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Annals of Oncology (ORR) and secondary endpoints were toxicities, disease control rate (DCR), progression free survival (PFS), and overall survival (OS). The planed sample size was 26 pts. Results: From March 2010 to May 2012, 20 pts were enrolled and eligible: males/ females 10/10; median age 66 (range 59-75); PS 0/2 2/18; stage III/IV 1/19; adeno/ others 20/0. Nineteen pts were eligible for efficacy and toxicity; a total of 226 cycles (median 12 cycles, range 1-27) was given. Major grade 3/4 toxicities were neutropenia, leucopenia, liver dysfunction and infection, respectively. There was no treatment-related death. ORR was 68.8%, and DCR was 100%. Median PFS is 18.2 months and median OS is not reached. Conclusions: This combination showed longer median PFS and acceptable toxicity. Randomized trial of PEM + G compare with G alone is warranted. Disclosure: All authors have declared no conflicts of interest. 1259P GEFITINIB FOR NON-SMALL CELL LUNG CANCER (NSCLC) WITH MINOR EGFR MUTATIONS: A RETROSPECTIVE STUDY FROM THE NORTH EAST JAPAN STUDY GROUP (NEJ) S. Watanabe 1 , H. Yoshizawa 1 , M. Maemondo 2 , A. Inoue 3 , S. Sugawara 4 , H. Isobe 5 , M. Harada 6 , Y. Ishii 7 , K. Hagiwara 8 , K. Kobayashi 9 1 Bioscience Madecal Research Center, Niigata University Medical and Dental Hospital, Niigata-City, JAPAN, 2 Department of Respiratory Medicine, Miyagi Cancer Center, Natori, JAPAN, 3 Department of Respiratory Medicine, Tohoku University, Sendai, JAPAN, 4 Department of Respiratory Medicine, Sendai Kousei Hospital, Sendai, JAPAN, 5 Clinical Oncology, KKR Sapporo Medical Center, Sapporo, JAPAN, 6 Department of Pulmonary Disease, National Hospital Organization Hokkaido Cancer Center, Sapporo, JAPAN, 7 Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University School of Medicine, Mibu, JAPAN, 8 Department of Respiratory Medicine, Saitama Medical University, Saitama, JAPAN, 9 Respiratory Medicine, Saitama International Medical Center, Saitama, JAPAN Background: In NSCLC, the sensitive mutations of epidermal growth factor receptor (EGFR), such as exon 19 deletion and L858R point mutation, are predictors of response to EGFR tyrosine kinase inhibitors (TKIs). However, it is still uncertain whether minor EGFR mutations are associated with sensitivity to EGFR-TKIs. Materials and methods: Retrospective review of 221 EGFR mutated (exon 19 deletion, L858R, G719X and L861Q) patients who were treated with gefitinib in a NEJ002 study was performed. We identified 7 patients with G719X and 3 patients with L861Q. Results: Among 10 patients harboring minor EGFR mutations (G719X or L861Q), 5 patients were treated with gefitinib as the 1st line treatment, and 5 patients were treated with carboplatin/paclitaxel as the 1st line chemotherapy, and then received gefitinib as the 2nd line treatment. Only 2 patients showed PR, 4 achieved SD, and 4 had PD with gefitinib treatment. The overall response rate was 20% and the disease control rate was 60%. The overall survival (OS) from enrollment was significantly shorter in patients with minor mutations (median OS, 12 months (95% CI, 5.8 - 30.5)) compared to patients with 19 deletion or L858R (median OS, 28 months (95% CI, 24.1 – 33.2), P = 0.0057). Tendency of longer progression free survival and OS were observed in minor EGFR mutation patients who received carboplatin/paclitaxel as the 1st line treatment (median PFS, 5.3 months (95% CI, 3.7 – 8.9) and median OS, 22.8 months (95% CI, 9.9 – 41.8)) compared to those who were treated with gefitinib as the 1st line treatment (median PFS, 2.2 months (95% CI, 0.5 – 10.6), P = 0.997 and median OS, 11.9 months (95% CI, 5.8 – 22.6), P = 0.1021). Conclusions: Our results indicate that NSCLC patients with G719X or L861Q minor EGFR mutations are less responsive to gefitinib than those with 19 deletion or L858R. Disclosure: All authors have declared no conflicts of interest. 