients than in controls. Individuals with the referred genotypes were under a 13.5 (95%CI: 2.47-252.3) and 8.05 (95%CI: 2.21-39.24) fold increased risks for CM than others. Conclusions: Our data present for the first time that: 1) ERP29 c.293A > G, PTCH1 g.79755C > T and g.79456C > T, IKBKAP p.Cys1072Ser, and ZNF415 c.443A > G SNPs are important inherited risk factors for CM and; 2) healthy individuals with these SNPs should receive recommendation to avoid sunlight exposition and should be frequently evaluated by a dermatologist to perform an early diagnosis of the tumor. Financial support: FAPESP and FINEP. Disclosure: All authors have declared no conflicts of interest. 1120P TIME TREND INFLUENCE OF SOCIECONOMIC STATUS ON SURVIVAL, BRESLOW THICKNESS, TIME FROM ONSET OF SYMPTOMS AND SURGICAL RESECTION IN STAGE I-II PRIMARY CUTANEOUS MELANOMA M. Mandala 1 , G. Imberti 2 , D. Piazzalunga 3 , R. Labianca 1 , G. Lucisano 4 , B. Merelli 1 , S. Mosconi 1 , L. Marchesi 2 , A. Gianatti 5 , C. Tondini 1 1 Oncology and Haematology, Ospedali Riuniti di Bergamo, Bergamo, ITALY, 2 Dermatology, Ospedali Riuniti Bergamo, Bergamo, ITALY, 3 Surgical Oncology, Ospedali Riuniti Bergamo, Bergamo, ITALY, 4 Epidemiology, Mario Negri Sud, Santa Maria Imbaro, ITALY, 5 Pathology, Ospedali Riuniti Bergamo, Bergamo, ITALY Objective: To investigate the time trend influence of socioeconomic status (SES) on Breslow thickness (BT) and survival in patients (pts) with stage I-II primary cutaneous melanoma (PCM). Patients and methods: Pathologic and sociodemographic characteristics of prospectively collected, consecutive pts diagnosed with PCM between November 1, 1998, and July 31, 2009 were evaluated. We categorized SES into 3 levels: low (manual employees with primary education level), middle (non-manual employees with middle education level), and high (professionals, executives with tertiary education). We divided the representative years between 2000 and 2009 into three four-year (table 1). In the multilvariate analysis models the following variables were tested: SES, marital status, sex and age. Results: A total of 1274 available pts were analyzed. Overall a progressive decrease of BT was observed (table 1). In the first four year period gender and age correlated with BT and ulceration [m vs f OR (95%CI): 1.66 (1.10-1.52) and (>60 vs G, PTCH1 G.79755C > T AND PTCH1 G.79456C > T POLYMORPHISMS WITH INHERITED RISK OF CUTANEOUS MELANOMA G.A.S. Nogueira, G.J. Lourenço, C. Oliveira, J.A. Rinck-Junior, E.F.D. Costa, A.M. Moraes, C.S.P. Lima Clinical Medical, University of Campinas, Campinas, BRAZIL Background: Recently we found that SNPs alter the oropharynx carcinoma risk in tumor suppressor MCC c.*5077A > G, PTCH1 g.79755C > T, and PTCH1 g.79456C > T. This study was conducted using high-resolution large-scale DNA microarray genotyping (5.0 SNP array, Affymetrix ®), and the quantities and functions of the proteins encoded by distinct alleles of the polymorphisms are being examined by our research group. Objective: We aimed to verify whether the different genotypes of polymorphisms in MCC c.*5077A > G, PTCH1 g.79755C > T, and PTCH1 g.79456C > T alter the CM susceptibility. Materials and methods: Genomic DNA of 149 CM patients and 153 controls was analyzed by TaqMan genotyping (Applied Biosystems®). Statistical significance of differences between groups was calculated by using chi-square (χ2) and Fisher’s exact tests. Power analysis (PA) was used to verify the effect of sample size on the results obtained in the study. Results: Samples from patients with MC and controls were in Hardy-Weinberg equilibrium for MCC and PTCH1 loci. Similar frequencies of MCC and PTCH1 genotypes were observed in patients and controls. Individuals with distinct isolated genotypes of the genes were under similar risks for CM. The frequencies of the combined genotypes MCC 5077AA + PTCH1 79755CC (90.4% versus 72.3%, P= 0.004; PA: 99.0%), MCC 5077AA + PTCH1 79456CC (89 0% versus 71.6%, P= 0.008; PA: 98.0%), and MCC 5077AA + PTCH1 79755CC + PTCH1 79456CC (91.3% versus 76.1%, P= 0.004; PA: 99.0%) were higher in patients than in controls. Individuals with these genotypes were at 4.44 (CI95%: 1.68 – 13.17), 