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550s Melanoma/Skin Cancers 8540 General Poster Session (Board #31F), Sun, 8:00 AM-12:00 PM Prognostic value of BRAFV600 mutations in melanoma patients after resection of metastatic lymph nodes. Presenting Author: Philippe Saiag, Hospital Ambroise Pare, APHP, University Versailles-SQY, Boulogne- Billancourt, France Background: Prognosis of AJCC stage III melanoma is heterogeneous. BRAF V600 mutations are frequent in melanomas. BRAFV600-targeted therapy has dramatic, but often transitory, efficacy in stage IV patients (pts). We aimed to determine for the first time the prognostic value of BRAFV600 mutations and other known prognostic criteria in stage III pts with sufficient nodal invasion. Methods: We searched all pts with cutaneous melanoma who had radical lymphadenectomy in our institution between 1/1/00 and 15/6/10 and included those with a nodal deposit �2 mm. BRAFV600 mutations were detected by DNA sequencing and pyrosequencing in formalin-fixed nodal samples containing �60% melanoma cells. Samples were considered mutated when �15% of DNA was positive. Endpoints were overall survival (OS) and distant metastasis free survival (DMFS). 92 patients had to be included to demonstrate a doubling of OS in patients without (40 months (m)) and with BRAFV600 mutation (20 m). Log-rank test and multivariate Cox proportional hazards regression model were used. Results: 105 consecutive pts were included, with 72% prospectively followed-up pts. BRAFV600 mutations (E: 83%; K: 14% of pts) were detected in 40% of pts. Median follow-up was 19 m (range: 3-139). Death occurred in 83% and 60% of pts with and without BRAF mutations, respectively, with median OS of 1.4 and 2.8 years. Pts’ age, primary melanoma ulceration, number of invaded nodes, AJCC staging, and BRAF status influenced OS and DMFS in the univariate analysis. The multivariate analysis showed the major prognostic role of BRAF status and of the number of invaded nodes (table). Conclusions: Provided our findings are independently replicated, BRAFV600 status should be used to stage melanoma pts with nodal metastasis. Our results also help to plan adjuvant trials with BRAFV600-targeted therapy in such patients, for whom the low tumor load may induce longer efficacy of BRAF-targeted therapies. OS DMFS P HR[IC95%] P HR[IC95%] N invaded nodes (1,2-3,4) 0.005 2.2 [1.3-3.9] 0.005 2.4 [1.3-4.3) BRAF mutated (Y/N) 0.005 1.9 [1.2-3.1] 0.002 2·1 [1·3-3·4] Ulceration of primary (Y/N) NS - 0.04 1.7 [1.0-2.8] AJCC staging, extracapsular spread, macro/micrometastasis, Breslow index: NS. 8542 General Poster Session (Board #31H), Sun, 8:00 AM-12:00 PM Role of cytokine-induced plasticity in melanoma on invasive, therapyresistant cells that express EMT-related genes and pathways. Presenting Author: Jonathan S. Cebon, Ludwig Institute for Cancer Research, Melbourne, Australia Background: The acquisition of new mutations can explain resistance to targeted therapies; however resistance also develops without demonstrable new mutations. To better understand potential mechanisms for treatment failure we studied subpopulations of chemo-resistant cells that can be identified in early passage cell lines and the cellular plasticity that yields these. Methods: Melanoma subpopulations were identified and sorted on the basis of functional assays. Gene expression was evaluated with Illumina HT12 arrays and qPCR to identify potential mechanisms and targets. Sorted cells were evaluated in vitro for the induction of phenotype switching and effects of target inhibition. Results: A subset of slow proliferating label-retaining cells (LRC) was identified using a membrane dye. Direct isolation of LRC from a pt showed these were not an in vitro artefact. LRC isolated from multiple cell lines comprised the majority of cells that resisted cytotoxic drugs and could invade through an artificial extracellular membrane. Gene expression profiling identified a network of over-expressed genes related to epithelial-to-mesenchymal transition (EMT) notable for the expression of Thrombospondin-1 (TSP-1), Transforming- Growth Factor, Beta Induced, (TGFBI) and other extracellular matrix molecules. Initial studies show that LRC shared gene expression characteristics with PLX4032-resistant cells. Although interrogating LRC by qPCR showed up-regulation of the putative melanoma stem cell marker ABCB5 and the lysine specific demethylase Jarid1B, cell sorting and serial re-labelling experiments revealed a dynamic and interchangeable phenotype for these cells, challenging the hierarchical stem cell model for melanoma. The observed slow-cycling and chemo-resistant phenotype could be induced in vitro through TGF beta-mediated phenotype switching and cellular invasion was blocked using an antibody against TSP-1. Conclusions: Cytokine-induced plasticity in melanoma yields invasive, therapy-resistant cells which express EMT-related genes and pathways. We hypothesize that these cells are a source of treatment resistance in vivo and blocking their emergence may prevent treatment failure. 