Annual Meeting Proceedings Part 1 - American Society of Clinical ...

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606s Pediatric Oncology 9500 Oral Abstract Session, Sat, 1:15 PM-4:15 PM Efficacy of crizotinib in children with relapsed/refractory ALK-driven tumors including anaplastic large cell lymphoma and neuroblastoma: A Children’s Oncology Group phase I consortium study. Presenting Author: Yael P. Mosse, The Children’s Hospital of Philadelphia, Philadelphia, PA Background: Genetic aberrations in the anaplastic lymphoma kinase (ALK) gene are found in anaplastic large cell lymphoma (ALCL), neuroblastoma (NB) and other tumors.Crizotinib,a small molecule inhibitor of ALK and c-Met, is active in non-small cell lung cancers (NSCLC) harboring an ALK translocation. We performed a phase 1 dose-escalation and pharmacokinetic (PK) trial of crizotinib in patients (pts) with refractory solid tumors and ALCL. Methods: Crizotinib was administered bid without interruption in 28 day cycles using the rolling-six design. Six dose levels (100, 130, 165, 215, 280, 365 mg/m2 /dose) have been evaluated (A1). Pts with confirmed ALK fusion proteins, mutations or amplification (A2) could enroll at one dose level lower than part A1 and those with NB could enroll on a separate stratum (A3). PK studies were performed on day 1 and at steady state (SS). ALK genomic status in tumor tissue was evaluated and qPCR was used to measure NPM-ALK fusion transcript in bone marrow and blood samples of ALCL pts. Results: 70 pts were enrolled, 57 fully evaluable for toxicity, [median (range) age 9.9 yrs (1.1–21.3)]: 29 on A1, 18 on A2, and 10 on A3. In A1, 2/7 pts developed DLT (grade 3 dizziness, grade 5 intra-tumoral hemorrhage) at 215 mg/m2 and 1/6 pts developed DLT (grade 4 liver enzyme elevation) at 365 mg/m2 . In A2, 1 grade 4 DLT (neutropenia) occurred at 165 mg/m2 ; in A3, no DLTs occurred. Mean (�SD) Cave (�AUC0-12h/12h) of crizotinib at SS was 466�114 ng/mL at 215 mg/m2 / dose (n�5), 443�121 ng/mL at 280 mg/m2 /dose (n�8), and 720�230 ng/mL at 365mg/m2 /dose (n�4). Response data for pts with ALCL (six at 165 mg/m2 , two at 280 mg/m2 ) approved for release by the Data Safety Monitoring Committee demonstrates 7/8 (88%) complete response (CR) rate to date. RT-PCR data for 6 of these pts at 57 time points was obtained and will be described. In addition, 2 pts with NB have had CRs, one with a documented ALK mutation. One patient with an inflammatory myofibroblastic tumor and one with NSCLC had PRs. Conclusions: Inhibition of ALK in pediatric pts with ALK-driven tumors occurs with minimal toxicity and is associated with objective anti-tumor activity. 9502 Oral Abstract Session, Sat, 1:15 PM-4:15 PM Stanford V chemotherapy and involved field radiotherapy for children and adolescents with unfavorable risk Hodgkin lymphoma: Results of a multiinstitutional prospective clinical trial. Presenting Author: Monika Metzger, University of Tennessee Health Science Center, Memphis, TN Background: To evaluate the efficacy of 12 weeks of Stanford V chemotherapy (prednisone, vinblastine, doxorubicine, nitrogen mustard, etoposide, vincristine, and bleomycin) without routine growth factor support plus response-adapted low-dose, involved-field radiotherapy (IFRT) in children and adolescents with unfavorable risk Hodgkin lymphoma (HL). Methods: Multi-institutional (St. Jude Children’s Research Hospital, Stanford University, Children’s Hospital Boston, Massachusetts General Hospital and Maine Children’s Hospital) clinical trial. One hundred forty-one patients with clinical stages IIB (n�43), IIIB (n�19), IVA (n�27), and IVB (n�52) HL were treated with 12 weeks of Stanford V chemotherapy and low dose IFRT between June 2002 and May 2011. Involved nodal sites in complete remission (CR, defined as � 75% shrinkage of the original tumor and PET negative) after 8 weeks of Stanford V received 15 Gy IFRT; those sites that achieved only partial response received 25.5 Gy IFRT after completion of all 12 weeks of chemotherapy. Results: With a median follow-up of 4.6 years, the 3-year overall and event-free survival (EFS) are 97% (SE�2%) and 79% (SE�4%) respectively. There was no significant difference in EFS by stage (IIB vs. IIIB vs. IV; P�0.84). Ten patients developed progessive disease and 18 relapsed, while 5 have died (1 after relapse in an accident and 4 of refractory disease). Most common toxicities were grade 3 hematologic with 234 episodes of neutropenia in 101 patients (72%) and 85 episodes of anemia in 52 patients (37%); Fever and neutropenia occurred 13 times in 12 patients (9%). Conclusions: Risk-adapted, combined-modality therapy using 12 weeks of Stanford V chemotherapy plus IFRT is well tolerated in this population with manageable acute toxicities. Overall survival is comparable to other more intense chemotherapy regimens. Future high-risk front line therapies may consider a Stanford V backbone with targeted intensification and further tailoring of radiation therapy. 