3.60 (CI95%: 1.45 – .87), and 4.70 (CI95%: 1.75 – 14.63)-fold increased risks for CM than others, respectively. Conclusion: Our results suggest that combined MCC and PTCH1 polymorphisms are an important inherited risk factor for CM. We believe that healthy carriers with these genotypes deserve recommendations for protecting their skin from the harmful effects of UV rays to prevent tumor disease and periodic follow-up with the dermatologist for early tumor diagnosis. Financial support: State of São Paulo Research Foundation (FAPESP) and Research and Project Financing (FINEP) Disclosure: All authors have declared no conflicts of interest. 1122P INHERITED ABNORMALITIES IN GENES THAT DURING THE APOPTOSIS PROCESS AND CUTANEOUS MELANOMA RISK C. Oliveira 1 , J.A. Rinck-Junior 1 , G.J. Lourenço 1 , M.L. Cintra 2 , A.M. Moraes 1 , C.S.P. Lima 1 1 Department of Internal Medicine, State University of Campinas, Distrito de Barão Geraldo, Campinas, São Paulo, Brazil, BRAZIL, 2 Department of Pathology, State University of Campinas, Distrito de Barão Geraldo, Campinas, São Paulo, Brazil, BRAZIL Background: P53 (guardian of the genome), MDM2 (p53 inhibitor), BCL2 (anti-apoptotic) and BAX (proapoptotic) genes remove cells damaged by ultraviolet (UV) rays of sunlight and, therefore, are related to the origin of cutaneous melanoma (CM). All these genes are polymorphic in humans. The Arg wild allele of the P53 Arg72Pro polymorphism is more efficient than the variant Pro allele at inducing apoptosis. The variant G and A alleles of MDM2 T309G and the BCL2 C (-948) A polymorphisms, and the variant A allele of the BAX G(-248)A polymorphism are related to higher and lower expressions of the encoded proteins, respectively, than their wild T, C and G alleles. This study aimed to clarify the roles of the above-mentioned genetic polymorphisms in the risk and clinical manifestation of the tumor. Material and methods: In this case-control study, genomic DNA from peripheral blood of 150 consecutive CM patients (75 males and 75 females, 138 Caucasians and 12 non-Caucasians aged 20-89 years) and 150 healthy subjects, matched by age, gender and race, was analyzed by polymerase chain reaction followed by enzymatic digestion. Results: The frequencies of the P53 ArgArg and the BCL2 AA genotypes were higher in patients than in controls (58.7% versus 44.7%, P= 0.01) and (28.0% versus 15.3%, P= 0.004), respectively. Carriers of these genotypes had a 1.86 and 2.87-fold increased risk for CM than those with the remaining genotypes, respectively. Excesses of the P53 ArgArg plus BCL2 AA and P53 ArgArg plus BAX AA were seen in patients when compared to controls (36.1% versus 16.9%, P= 0.002) and (29.5% versus 15.3%, P= 0.008). Carriers of these genotypes had a 3.43 and 2.71-fold increased risk for CM than others, respectively. Conclusions: The data suggest that P53 Arg72Pro, BCL2 C(-248)A and BAX G (-248)A polymorphisms, alone or combined, alter the risk for CM in our region. We believe that carriers of specific genotypes of the above-mentioned genes should receive additional recommendation to avoid exposition to sunlight, in addition to frequently being evaluated by a dermatologist for early disease diagnosis. Financial support: (FAPESP) Disclosure: All authors have declared no conflicts of interest. 1123P BRAF-V600 AND C-KIT MUTATION ANALYSIS IN CYTOLOGYCAL SAMPLES FROM METASTATIC MELANOMA T. Labiano 1 , M.D. Lozano 1 , J.I. Echeveste 1 , M. Montañana 1 , M.F. Sanmamed 2 , E. Castanon Alvarez 2 , N. Gómez 1 , A. Gurpide 2 , M.A. Idoate 1 , S. Martin Algarra 3 1 Pathology, University of Navarra, Pamplona, SPAIN, 2 Medical Oncology, Clinica Universitaria de Navarra, Pamplona, SPAIN, 3 Medical Oncology, Clinica Universidad de Navarra, Pamplona, SPAIN Background: Vemurafenib is approved for the first-line treatment of BRAF-V600E+ metastatic melanoma (MM). Also, preliminary clinical experience with imatinib in MM patients with gene amplification or activating mutations of c-KIT, have shown Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds404 | ix365