8541 General Poster Session (Board #31G), Sun, 8:00 AM-12:00 PM Characterization of ipilimumab exposure-efficacy/safety response relationships in subjects with previously treated or untreated advanced melanoma. Presenting Author: Yan Feng, Bristol-Myers Squibb, Princeton, NJ Background: Ipilimumab (IPI) is a fully human monoclonal antibody directed against CTLA-4 that is being developed as a novel immunotherapeutic agent against melanoma and other solid tumors. The objective of this analysis was to retrospectively characterize the exposure-response (E-R) relationships for efficacy (overall survival, OS) in subjects with previously untreated advanced melanoma (pu-MEL), and safety (immune related adverse-events, irAEs) in subjects with previously treated advanced melanoma (pt-MEL) or pu-MEL. Methods: The E-R analysis of OS included 498 pu-MEL from a phase III study (CA184024) of IPI administered at 10 mg/kg � dacarbazine (DTIC) or DTIC � placebo; and the E-R analyses of irAE included 1036 subjects from a phase I study (CA184078), 4 phase IIstudies (CA184004/007/008/022) and CA184024 of IPI administered at doses of 0.3, 3 or 10 mg/kg. The relationship between steady-state IPI trough concentration (Cminss) and OS was described using a Cox proportional hazards model, and the relationships between Cminss and incidence of irAEs were described by ordinal logistic regression models (separate models for any irAE, as well as skin, liver and GI irAE). Results: The risk of death decreased with increasing Cminss, and is higher for subjects with elevated baseline LDH level. The risk of death was higher for subjects with baseline ECOG status � 0 and was higher with increasing stage of disease (M1C�M1B�M1A�M0). The hazard ratio for OS corresponding to the median Cminss of 49.99 �g/mL was 0.745 relative to subjects in DTIC � placebo group. The probability of Grade 2� or Grade 3� GI, skin, liver and any irAEs also increases with Cminss. Prior anti-cancer therapy (including prior DTIC) or concomitant DTIC were the only significant covariates in the E-R irAE models. Conclusions: These model-based analyses suggest that higher Cminss of IPI appears to be associated with improved survival in pu-MEL (based on data from CA184024) and higher Cminss also appears to be associated with increased probability of irAEs in pu-MEL or pt-MEL. 8543 General Poster Session (Board #32A), Sun, 8:00 AM-12:00 PM Gene expression profile signature (DecisionDx-Melanoma) to predict visceral metastatic risk in patients with stage I and stage II cutaneous melanoma. Presenting Author: Navneet Dhillon, Emory University , Atlanta, GA Background: The current AJCC TNM staging system has poor specificity for predicting visceral metastatic risk in patients diagnosed with stage I or stage II cutaneous melanoma. We, therefore, developed a gene expression profile signature (GEP) following in silico investigation of previously published microarray analyses. Methods: 60 formalin fixed paraffin embedded primary cutaneous melanoma samples from patients with stage I or II cutaneous melanoma with at least a follow up period of at least 6 years were macrodissected and analyzed blindly. RNA was isolated, converted to cDNA and RT-PCR was performed to assess the expression of the gene set. Expression data and biostatistical analysis was performed using GeNorm and JMP Genomics (SAS) Predictive modeling included Radial Basis Machine (RBM) and Partition Tree Analysis (PTA) Metastasis-free survival (MFS) was assessed using Kaplan-Meier analysis. The following clinical data was retrieved from medical records: survival, metastases, types of metastases. 20 out of 60 patients had developed visceral metastases in the follow up period. Results: GEP was developed following multiple analytical approaches.Two types of signatures emerged: Low risk (Class 1) and High risk (Class 2). Without optimizing for sensitivity, the analyses of the 60 sample cohort by radial basis machine (RBM) resulted in 92% ROC (met. accuracy � 90%, non-met. accuracy � 85%), while partition tree analysis (PTA) yielded 99% ROC (met. accuracy � 100%, non-met. accuracy � 95%). RBM classification showed 6-year MFS rates of 97% for Class 1 and 19% for predicted Class 2 of metastasis (median MFS � NR and 5.6 yrs, resp., P�0.0001 Log-Rank respectively). PTA showed 6-year MFS rates of 100% for predicted Class 1 and 14% for Class 2 of metastasis (median MFS � NR and 5.4 yrs, resp., P�0.0001 Log-Rank respectively). Conclusions: This study shows that DecisionDx-Melanoma GEP signature can provide excellent accuracy in predicting metastatic risk in stage I and II cutaneous melanoma.To our knowledge, the GEP provides the most accurate predictor to date for development of visceral metastases in patients with Stage I and II cutaneous melanoma. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