1260P A PHASE II STUDY OF ERLOTINIB AS FIRST-LINE TREATMENT IN JAPANESE ADVANCED NSCLC PATIENTS HARBORING EGFR MUTATIONS A. Horiike 1 , M. Nishio 1 , K. Goto 2 , N. Yamamoto 3 , K. Chikamori 4 , M. Maemondo 5 , T. Hida 6 , N. Katakami 7 , T. Tamura 3 1 Thoracic Oncology Center, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Koto-ku, Tokyo, JAPAN, 2 Division of Thoracic Oncology, National Cancer Center Hospital East, Kashiwa, JAPAN, 3 Division of Internal Medicine and Thoracic Oncology, National Cancer Center Hospital, Chuo-ku, Tokyo, JAPAN, 4 Oncology Medicine, National Hospital Organization, Yamaguchi - Ube Medical Center, Ube, JAPAN, 5 Department of Respiratory Medicine, Miyagi Cancer Center, Natori, JAPAN, 6 Department of Thoracic Oncology, Aichi Cancer Center Hospital, Nagoya, JAPAN, 7 Integrated Oncology, Institute of Biomedical Research and Innovation Hospital, Kobe, JAPAN Background: Several studies of EGFR TKIs have shown a benefit in response and progression-free survival (PFS) for NSCLC patients harboring EGFR mutations in the first-line setting. This is the first prospective study to investigate erlotinib for the first-line treatment of NSCLC patients harboring EGFR mutations in Japanese patients. Methods: We undertook the single-arm phase II study at 25 centers. Eligible patients were adults (over 20 years) with advanced or recurrent NSCLC harboring EGFR mutations (Exon 19 deletions (19del) or Exon 21 L858R mutation) with no prior chemotherapy for NSCLC. The primary endpoint was progression-free survival (PFS) and safety. Secondary endpoints were overall response rate (ORR), disease control rate (DCR), overall survival (OS), and response duration. Results: Between April 8 and October 6 2010, 103 patients were enrolled. All patients were administered erlotinib and included in the safety analysis. One patient was excluded from efficacy analysis, because of the deviation of GCP. Thus 102 patients were analyzed in the efficacy analysis. At Data cut-off (Sep 1, 2011), median PFS assessed by Independent Review Committee was 11.8 months [95 % CI 9.7- not reached]. The updated median PFS incorporated with follow up assessments will be obtained in August 2012. The most common adverse events were rash and diarrhea in 82.5 % and 80.6 % respectively, with Grade 3 was 13.6 % and 1.0 % respectively, and there were no Grade 4/5 rash and diarrhea. Six treatment-related ILD like events were reported by investigators, and of which two were fatal. ORR was 78.4 %, DCR was 95.1 %, and response duration was 11.1 months [95 %CI 9.4- not reached], OS data is immature at this time (only ten deaths events). Median PFS in 50 patients with 19del was 12.5 months, in 50 patients with L858R was 11.0 months, and two patients with L858R/T790M was 3.8months. Conclusion: This study showed a promising efficacy and safety profile of erlotinib in Japanese advanced NSCLC patients harboring EGFR mutations. Disclosure: A. Horiike: Corprate-sponsored research: Chugai, Pfizer, Merck, KyowaKirin, Taiho, Eisai, Novartis, AMGEN. M. Nishio: Corporate-sponsored research: Chugai, Eli Lillly, Pfizer, DiichiSankyo, KyowaKirin, Taiho, Eisai, Novartis. Lecture fees: Chugai. K. Goto: Corporate-sponsored research: Chugai, Pfizer, KyowaKirin, Taiho, Eisai, Merckserono, Boehringer Ingelheim Lecture fees: Chugai, Taiho, Ono. N. Yamamoto: Corporate-sponsored research: Chugai, Pfizer, KyowaKirin. K. Chikamori: Corporate-sponsored research: Chugai, Taiho, Nippon Kayaku Lecture fees: Eli Lilly. M. Maemondo: Corporate-sponsored research: Chugai, Taiho, Janssen Lecture fees: Chugai, Eli Lilly. T. Hida: Corporate-sponsored research: Chugai, Eli Lilly, Bayer, Pfizer, DaiichiSankyo, KyowaKirin, Taiho, Boehringer Ingelheim, Merck, Aventis. N. Katakami: Corporate-sponsored research: Chugai, Pfizer, Kyowakirin, Ono, Janssen, Merckserono, Boehringer Ingelheim, Dainipponsumitomo, Eisai, Shionogi. T. Tamura: Corporate-sponsored research: Chugai, DaiichiSankyo, Boehringer Ingelheim, Abbott, Eisai, Bristol-Myers Squib, KyowaKirin Lecture fees: Taiho, Eli Lilly, Chugai 1261P ERLOTINIB AS NEOADJUVANT TREATMENT IN PATIENTS WITH IIIA-N2 NON-SMALL CELL LUNG CANCER(NSCLC) WITH ACTIVATING EPIDERMAL GROWTH FACTOR RECEPTOR (EGFR) MUTATION (NCT01217619, ESTERN) B. Han, L. Xiong, R. Li, J. Sun, Y. Lou, Y. Zhang Department of Pulmonary Medicine, Shanghai Chest Hospital affiliated to Shanghai Jiaotong University, Shanghai, CHINA Background: Patients with stage IIIA N2 NSCLC have poor outcomes with 5-year survival rate of approximately 15% after treatment with surgical resection or chemo-radiotherapy. Tyrosine kinase inhibitor monotherapy have been demonstrated a significant improvement in tumor response rate and progression free survival as the first line treatment for metastatic NSCLC patients with activating EGFR mutation. The objective of this trial is to explore the efficacy and safety profile of erlotinib as neoadjuvant treatment in patients of stage IIIA-N2 NSCLC with activating EGFR mutation. Material and methods: This is a single arm, one center, phase II study of erlotinib as neoadjuvant treatment in patients with Endobronchial Ultrasound (EBUS) confirmed stage IIIA-N2 NSCLC with activating EGFR mutation in exon 19 or 21. The primary endpoint is to evaluate radical resection rate. A total of 44 patients will be enrolled. Major inclusion criteria: IIIA-N2 NSCLC Patients with pathologically confirmed ipsilateral mediastinal metastasis by EBUS. The biopsy specimen shows activating EGFR mutation in exon 19 or 21. Treatment schedule: All the recruitment patients will be treated by erlotinib 150mg orally per day for 56 days for neoadjuvant period. Patients will be assessed by Chest CT for the efficacy evaluation in day 29 and right after day 56. All the post-operative patients will receive standard adjuvant treatment which will be decided by the investigator. Current enrollment: 48 patients have been screened, and 7 patients met the inclusion criteria and were enrolled. 2 patients are still on neoadjuvant treatment, 5 patients have completed the neoadjuvant therapy, and RECIST evaluation showed partial response in 2 patients, disease progression in 2 patients, and disease stable in 1 patient. Due to active hepatitis and technical infeasibility, 2 patients with PR didn’t receive surgery, only one SD patient received R0 surgery. Disclosure: All authors have declared no conflicts of interest. Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds409 | ix413
1262P DISTINCT SPREAD OF EGFR MUTATED PULMONARY ADENOCARCINOMAS D. Shin 1 , S.Y. Kwon 2 , C.H. Kim 1 , S.H. Yang 1 , I.I. Na 1 1 Internal Medicine, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, KOREA, 2 Hospice and Palliative Care Team, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, KOREA Introduction: Our aim in this study was to explore the potential association of epidermal growth factor receptor (EGFR) with characteristics of tumor spread in patients with pulmonary adenocarcinoma. Clinical implication of EGFR mutational status on brain metastasis was also evaluated in surgically treated patients. Methods: We analyzed clinical data on 317 patients who were tested for EGFR mutation and who underwent brain MRI at diagnosis between October 2005 and December 2011. The relationship between EGFR mutation status and clinical factors were analyzed. Initial metastatic disease was stratified according to brain metastases and their association with EGFR mutations was evaluated using multinomial logistic regression. Results: Of the 317 patients, 139 patients (43.85%) harbored EGFR mutations. EGFR mutations was more commonly found in patients with early nodal stage (71.9 % versus 28.1%, adjusted odds ratio [OR] = 1.90, p = 0.030) and distant metastases (54.0% versus 46.0%, adjusted OR = 2.05, p = 0.011). Further analysis showed that EGFR mutations were more likely to be detected in brain metastases (64.7% versus 35.3%, p = 0.005), whereas their association with noncranial metastases was not significant (55.4% versus 44.6%, p = 0.960). In addition, survival analysis of 133 patients treated with surgical resection showed that EGFR mutation status was a poor prognostic factor for brain metastasis (HR = 5.94, 95% CI = 1.08-16.28, p = 0.039) after adjustment of pathologic N stage. Conclusions: In this study, EGFR mutation status was significantly associated with early nodal and distant metastasis, in the patients with pulmonary adenocarcinoma. The current study also suggests the preference of brain metastases in mutant EGFR tumors at initial presentation and after curative resection. Disclosure: All authors have declared no conflicts of interest. 