high response rates and prolonged progression free survival. These results emphasise the importance of molecular information, even in those cases in which the diagnosis is made on small samples obtained through minimally invasive approaches. Cytology is an accurate and cost-effective tool for the diagnosis of MM and cytological smears are occasionally the only samples available from these patients. Methods: We have studied BRAF and c-KIT mutations in 62 cytological samples from MM patients. Preliminary results of 56 cases (32 men (58%) and 23 women (42%); median age 52 years) are included in this abstract. Diagnosis was made on fine needle aspiration in 41 cases, imprints in 10, direct eye touch in 1, a smear from cellular culture in 1, and pleural and peritoneal fluid in 3. To assure tissue quality, DNA was extracted directly from Papanicolau stained smears on which cytological diagnosis was made. BRAF and c-KIT mutations were analysed by PCR and direct sequencing using an ABI PRISM TM 310XL. Results: BRAF mutations was found in 30 cases (53.5%): V600E mutation in 26 (86,7%) and V600K in 4 (13,3%). c-KIT mutations were studied in 18 cases. L576P mutation was present in 1 patient with liver metastasis from acral melanoma (5.56%). BRAF status did not correlated with primary melanoma histology, age at diagnosis, disease free survival, brain metastases rate and overall survival. Conclusions: The frequency of activating mutations in BRAF is 53.5% in this series. V600E is the most commonly observed mutations, but V600K appears in 13.3% of the cases. c-KIT mutations incidence is low (5.56%). Mutational analysis of BRAF and c-KIT using cytological samples from patients with metastatic melanoma is feasible and can be used to extend the benefits of targeted therapy to those patients from which biopsies are not available. Updated results will be presented. Disclosure: S. Martin Algarra: Participation in Advisory Boards of Roche. All other authors have declared no conflicts of interest. 1124P AN OPEN-LABEL, MULTICENTRE SAFETY STUDY OF VEMURAFENIB IN PATIENTS WITH METASTATIC MELANOMA C. Blank 1 , M. Del Vecchio 2 , P.A. Ascierto 3 , P. Queirolo 4 , A. Hauschild 5 , A. Arance 6 ,M.Brown 7 , L. Mitchell 8 , L. Veronese 8 , J. Larkin 9 1 Immunology, The Netherlands Cancer Institute Antoni van Leeuwenhoek Hospital, Amsterdam, NETHERLANDS, 2 Department of Medical Oncology, Instituto Nazionale dei Tumori, Milan, ITALY, 3 Unit of Medical Oncology and Innovative Therapy, Istituto Nazionale Tumori Fondazione G. Pascale, Naples, ITALY, 4 National Institute for Cancer Research, San Martino Hospital, Genova, ITALY, 5 Klinik für Dermatologie, Venerologie und Allergologie, Universitätsklinikum Schleswig-Holstein, Kiel, GERMANY, 6 Medical Oncology, Hospital Clinic, Barcelona, SPAIN, 7 Oncology, Royal Adelaide Hospital Cancer Centre, Adelaide, AUSTRALIA, 8 F. Hoffmann-La Roche Ltd, Basel, SWITZERLAND, 9 Department of Medicine, Royal Marsden Hospital, London, UNITED KINGDOM Background: Vemurafenib, a BRAF inhibitor, is associated with improved progression-free survival and overall survival in patients (pts) with BRAF V600 -mutant metastatic melanoma (mM). Here we present findings from a safety study of vemurafenib in pts with unresectable Stage IIIC/IV BRAF V600 -positive mM. Methods: Pts with untreated or previously treated Stage IIIC/IV BRAF V600 mutation-positive (cobas® 4800 BRAF V600 Mutation Test) melanoma were enrolled. Pts received continuous oral vemurafenib 960 mg bid. Primary study endpoint was safety; efficacy (RECIST V 1.1) was a secondary endpoint. Results: Of 5273 screened pts (Mar 2011–Feb 2012), 2353 (45%) were enrolled and 2096 received ≥1dose of vemurafenib. Median age was 54 (16–95 years), 56% were male. Median time since first mM diagnosis was 6.4 months. Most pts were Stage IV (84%); 47.1% M1c, 2% Stage IIIC (stage not reported for 14% of pts). At baseline, 87% of pts had ECOG PS 0/1, 11% ECOG PS ≥2; 24% had brain metastases and 37% had elevated LDH. Most pts had received prior systemic therapy (60%) including ipilimumab (10%), MEK and BRAF inhibitors (3%). At data cut-off (29 Feb 2012), median treatment duration was 3.1 months (10%) of any grade were arthralgia (30.7%), rash (25.6%), fatigue (19.6%), alopecia (15.6%), nausea (15%) and photosensitivity (11%), and were