8544 General Poster Session (Board #32B), Sun, 8:00 AM-12:00 PM Elucidating distinct tumorigenic pathways in nodular versus superficial spreading melanoma. Presenting Author: Joshua Andrew Farhadian, New York University School of Medicine, New York, NY Background: Superficial spreading melanoma (SSM) and nodular melanoma (NM), which account for 70% and 20% of all melanoma diagnoses respectively, are believed to represent sequential phases of linear progression from radial to vertical growth. Recent evidence from several groups including ours challenges this linear progression model and suggests that SSM and NM are biologically distinct. In this study, we focused on identifying tumorigenic pathways that are differentially activated in melanoma subtypes and that can be therapeutically exploited. Methods: We performed Protein Pathway Array on SSM/radial growth phase (RGP) and NM/vertical growth phase (VGP) primary melanoma cell lines to determine expression levels of 141 tumorigenic proteins/phospho-proteins. Differential protein expression was determined using the Pavlidis Template Matching algorithm in TIGR Multi Experiment Viewer. Differentially expressed proteins were validated in an expanded panel of RGP, VGP, and metastatic melanoma cell lines using western blot. Constitutively active, overexpressed proteins in VGP melanoma were down-regulated in cell lines using several small molecule inhibitors and the effects on proliferation and migration were assessed. Results: 17 (12%) proteins/phospho-proteins are significantly overexpressed in VGP versus RGP melanoma (p�0.05). Western blot confirmed the results of 5 proteins/phospho-proteins. Each of those 5 was equally overexpressed in VGP and metastatic melanoma cell lines. Phospho-p90 ribosomal s6 kinase (RSK) was prioritized for functional studies based on its role in both the MAPK and AKT signaling cascades, two tumorigenic pathways often dysregulated in melanoma. Constitutive phosphorylation of p90 RSK in VGP, but not RGP melanoma was observed in response to serum starvation. Small molecule inhibition of phospho-p90 RSK attenuated proliferation and migration (p�0.05) in VGP melanoma. Conclusions: Data demonstrate discrete tumorigenic pathways are activated in nodular versus superficial spreading melanoma and suggest that phospho-p90 RSK might be a viable target against nodular melanoma. 8546 General Poster Session (Board #32D), Sun, 8:00 AM-12:00 PM BEVATEM: Phase II single-center study of bevacizumab in combination with temozolomide in patients (pts) with first-line metastatic uveal melanoma (MUM): First-step results. Presenting Author: Sophie Piperno- Neumann, Institut Curie, Paris, France Background: Overall survival (OS) of MUM pts remains poor. In our retrospective series of 470 MUM pts, median OS was 13 months, ranging from 3 to 12 and 21 months for best supportive care, systemic treatment and surgery groups respectively, stressing the lack of effective therapies in this rare cancer. Targeting angiogenesis seems to be promising in uveal melanoma. Intravitreal application of antiangiogenic agents is used to treat neovascular ocular diseases such as age-related macular degeneration or proliferative diabetic retinopathy. Bevacizumab suppressed in vitro growth and in vivo hepatic establishment of micrometastases in experimental uveal melanoma. Preclinical data suggest a potential clinical benefit of the combination of dacarbazine and bevacizumab. Methods: Phase II study, modified 2-step Fleming plan; with expected 6-month progression-free survival (PFS) rates of 15% with chemotherapy and 40% with BEVATEM, 35 pts are to be recruited for a power of 94% (� and � risk 3 and 6%). After the first 17 pts, the study will be continued and another 18 pts will be enrolled in the second step if �3 evaluable pts show stable disease or response. Primary endpoint: 6-month PFS according to RECIST. Secondary objectives: response and survival rates, safety; liver perfusion CT for functional imaging of response; impact of VEGF-A gene polymorphisms on bevacizumab pharmacodynamics. Treatment schedule: Temozolomide 150mg/m2 d1-d7 and d15-d21 oral route, Bevacizumab 10 mg/kg d8 d22 IV