9501 Oral Abstract Session, Sat, 1:15 PM-4:15 PM Efficacy of rituximab plus FAB group C chemotherapy without CNS radiation in CNS-positive pediatric Burkitt lymphoma/leukemia: A report from the Children’s Oncology Group. Presenting Author: J. Kimble Frazer, University of Utah, Salt Lake City, UT Background: Historically, CNS-positive (CNS�) mature B-NHL in children and adolescents has been associated with a dismal outcome (Miles/Cairo, Br J Haematol, 2012). Adding CNS radiation and high-dose MTX and cytarabine to group C therapy for children with CNS� B-NHL yielded a 77% 5-yr EFS in LMB89 (Patte et al., Blood, 2001). An ensuing FAB/LMB96 trial replaced cranial radiation with further HD-MTX and intrathecal therapy with similar results (75% 4-yr EFS) (Cairo et al., Blood, 2007). Here, patients with marrow and CNS� disease fared worse than isolated CNS� (61% vs. 83% 4-yr EFS, p�0.001), with �50% of CNS� patients who progressed or recurred having systemic, but not CNS, relapse. Rituximab, a chimeric anti-CD20 antibody, improved EFS, PFS, and OS when added to chemotherapy for adults with DLBCL (Coiffier et al., N Engl J Med, 2002; Pfreundschuh et al., Lancet Oncol, 2006). We tested whether adding rituximab to FAB group C chemotherapy in pediatric patients with CNS� B-NHL was safe and efficacious. Methods: Children and adolescents (�21 yrs.) with CNS� B-NHL received FAB group C1 therapy (Cairo et al., Blood, 2007). Rituximab (375 mg/m2 /dose) was given twice in COPADM courses 1&2andonce in CYVE courses (Cairo et al., ASCO, 2010). CSF blasts (�1), cranial nerve palsy (CNP), intra-cerebral mass (ICM), and/or parameningeal extension (PME) defined cases as CNS�. Results: Of 40 eligible Group C patients,15 (38%) were CNS�; all 15 had Burkitt morphology. Eight CNS� patients were CSF� [WBC median 35 (range 1-1104)] with 6 cases CNP�, 4 PME�, and 1 ICM�. No adverse events were attributed to rituximab. Fourteen of 15 CNS� patients (93%) are alive and disease-free. Of 7 BM- /CNS� patients, 100% are NED. In BM�/CNS� cases, 7/8 (88%) are NED, with one patient progressing with systemic and CNS disease. Conclusions: Addition of rituximab to group C FAB therapy was well tolerated. Outcomes in this small cohort of 15 children and adolescents with CNS� BL (93%) suggest that adding rituximab to FAB group C therapy without CNS radiation may reduce systemic relapse. Large randomized studies are warranted to test this hypothesis in this previously high-risk clinical subgroup. 9503 Oral Abstract Session, Sat, 1:15 PM-4:15 PM The effects of dexrazoxane on cardiac status and second malignant neoplasms (SMN) in doxorubicin-treated patients with osteosarcoma (OS). Presenting Author: Lisa M. Kopp, The University of Arizona, Tucson, AZ Background: Anthracyclines are highly efficacious in OS but associated with risk of cardiotoxicity. We conducted two studies using dexrazoxane as a cardioprotectant: i) AOST0121, a phase II study for metastatic OS and ii) P9754, a series of pilot studies including doxorubicin dose intensification in patients with localized OS. Methods: Patients on AOST0121 received methotrexate, doxorubicin (375 mg/m2 ), cisplatin, ifosfamide and etoposide (MAPIE). Those with HER2-positive tumors also received trastuzumab (4 mg/kg loading dose, 2 mg/kg weekly). On P9754, patients received MAP in Pilot 1, MAPI or MAPIE in Pilots 2 and 3. Total doxorubicin was 450 mg/m2 or 600 mg/m2 with each dose preceded by dexrazoxane (10:1 ratio). Etoposide was never given simultaneously with dexrazoxane. Measurements of left ventricular systolic function by echocardiography, serum troponin-T (cTnT, a myocardial injury marker) and N-terminal pro-brain natriuretic peptide (NT-proBNP, a cardiomyopathy marker) were obtained at baseline and repeated during therapy. Secondary malignancies were reported to the NCI. Results: None of the 47 patients (17 receiving