1263P IMPACT OF EPIDERMAL GROWTH FACTOR RECEPTOR-TYROSINE KINASE INHIBITOR TREATMENT IN ADVANCED NON-SMALL CELL LUNG CANCER: A META-ANALYSIS C.K. Lee 1 , C. Brown 2 , R. Gralla 3 , V. Hirsh 4 , A. Inoue 5 , V. Gebski 6 , C.J. Yang 7 1 NHMRC Clinical Trials Centre, University of Sydney, Sydney, NSW, AUSTRALIA, 2 Clinical Trials, NHMRC Clinical Trials Centre, University of Sydney, Sydney, AUSTRALIA, 3 Department of Medicine, Hofstra University School of Medicine, New York, UNITED STATES OF AMERICA, 4 Oncology, McGill University Health Centre, Montreal, QC, CANADA, 5 Department of Respiratory Medicine, Tohoku University, Sendai, JAPAN, 6 Biostatistics and Research Methodology, NHMRC Clinical Trials Centre, University of Sydney, Sydney, AUSTRALIA, 7 Department of Oncology, National Taiwan University Hospital, Taipei, TAIWAN Background: Previous meta-analyses have reported that epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) improves progression-free survival (PFS) in patients with advanced non-small cell lung cancer (NSCLC) harbouring EGFR mutation. We examined the influence of EGFR-TKI on PFS and overall survival (OS) in those with (EGFR+) and without mutation (EGFR-). Methods: We included published and unpublished randomised trials of advanced NSCLC that compared EGFR-TKI monotherapy or combination EGFR-TKI chemotherapy with chemotherapy or placebo. We used published hazard ratios (HR) if available, or derived treatment estimates from other survival data. We investigated treatment effects in different treatment settings and trial regimens. Results: We identified 20 eligible trials investigating EGFR-TKI in front-line (n = 12), second or subsequent (n = 5), and maintenance (n = 3) treatment, with EGFR status known in 3198 (23%) patients. Overall, HR for EGFR-TKI over control for PFS were (EGFR+) 0.37 (95% CI, 0.32 to 0.42; p < 0.001) and (EGFR-) 1.02 (95% CI, 0.93 to 1.12; p = 0.67). EGFR mutation is predictive of PFS benefit with EGFR-TKI in all settings: front-line HR (EGFR+) 0.39, p < 0.005, HR (EGFR-) 1.07, p = 0.27, interaction p < 0.001; second or subsequent lines HR (EGFR+) 0.38, p = 0.01, HR (EGFR-) 1.22, p = 0.07, interaction P = 0.003; maintenance HR (EGFR+) 0.15, p < 0.001, HR (EGFR-) 0.81, p = 0.02, interaction p = 0.02. There was no difference in OS for patients treated with EGFR-TKI or control in these subgroups of patients: HR (EGFR+) 0.95, p = 0.21; HR (EGFR-) 0.95; p = 0.29. Conclusions: In this meta-analysis, treatment with EGFR-TKI was found to significantly delay disease progression in EGFR+ patients; however, no impact on OS was identified. EGFR mutation is a predictive biomarker of PFS benefit with EGFR-TKI treatment in all settings. These findings support assessment for Annals of Oncology EGFR mutation before initiation of EGFR-TKI treatment and that EGFR-TKI should be considered as front-line therapy in EGFR+ patients with advanced NSCLC. Disclosure: R. Gralla: Consultant or advisory role for Boehringer Ingelheim. V. Hirsh: Advisory role for Boehringer Ingelheim. A. Inoue: Received lecture fees and research grants from AstraZeneca. C.J. Yang: Advisory roles for Boehringer Ingelheim, AstraZeneca, Roche and OSI, and have received honoraria from AstraZeneca, Roche and OSI. All other authors have declared no conflicts of interest. 