similar irrespective of brain metastases and ECOG PS. AEs caused treatment interruption in 492 (23.5%) pts. Of 774 pts (37%) who discontinued treatment, most withdrew due to progressive disease (71%) or death (14%) but 6% had AEs (most commonly general physical deterioration). Tumour assessments at Week 8 of treatment were available for 1356/2096 (65%) pts; 60% of pts achieved a CR or PR; 31% had SD. Conclusions: In a setting representative of routine clinical practice, vemurafenib is well tolerated and both safety profile and activity resemble the Phase I–III data, although this analysis is limited by the study duration. Disclosure: C. Blank: Financial disclosure: Roche global steering committee, Roche NL presentations, conference travel, Novartis NL: conference travel, advisory board; MedImmune: research grant; BMS: advisory board, clinical research funding. M. Del Vecchio: Consultant or Advisory Role: Merck/Schering-Plough (U); Research Funding: Celgene, Novartis, Roche. P.A. Ascierto: Consultant for MSD; Advisory role for BMS, MSD, Roche-Genetech, GSK, Amgen, Celgene, Medimmune, Novartis; Annals of Oncology received honoraria from BMS, MSD, and Roche-Genentech. P. Queirolo: Advisory Board of Bristol Myers Squibb, Roche-Genentech, GSK, MSD and received honoraria from Brystol Myers Squibb and Roche-Genentech. A. Hauschild: Honoraria for adboard membership, and payments for lectures/speakers bureaus from Amgen, AstraZenica, Biovex, BMS, Boehringer, Ingelheim, Celgene, Eisai, GSK, IGEA, Lilly, Medac, MelaSciences, MSD?Merck, Novartis, Roche Pharma, SOBI, Vical, Janssen. A. Arance: Steering committee of this safety study (Roche). M. Brown: Membership of a Roche Melanoma Advisory Board. L. Mitchell: Full-time employee at F. Hoffmann-la-RocheL. Veronese: Full-time employee at F. Hoffmann-la-Roche. All other authors have declared no conflicts of interest. 1125P OPEN-LABEL PILOT STUDY OF VEMURAFENIB IN PREVIOUSLY TREATED METASTATIC MELANOMA (MM) PATIENTS (PTS) WITH SYMPTOMATIC BRAIN METASTASES (BM) R. Dummer 1 , S. Goldinger 2 , C. Turtschi 2 , N. Eggmann 2 , O. Michielin 3 , L. Mitchell 4 , L. Veronese 4 , P.R. Hilfiker 5 , J.D. Rinderknecht 2 1 Department of Dermatology, Universitätsspital Zürich, Zürich, SWITZERLAND, 2 Department of Dermatology, University Hospital of Zurich, Zurich, SWITZERLAND, 3 Melanoma Clinic, Multidisciplinary Oncology Center, Lausanne, SWITZERLAND, 4 F. Hoffmann-La Roche Ltd, Basel, SWITZERLAND, 5 Radiology, MRI Bethanien, Zurich, SWITZERLAND Background: The BRAF inhibitor vemurafenib has shown high response rates and improved progression-free and overall survival in mM harbouring V600-mutated BRAF. BMs are often observed with mM and indicate a poor prognosis. The aim of this preliminary investigation is to determine the feasibility of vemurafenib therapy in mM with BM. Methods: 24 evaluable pts with BRAF V600 mutation positive (cobas® 4800 BRAF V600 Mutation Test) mM and BMs, requiring corticosteroids for symptom control, were enrolled (Nov 2010–Nov 2011). Pts received twice-daily vemurafenib 960 mg. Primary endpoint is safety; secondary endpoint is best overall response rate (RECIST v1.1). Results: All pts were white, median age 47 (24–70) years. Median baseline number of BMs was 3.5 (1–20). Median time since BM diagnosis was 3.2 (0–64) months. Other lesion sites included skin, lung, liver, bone, lymph nodes, colon/large intestine, stomach, breast and adrenal. All pts had prior treatment for BM: radiotherapy 83% (58% whole brain, 25% precision), 2 pts had surgery and 83% of pts had systemic therapy. As of clinical data cut-off (15 Dec 2011), median treatment duration was 117 (3–304) days. 9 pts are ongoing; 15 (63%) discontinued treatment because of progression of disease (PD), 8 of whom died because of PD. 22 pts (92%) reported ≥1 adverse event (AE), which were mainly mild or moderate. Most common AEs were arthralgia (33%), photosensitivity (21%) and seizures (20%, pre-existing). 3 pts reported 1 of each of the following grade 3 AEs: epilepsy, cutaneous squamous cell carcinoma (cuSCC), increased amylase, elevated γ-glutamyltransferase and ileus with perforation. Overall, cuSCC occurred in 3 pts (12.5%), skin papilloma in 3 pts (12.5%) and keratoacanthoma in 1 pt (4.2%). 