trastuzumab) evaluated for cardiac toxicity on AOST0121 had significant changes in left ventricular fractional shortening, measurable cTnT, elevation of NT-proBNP or clinical evidence of cardiotoxicity (CTCv2.0). In P9754, 242 patients were evaluated for cardiotoxicity. Only 1 patient had CTCv2.0 grade 3 toxicity and 1 patient had a measurable cTnT. Three of 96 patients treated on AOST0121 and two of 272 patients on P9754 developed AML. Combining both studies: 5/398 or 1.4%. Conclusions: This large group of OS patients demonstrates that dexrazoxane is an effective cardioprotectant for doxorubicin alone (375-600 mg/m2 ), and in combination with trastuzumab. Dexrazoxane did not lead to an increase in secondary malignancies in OS patients treated with these regimens as compared to historical rates of 1-2%. Our results do not support the findings of a recent European Medicines Agency safety review that concluded dexrazoxane was unsafe for use in children and adolescents due to risk of SMN. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
9504 Oral Abstract Session, Sat, 1:15 PM-4:15 PM Cardioprotection and safety of dexrazoxane (DRZ) in children treated for newly diagnosed T-cell acute lymphoblastic leukemia (T-ALL) or advanced stage lymphoblastic leukemia (T-LL). Presenting Author: Barbara Asselin, University of Rochester, Rochester, NY Background: POG 9404 evaluated the efficacy of DRZ as a cardioprotectant and its side effects in children receiving doxorubicin (DOX) as part of chemotherapy for T-ALL/T-LL. Methods: Between 6/1996 and 9/2001, 537 T-ALL/T-LL patients were treated with multi-agent chemotherapy that included 12 DOX doses of 30 mg/m2 . Patients were randomized at diagnosis to treatment with or without DRZ (300 mg/m2 IV immediately prior to each DOX dose). Cardiac effects were assessed by serial echocardiograph measurements of left ventricular (LV) function (fractional shortening) and structure (end-diastolic dimension, wall thickness, and mass). Adverse events, grades 3-5 were recorded using CTCAE version 2.0. Results: Five-year EFS was similar for the DRZ (0.77�0.03%) and no-DRZ (0.76�0.03%) groups (p�0.9). Acute cardiac toxicity occurred in 1 patient (arrhythmia) on DRZ and 4 patients treated without DRZ (1arrhythmia, 3-decreased LV fractional shortening). At each of the three time-points post-baseline (end-induction, after the last DOX dose and two years post study entry) LV dimensions were larger from baseline for patients who did not receive DRZ. In univariate analyses, change in LV end-diastolic dimension from baseline was the only variable that was significantly different between DRZ and no-DRZ arms. This was true at each of the three time points (p�0.005-0.02). The frequencies of grade 3 or 4 toxicity (hematologic, infection, CNS events, mucositis) or death were similar in groups with or without DRZ (p�0.24). There were 13 second malignancies, 10 patients had received DRZ and 3 had not (p�0.07). Conclusions: Our LV dimension measurements suggest that DRZ may protect against the early LV remodeling and enlargement that is seen with DOX cardiotoxicity. Addition of DRZ did not interfere with the anti-tumor efficacy of this DOX-containing, multi-agent regimen, and there was no significant increase in toxicities. An increased rate of second malignancies with DRZ did not reach conventional levels of statistical significance. The study was not powered to assess second malignancy rates and this trend is of unknown clinical significance. 9506 Oral Abstract Session, Sat, 1:15 PM-4:15 PM In vivo monitoring of JAK/STAT and PI3K/mTOR signal transduction inhibition in pediatric CRLF2-rearranged acute lymphoblastic leukemia (ALL). Presenting Author: Sarah Kathleen Tasian, The Children’s Hospital of Philadelphia, Philadelphia, PA Background: Therapy intensification for children with B-precursor ALL with high-risk genetic lesions has improved relapse-free survival. CRLF2 rearrangements and JAK2 and IL7RA mutations occur in 10-15% of adult and pediatric ALL patients, most of whom relapse. We and others identified aberrant kinase signatures and perturbed JAK/STAT and PI3K/mTOR signal transduction via in vitro studies of CRLF2-rearranged (CRLF2r) ALLs, suggesting the therapeutic relevance of signal transduction inhibitors (STIs). Our creation of CRLF2r ALL xenograft models has enabled rapid preclinical testing of STIs and measurement of in vivo target inhibition. We