1264P CLINICOPATHOLOGIC FEATURES OF NEVER-SMOKING WOMEN LUNG CANCER (WLC): A REVIEW FROM THE SPANISH WORLD07 DATABASE J. De Castro 1 , D. Isla Casado 2 , M. Provencio Pulla 3 , M. Majem Tarruella 4 , N. Vinolas Segarra 5 , E. Felip 6 , A. Artal-Cortes 7 , R. García-Campelo 8 , M. Domine 9 , P. Garrido Lopez 10 1 Medical Oncology, Hospital Universitario La Paz, Madrid, SPAIN, 2 Oncology Service, Hospital Clínico Universitario Lozano Blesa, Zaragoza, SPAIN, 3 Medical Oncology, Hospital Universitario Puerta de Hierro Majadahond, Majadahonda, SPAIN, 4 Medical Oncology, Hospital de la Santa Creu i Sant Pau, Barcelona, SPAIN, 5 Medical Oncology, Hospital Clinic y Provincial de Barcelona, Barcelona, SPAIN, 6 Oncologia Médica, Vall d’Hebron University Hospital Institut d’Oncologia, Barcelona, SPAIN, 7 Servicio de Oncologia Medica, Hospital Miguel Servet, Zaragoza, SPAIN, 8 Medical Oncology, Complexo Hospitalario Universitario de A Coruña, La Coruña, SPAIN, 9 Oncology, Fundación Jiménez Díaz, Madrid, SPAIN, 10 Medical Oncology, Hospital Ramon y Cajal, Madrid, SPAIN Background: Lung cancer in never-smoker appears to be a distinct entity from lung cancer in smoker, with specific molecular characteristics and potential different treatment. Several factors like hormonal, environmental, genetic, pre-existing lung diseases, and virus, may play etiologic roles, and an in-depth understanding of them is needed. So, new clinicopathologic aspects of never-smoking WLC should be very important to know the biology of this tumoral disease. Methods: Information has been extracted from WORLD07 database, a prospective, from 32 Spanish centers, epidemiologic female-specific lung cancer e-database performed by ICAPEM, an association to research WLC. Results: From October 2007 to October 2011, 539 newly diagnosed never-smoking WLC were included in World07 database (39.3% of 1371 patients(p). P characteristics are: median age 71.1 years(y) (range: 22-91). Previous history of cancer (%): 13(breast, lung, cervix: 41.4,5.7,2.9). Gynecological features: median age of menarche 13y, Postmenopausal 88.9%, median age of menopause 49y. Median age of first child 26.4y Children: 91.2% (median: 2.3). Oral contraceptive: 11.9%. HRT: 5.2%. Tobacco exposure: Second-hand smokers: 40%, work-exposure 17.1%, home-exposure 88.8%. Obesity: 16.3%. Familiar history of cancer: 39.9% (lung cancer 29.8%).Lung cancer histology (%): adenocarcinoma/BAC/squamous/large cell/SCLC/ others: 69.2/6.8/5.7/5.0/3.8/3.8. EGFR mutated p (268 p analized): 55.5%, exon 19/ 20/21(%): 61.1/7.4/36.9. TNM NSCLC I/II/III/IV (%): 14/3.3/19.8/60.3. Treatment: EGFR-TKI in p harboring EGFR mutations stage IV (1 st -/2 nd -line)(%): 51.7/15.4; stage IV NSCLC(1 st -line)(%): platinum-based chemotherapy 42.5, combinations with bevacizumab 2.9. Overall survival: median 27 months (m), 1/2-y(%) 74.8/55.2; stage IV NSCLC: median 20.5m, 1/2-y(%) 67/46; EGFR mutated p: median 27.3m, 1/2-y (%) 75/54.3. Conclusions: Never-smoking WLC represents 39% of Spanish World07 database. The high incidence of adenocarcinoma histology (69.2%) and EGFR mutated tumors suggests a different clinical and genetic profiling and recommend a different treatment approach for this group of patients. Disclosure: All authors have declared no conflicts of interest. 1265P IS THERE A BENEFIT ON SURVIVAL OF TYROSINE-KINASE INHIBITORS VERSUS CHEMOTHERAPY IN FIRST LINE IN MUTATED EGFR PATIENTS WITH ADVANCED NON-SMALL CELL CANCER (NSCLC)? A META-ANALYSIS G. Des Guetz 1 , B. Uzzan 2 , K. Chouahnia 1 , P. Nicolas 2 , L. Zelek 1 , M. Pailler 1 , J. Morère 1 1 Oncology, Hôpital Avicenne, Bobigny, FRANCE, 2 Pharmacology, Hôpital Avicenne, Bobigny, FRANCE Background: Tyrosine-Kinase Inhibitors (TKIs) markedly improve Progression Free Survival (PFS) of advanced NSCLC patients mutated for Epidermal Growth Factor Receptor (EGFR). Results on Overall Survival (OS) are more questionable. Therefore, we performed a publication-based meta-analysis to further assess this issue. ix414 | 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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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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312: Table: Chemotherapy uptake wit
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abstracts breast cancer, locally ad
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Results: 8 trials (2092 pts) with 1
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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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509TiP LUX-LUNG 8: A RANDOMIZED, OP