infusion, 6 cycles (d1�d28) then Bevacizumab maintenance until toxicity or progression. Results: From May 2010 to January 2011, 17 pts were enrolled according to the first step of the study: 3/17 achieved disease control at 6 months, second step is on going with 26/35 pts already recruited. One patient with minor response in liver and lung metastases is under Bevacizumab maintenance for 12 months. Safety of BEVATEM is as good as expected. Liver perfusion CT study showed decrease in blood flow and blood volume before lesion size decrease in one stable patient. Conclusions: BEVATEM study in first line MUM pts is on going, showing promising results in the first step of 17 pts. Melanoma/Skin Cancers 551s 8545 General Poster Session (Board #32C), Sun, 8:00 AM-12:00 PM Serum IL-6 as a prognostic biomarker in patients with stage IIB-III melanoma. Presenting Author: Lise Hoejberg, Department of Oncology, Odense University Hospital, Odense, Denmark Background: Interleukin (IL)-6 is an immunomodulatory cytokine produced by cancer cells and different immune cells. The specific function of IL-6 in cancer is unknown. Serum IL-6 is elevated in patients with different types of cancer. Elevated serum concentration of IL-6 is related to short survival in patients with stage IV melanoma. Methods: IL-6 was measured by ELISA (R&D) in pretreatment serum samples from 435 patients with stage IIB-III melanoma (151 women and 284 men, median age 51 years, range 18-77). After surgery patients were treated in a randomized study (The Nordic IFN trial) with either adjuvant interferon for 1 or 2 years, or observation. Results: Median serum concentration of IL-6 after surgery and before treatment was 1.8 ng/l, range 0.23-24 ng/l. Patients with serum IL-6 above the median had shorter overall survival (OS) compared to patients with serum IL-6 below the median (p�0.004). Median OS was 4.5 years in patients with serum IL-6 above the median (95% confidence interval (CI): 3.05-7.60). In patients with serum IL-6 below the median, median OS was not reached at the last survival-update. Multivariate Cox analysis including serum IL-6, ulceration in primary melanoma, LDH, white blood cells, lymph node metastases and Breslow thickness of primary melanoma showed that only serum IL-6 (hazard ratio (HR) � 1.48, 95% confidence interval (CI) : 1.13-1.94, p�0.004) was an independent prognostic factor for OS. In subgroup analysis of the control group and the two treatment groups, serum IL-6 demonstrated a negative prognostic impact in the control group (HR � 1.62, 95% CI: 1.02-2.57, p�0.04) and in the group treated with 2 years interferon HR � 1.69, 95% CI: 1.06-2.7, p�0.03). In the group treated with 1 year interferon this negative impact was not significant (HR � 1.15, 95% CI: 0.71-1.85, p�0.58). An interaction between IL-6 and treatment arm was not significant (p�0.45), suggesting that the negative prognostic effect of elevated pretreatment serum IL-6 is independent of treatment. Conclusions: Serum IL-6 above the median is an independent prognostic biomarker of short OS in patients operated for stage IIB-III melanoma. 8547 General Poster Session (Board #32E), Sun, 8:00 AM-12:00 PM Phase II study of the anti-ganglioside GD3 mouse/human chimeric antibody KW2871 combined with high dose interferon-a2b in patients with metastatic melanoma. Presenting Author: Stergios J. Moschos, University of Pittsburgh Medical Center, Pittsburgh, PA Background: Immunotherapy has demonstrated notable effects in metastatic melanoma (MM) with durable responses achieved by high-dose IL-2 and IFN�2b, leading to approval of these therapies for treatment of melanoma. However, complete responses occur in only a minority of patients. KW2871 is a chimeric monoclonal antibody (mAb) targeting the GD3 ganglioside with demonstrated antitumor activity and enhancement of antibody-dependent cell-mediated cytotoxicity (ADCC) and complementdependent cytotoxicity (CDC). IFN�2b has potent immunoregulatory, antiproliferative, differentiation-inducing, pro-apoptotic, and anti-angiogenic properties against a variety of malignancies including melanoma. Combining high dose IFN�2b (HDI) � KW2871 was hypothesized to have synergistic anti-tumor activity due to (1) the ability of HDI to enhance KW2871 induced ADCC in vitro (Liu, Cancer Immun 2002); (2) improved mAb targeting due to increased GD3 expression and induced inflammatory cytokines (TNF-�, IL-4 and IFN-�) (Hoon, Cancer Res, 1991); (3) increased tumor-infiltrating immune cells (Kirkwood, Cancer 2002; Moschos, J Clin Oncol 2006). Methods: This is an open label, dose-escalation, phase II study of KW2871 plus HDI in patients with measurable MM. Primary objectives are progression-free