hypothesized that inhibition of JAK/STAT and PI3K/mTOR phosphosignaling correlates with therapeutic responses in these models. Methods: NOD/SCID/�c-null (NSG) mice well-engrafted with pediatric ALL samples were treated with the JAK inhibitor ruxolitinib, the mTOR inhibitor sirolimus, or vehicle for 72 hours (for signaling response) or 4 weeks (for therapeutic response). Splenocytes were briefly stimulated ex vivo with thymic stromal lymphopoietin (ligand for CRLF2) and stained with humanspecific surface and intracellular phosphoantibodies for multi-parameter phosphoflow cytometry analysis. Results: Ruxolitinib-induced inhibition of phospho (p)-JAK2 and pSTAT5 was most pronounced in non-CRLF2r ALLs with novel JAK2-activating BCR-JAK2 and IL7RA/LNK mutations. Sirolimus potently inhibited pS6 and other PI3K/mTOR pathway phosphoproteins in the CRLF2r r ALLs. PSTAT5 and pS6 inhibition correlated with longer-term ruxolitinib- and sirolimus-induced decreases in ALL cell burden, demonstrating therapeutic responses to STIs. Conclusions: Ruxolitinib inhibited JAK/STAT phosphosignaling and markedly decreased leukemic burden in the JAK2-activating BCR-JAK2 and IL7RA/LNK mutant ALL xenografts. Sirolimus potently inhibited PI3K/mTOR (as well as some JAK/STAT) phosphosignaling and had greater therapeutic efficacy than ruxolitinib in the CRLF2r ALLs. The safety of ruxolitinib and of temsirolimus with cytotoxic chemotherapy are currently being established in Children’s Oncology Group Phase I trials. Pediatric Oncology 9505 Oral Abstract Session, Sat, 1:15 PM-4:15 PM Efficacy of the Children’s Oncology Group (COG) long-term followup (LTFU) guidelines in reducing risk of congestive heart failure (CHF) in childhood cancer survivors (CCS). Presenting Author: F. Lennie Wong, City of Hope, Duarte, CA Background: CCS are at risk for left ventricular dysfunction (LVD) and subsequent CHF due to exposure to anthracyclines and chest radiation (RT). COG LTFU guidelines recommend screening for LVD using echocardiograms (ECHOs) every 1-5y depending on anthracycline dose, RT, and age at cancer diagnosis. The relevance and cost-effectiveness of these consensus-based guidelines are unknown. Methods: Life expectancy and age at onset of CHF were projected in a simulated cohort (�1 million) of CCS undergoing screening ECHO per COG guidelines. Intervention for LVD was modeled to reduce annual CHF risk by 30%. Quality-adjusted life-years (QALYs) and lifetime costs with and without ECHO screening were calculated. Non-CHF mortality was estimated from the Childhood Cancer Survivor Study and US population rates. Costs and QOL adjustments were obtained from the Healthcare Cost and Utilization Project and medical literature. Screening was considered cost-effective if it resulted in a �6 month delay in onset of CHF and �$50,000/QALY gained. Results: Recommended screening strategies (Table) were cost-effective in: i) CCS exposed to �300mg/m² of anthracycline regardless of RT or age; and ii) CCS diagnosed at age 1-4y, exposed to RT and �300mg/m² of anthracycline. Screening was most cost-effective for CCS diagnosed at age 1-4y exposed to RT � �300 mg/m² of anthracycline (1.4y delay in CHF onset; $15,821/QALY gained). Screening as currently proposed was not costeffective for other age/anthracycline/RT combinations. Conclusions: Recommended ECHO screening strategies are cost-effective for all CCS exposed to �300 mg/m² of anthracycline; screening was also cost-effective for those 1-4y at diagnosis, exposed to anthracycline �300 mg/m² � RT. Alternate screening strategies are needed for CCS with other exposure conditions. Age Dx (years) RT Anthracycline dose (mg/m²) Recommended ECHO interval (years) Delay in CHF onset age (years) 607s Cost / QALY gained (US$) 1-4 Yes �300 1 0.8 $49,750 �300 1 1.4 $15,821 No �100 5 0.3 $17,798 100-299 2 0.4 $29,415 �300 1 1.2 $25,065 >5 Yes �300 2 0.4 $36,874 �300 1 0.8 $28,093 No � 200 5 0.1 $50,750 200-299 2 0.2 $86,867 �300 1 0.7 $36,401 9507 Oral Abstract Session, Sat, 1:15 PM-4:15 PM Relapse-specific mutations in cytosolic 5’-nucleotidase II in childhood acute lymphoblastic leukemia. Presenting Author: Julia Meyer, New York University Langone Medical Center, New York, NY Background: Relapsed childhood acute lymphoblastic leukemia (ALL) carries a very poor prognosis despite intensive retreatment that often includes allogeneic stem cell transplantation, due to intrinsic drug resistance. Novel