7/24 pts (29%) had a confirmed partial response: 9 pts (38%) had stable disease, 3 (12%) PD and 5 (21%) were not evaluable for response. Median duration of response was 3.8 (0.8–4.7) months. Conclusions: Vemurafenib therapy is feasible in advanced melanoma patients with symptomatic BM. Interpretation of efficacy is currently limited because of a short follow-up time, but there are strong indications of vemurafenib activity in BM. Disclosure: R. Dummer: Research funding: Astra Zeneca, Novartis, Cephalon, MSD, Transgene, BMS, Roche, GlaxoSmithKline, Bayer. Ad-board: Astra Zeneca, Novartis, Cephalon, MSD, Transgene, Genta, Bayer, Roche, BMS, GSK, Spirig. L. Mitchell: Full-time employee of F. Hoffmann-la-Roche. L. Veronese: Full time employee at F. Hoffmann-la-Roche. All other authors have declared no conflicts of interest. 1126P PHASE II STUDY OF IPILIMUMAB PLUS TEMOZOLOMIDE IN PATIENTS WITH METASTATIC MELANOMA S. Patel 1 , R. Bassett 2 ,W.Hwu 1 , K. Kim 1 , N. Papadopoulos 1 ,P.Hwu 1 , A. Bedikian 1 1 Melanoma Medical Oncology, MD Anderson Cancer Center, Houston, TX, UNITED STATES OF AMERICA, 2 Biostatistics, MD Anderson Cancer Center, Houston, TX, UNITED STATES OF AMERICA Background: Ipilimumab (Ipi) alters the immune system balance by inhibiting the suppression of T-cell function. In two Phase III trials, Ipi has shown an overall survival benefit alone and in combination with dacarbazine in previously treated and treatment-naïve patients (pts) with metastatic melanoma (MM), respectively. We performed a single-institution, Phase II clinical trial of Ipi plus temozolomide (Tem) in pts with MM. Methods: Pts between the ages of 18 and 75 with previously untreated unresectable Stage III or Stage IV MM and an ECOG Performance Status (PS) of 0 to 1 were enrolled in a Phase II trial of Ipi plus Tem. Induction phase consisted of Ipi 10mg/kg intravenous on Day 1 and oral Tem 200 mg/m 2 on Days 1 – 4 every 3 weeks for 4 doses. Maintenance consisted of Ipi 10 mg/kg intravenous on Day 1 starting week 12 and repeated every 12 weeks and oral Tem 200 mg/m 2 on Days 1 – 5 starting week ix366 | 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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Material and methods: We searched P
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Results: The median concentration o
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Table: 226P Methods: Pts were rando
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However, additional analysis sugges
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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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261P BREAST CANCER SUBTYPES AND OUT
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90 mg/m2-cyclophophamide 600 mg/m2
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to 9 weeks after dosing. Trastuzuma
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Patients and methods: We reviewed d
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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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abstracts breast cancer, locally ad
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absolute difference of median value
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Novartis, Genentech, and sanofi-ave
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Results: Three RCTs with 1023 patie
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collected from all patients for det
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355P FIRST REPORT OF LONG-TERM RESP
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361P A RETROSPECTIVE ANALYSIS OF PL
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publications and aggregated in a me
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Thus the primary aim to target BCSC
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383 WHY DO WOMEN WITH BREAST CANCER
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Results: We evaluated 76 pts with M
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more than 6 cycles of capecitabine.