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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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oxaliplatin (100 mg/m 2 )/raltitrex
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585P CHANGES IN THE INTESTINAL ENVI
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592P PHASE II TRIAL OF COMBINED CHE
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minutes. In a previous study, 30-mi
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Patients and methods: Chemotherapy-
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612P ARE PATIENTS WITH RESECTABLE R
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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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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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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
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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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928P LHRH AGONIST-INDUCED SUPPRESSI
Page 309 and 310:
Disclosure: S. Oudard: Has acted as
Page 311 and 312:
939P NEOADJUVANT SIPULEUCEL-T IN LO
Page 313 and 314:
945 BONE TURNOVER MARKERS AND POTEN
Page 315 and 316:
952 SEQUENTIAL ANDROGEN DEPRIVATION
Page 317 and 318:
managed in a multidisciplinary (MD)
Page 319 and 320:
or hypercalcemia at screening; prio
Page 321 and 322:
meeting. The prevalence of LGSC is
Page 323 and 324:
Table: 975PD Continued AMG 386 + pa
Page 325 and 326:
physicians in the U.S. and Europe.
Page 327 and 328:
989P PHASE II STUDY OF COMBINATION
Page 329 and 330:
elated with stage, nodal involvemen
Page 331 and 332:
1004P CASE CONTROL STUDY ON TWO DIF
Page 333 and 334:
eight patients who had infertility
Page 335 and 336:
abstracts head and neck cancer 1016
Page 337 and 338:
same CT/RT; Arm B2: 3 cycles of ind
Page 339 and 340:
induction chemotherapy in the treat
Page 341 and 342:
patients. We have developed a rando
Page 343 and 344:
evaluated by the screening instrume
Page 345 and 346:
morbidities that radiation would le
Page 347 and 348:
Conclusions: Through adequate selec
Page 349 and 350:
abstracts hematological malignancie
Page 351 and 352:
anthracyclines in vitro. A favorabl
Page 353 and 354:
1076P RITUXIMAB PLUS SUBCUTANEOUS C
Page 355 and 356:
than the standard target of ≥2.5
Page 357 and 358:
Patients: From November 2002 to May
Page 359 and 360:
lymphadenopathy and multiple cutane
Page 361 and 362:
prospective non-interventional stud
Page 363 and 364: Funding: GSK Biologicals Disclosure
Page 365 and 366: survival rates of 13-25% (Prieto et
Page 367 and 368: high response rates and prolonged p
Page 369 and 370: GlaxoSmithKline, Merck Sharp & Dohm
Page 371 and 372: advisor for Merck Sharp & Dohme, an
Page 373 and 374: or cutaneous melanoma. A survival u
Page 375 and 376: systemic therapy or were intolerant
Page 377 and 378: abstracts neuroendocrine tumors and
Page 379 and 380: morbidity, with G3 tumors behaving
Page 381 and 382: pts. Poorly differentiated endocrin
Page 383 and 384: Adenocarcinoma was present in 25 pa
Page 385 and 386: Method: Endobronchial ultrasound gu
Page 387 and 388: widely used by single agent or plat
Page 389 and 390: disease after surgery were treated
Page 391 and 392: stage IIIA NSCLC, EML4-ALK fusion-p
Page 393 and 394: 1200P CONCOMITANT CHEMORADIATION GI
Page 395 and 396: Patients and methods: The study was
Page 397 and 398: months (95% CI:13-25). The PFS and
Page 399 and 400: maintenance therapy had favourable
Page 401 and 402: abstracts non-small cell lung cance
Page 403 and 404: Ingelheim, GSK Biologicals (compens
Page 405 and 406: 1234PD RANDOMIZED PHASE III TRIAL O
Page 407 and 408: GlaxoSmithKline (myself, compensate
Page 409 and 410: 1243P IDENTIFICATION OF MICRORNA (M
Page 411 and 412: N-arm n=34 P-arm n=32 All n=66 Male
Page 413: 1255P POPULATION BASED EVALUATION O
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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