therapeutic approaches are urgently needed and identification of the biological pathways that mediate resistance might provide targets for the effective prevention and treatment of relapsed ALL. However, the spectrum of somatic mutations responsible for ALL relapse is not yet known. Methods: We profiled the transcriptome of matched diagnosis and relapse bone marrow specimens from 10 pediatric B lymphoblastic leukemia patients using massively parallel sequencing technology (RNAseq) to identify novel mutations specific at disease recurrence. Results: Transcriptome sequencing identified 20 newly acquired novel nonsynonymous mutations in 10 relapse specimens not present at initial diagnosis. Two patients harbored relapsed specific mutations in the same gene, NT5C2, which codes for the Cytosolic 5’-nucleotidase II protein at different sites in the protein sequence. Mutations were validated as relapse specific after Sanger resequencing of germline, diagnosis and relapse DNA. RNA-seq coverage of each mutation was �100X, indicating that if a relapsed clone were present at diagnosis it made up � 1% of the bulk leukemia. Full exon sequencing of NT5C2 was completed in 61 additional relapse specimens, identifying 5 additional mutations which were also confirmed as relapse specific. Structural modeling of the relapseassociated mutations in the encoded protein Cytosolic 5’-nucleotidase II suggests alteration of enzyme subunit association/dissociation. Clinically, patients who harbored NT5C2 mutations were more likely to relapse earlier following initial diagnosis than those patients without mutations (p�0.03). Conclusions: Mutations in NT5C2 are associated with the outgrowth of drug resistant cells in childhood ALL. 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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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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Gang, Wu 7091, e14511 Gangaram, Anj
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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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Mathieu-Nicot, Florence e19623 Math
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Mergenthaler, Hans-Guenther e15026
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Molero, Xavier e21035 Moles-Moreau,
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Munoz-Sanchez, MM e19590 Munsell, M
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Ng, Daniel e15050 Ng, Dawn Marie e1
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Oguri, Senri 5556 Oh, Do Youn 1003
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Palassini, Elena 10026, 10053, 1006
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Peisker, Uwe 10600 Peker, Deniz e18
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Piwnica-Worms, Helen 3047 Pizzo, Fa
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Rabinowits, Guilherme 5501, 5582, 9
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Reyes-Rivera, Irmarie CRA3503 Reyna
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Rose, Steven C. 3590 Rosell, Rafael
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Sakata, Shinya e18059 Sakata, Yuh 3
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Schenkein, David P. 6606 Schepp, Wo
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Sha, Dan 3564 Sha, Huifang e13528 S
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Silva, Jose D. 5567 Silva, Milton J
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Sousa, Carlos Eduardo Pires 643 Sou
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Su, Xinying 4124 Su, Yu-Chieh e1600
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Tan, Chee Seng 1064, e19523 Tan, Ch
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Tillmanns, Todd D. 5014, e15514 Til
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Uchiyama, Tomotaka e21108 Udovitsa,
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Videtic, Gregory M.M. e14611, e1466
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Wang, Yuan e15124 Wang, Yunfei 547
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Wischnewsky, Manfred 1078 Wischnik,
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Yasuda, Hiromi e14029 Yasuda, Hiroy
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Zhang, Xinmin e16022 Zhang, Xu Dong
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