survival (PFS) and safety. Secondary objectives include assessment for tumor response by RECIST, ADCC, CDC, pharmacokinetics, human antichimeric antibodies (HACA), tumor-infiltrating immune cells, biomarkers and OS. Patients with measurable disease by RECIST, stable brain metastases, and performance status ECOG 0 or 1 are eligible. Patients with severe comorbidities or autoimmune disease or prior exposure to anti-GD3 antibodies are excluded. Sequential enrollment to cohorts of KW2871 at 5, 10 , 20 mg/m2 IV every 2 week in combination with HDI 20 MU/m2 IV once daily x 5 Days for 4 weeks, then 10 MU/m2 SC three times weekly until disease progression. Results: To date, Cohort 1 (5 mg/m2 KW2871) and Cohort 2 (10 mg/m2 KW2871) have been completed safely. Cohort 3 (20 mg/m2 KW2871) has enrolled of 18 of 27 planned patients. Conclusions: Will be presented at study completion. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
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Volume 30, Issue 15S, Part I of II
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Editor: Michael A. Carducci, MD Man
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Volume 30, Issue 15S Supplement to
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Letter from the Editor The 2012 ASC
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JOURNAL of CLINICAL ONCOLOGY ......
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ASCO Conflict of Interest Policy an
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2012 ASCO Annual Meeting Proceeding
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Author Index Note: Numerals refer t
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Alexanian, Raymond 8093 Alexeev, Bo
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Arkenau, Hendrik-Tobias 2540, 3000,
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Ballen, Karen K. 6606, 6617, 6618,
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Ben-Aharon, Irit 548, 2556, e13080
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Blancas, Isabel e11535, e11545, e21
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Brandes, Johann Christoph 7048, 106
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Cakir, Betul 9567 Calabek, Bernadet
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Ceraulo, Domenica 4017 Cerbone, Lin
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Chinen, Ludmilla T.D. e16046 Chinen
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Come, Steven E. 9071, 9100 Comis, S
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Dahlheimer, Tambra 2546 Dahmane, El
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DeLacure, Mark D. e16052 Delage, Ju
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Domingo, Gelenis 6568, 6575, 6588 D
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El Sherbeiny, Esam e15129 El-Deiry,
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Fayad, Luis 6501, 8067 Fayette, Jer
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Foroni, Chiara e11546 Foroni, Letiz
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Gang, Wu 7091, e14511 Gangaram, Anj
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Gimenez Capitan, Ana 4068, 10596, e
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Granowetter, Linda 9537 Grant, Barb
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Hainsworth, John D. 618, 1018, 1086
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Heerschap, Arend e13111 Heersink, M
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Hong, Seung-Mo 3568 Hong, Sook Hee
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Im, Young-Hyuck 598^, 644, TPS649,
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Ji, Yongling e17527 Jia, Jingquan e
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Kaparelou, Maria 583 Kapaun, Christ
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Kim, Chan Kyu e14688 Kim, Chang Won
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Komatsu, Yoshihiro e14689 Komatsu,
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Laack, Nadia N. 2032, e14507 Laadem
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Lee, Ji-Hyun TPS3114, 6100 Lee, Jih
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Lim, Kian-Huat e14584 Lim, Kiat Hon
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Loupakis, Fotios 3518, 3540, 3546,
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Man, Shan e11061, e15177^ Manaloor,
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Yasuda, Hiromi e14029 Yasuda, Hiroy
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Zhang, Xinmin e16022 Zhang, Xu Dong
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