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406TiP PHASE II TRIAL OF PRIMARY SY
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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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432 GAMMA KNIFE RADIOSURGERY AS A M
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abstracts developmental therapeutic
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1PR), but no responses were seen in
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RO and Cd, as well as PD data for c
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and vulvar Ca), and 11 SDs were obs
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knowing HLA-A status double-blindly
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Acquired-resistance to EGFR inhibit
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474P PHASE 1 STUDY OF THE SELECTIVE
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TST is active in breast and gastric
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Treatment-induced shedding of circu
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Methods: Either co-cultures of peri
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501 PRECLINICAL DATA INVESTIGATING
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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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plus intravenous Bev(7.5mg/kg q 21d
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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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551P ADJUVANT CHEMOTHERAPY (AC) USE
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experienced significantly more ≥
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functioning scales. Exploratory ana
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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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Table: 632 633 AFLIBERCEPT/FOLFIRI
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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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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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effective in second or further line
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Conclusions: In pts with RCC treate
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using Drug inCode ® pharmacogeneti
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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
Page 293 and 294:
Median overall survival (OS) was 26
Page 295 and 296:
abstracts Genitourinary tumors, pro
Page 297 and 298:
and week 13 BPI-SF Q3 scores), 28%
Page 299 and 300:
Working Group (PCWG)-2 guidelines r
Page 301 and 302:
atio HR 0.39; CI 0.18, 0.83, p = 0.
Page 303 and 304:
We observed tumor responses and pro
Page 305 and 306:
Here we report emerging data from t
Page 307 and 308:
928P LHRH AGONIST-INDUCED SUPPRESSI
Page 309 and 310:
Disclosure: S. Oudard: Has acted as
Page 311 and 312:
939P NEOADJUVANT SIPULEUCEL-T IN LO
Page 313 and 314:
945 BONE TURNOVER MARKERS AND POTEN
Page 315 and 316: 952 SEQUENTIAL ANDROGEN DEPRIVATION
Page 317 and 318: managed in a multidisciplinary (MD)
Page 319 and 320: or hypercalcemia at screening; prio
Page 321 and 322: meeting. The prevalence of LGSC is
Page 323 and 324: Table: 975PD Continued AMG 386 + pa
Page 325 and 326: physicians in the U.S. and Europe.
Page 327 and 328: 989P PHASE II STUDY OF COMBINATION
Page 329 and 330: elated with stage, nodal involvemen
Page 331 and 332: 1004P CASE CONTROL STUDY ON TWO DIF
Page 333 and 334: eight patients who had infertility
Page 335 and 336: abstracts head and neck cancer 1016
Page 337 and 338: same CT/RT; Arm B2: 3 cycles of ind
Page 339 and 340: induction chemotherapy in the treat
Page 341 and 342: patients. We have developed a rando
Page 343 and 344: evaluated by the screening instrume
Page 345 and 346: morbidities that radiation would le
Page 347 and 348: Conclusions: Through adequate selec
Page 349 and 350: abstracts hematological malignancie
Page 351 and 352: anthracyclines in vitro. A favorabl
Page 353 and 354: 1076P RITUXIMAB PLUS SUBCUTANEOUS C
Page 355 and 356: than the standard target of ≥2.5
Page 357 and 358: Patients: From November 2002 to May
Page 359 and 360: lymphadenopathy and multiple cutane
Page 361 and 362: prospective non-interventional stud
Page 363 and 364: Funding: GSK Biologicals Disclosure
Page 365: survival rates of 13-25% (Prieto et
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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