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

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446s Leukemia, Myelodysplasia, and Transplantation 6620 General Poster Session (Board #24G), Mon, 1:15 PM-5:15 PM Azacitidine as induction therapy of elderly patients with acute myelogenous leukemia. Presenting Author: Cyrus Khan, West Penn Allegheny Health System, Pittsburgh, PA Background: Effective alternative treatment of elderly patients (aged � 60 years) with acute myelogenous leukemia (AML) remains challenging. Elderly patients with AML respond poorly to standard induction regimens and have high treatment related mortality. In a prior retrospective analysis of elderly patients with AML performed at our institution, azacitidine (AZA) showed an overall response rate (ORR) of 60% with limited toxicity. Methods: This is a prospective, phase II open-label study using AZA in patients �60 years with AML. Inclusion criteria: Newly-diagnosed non-M3 AML and ECOG � 2. Patients with circulating blast count �30,000/mcl were treated with hydroxyurea until � 30,000/mcl. AZA was administered at 100 mg/m2 subcutaneously for 5 consecutive days every 28 days until disease progression or significant toxicity. Results: In all, 15 patients were enrolled last follow-up being 8/2/11. The mean age of patients is 74 years (range: 64–82). Mean ECOG score was 1. Mean baseline bone marrow blast count was 52% (range: 25–92%). ORR was 46% (n�7) with complete response (CR) in 3 (20%) patients and partial response (PR) in 2 (13%) patients according to NCI response criteria, and hematologic improvement (HI) in 2 (13%) patients according to IWG response criteria. The mean number of days on treatment was 198 (range: 13–724). The mean time to best response among responders was 95 days (range: 44-279). The mean number of days hospitalized for diagnosis plus treatment or disease-related complication was 19 (range: 5–56), with the majority of therapy administered in an outpatient setting. Mean overall survival (OS) from diagnosis for all patients was 355 days (range: 13–908) and mean OS for responders was 532 days (range: 120–908). Nonhematological toxicity was limited to mild injection site skin reaction and fatigue in 73% (11/15). No treatment-related deaths were observed. The dose and schedule of AZA remained constant in a majority of the patients. Conclusions: This study suggests that a 5-day schedule of SC AZA at 100 mg/m2 to elderly patients with newly-diagnosed AML is a feasible, well-tolerated and effective alternative to standard induction chemotherapy. 6622 General Poster Session (Board #25A), Mon, 1:15 PM-5:15 PM Use of granulocytes concentrates from a single high yield apheresis to support more than one patient. Presenting Author: Fleur M. Aung, University of Texas M. D. Anderson Cancer Center, Houston, TX Background: Allogeneic granulocyte transfusion therapy is sometimes the only therapeutic option in immunocompromised neutropenic leukemic/ HSCT patients with life threatening bacterial and fungal infections. Collection of larger cell doses of granulocyte concentrates (GC) by automated apheresis following G-CSF/steroids administration has renewed interest and its use has grown steadily. Methods: Donors were recruited from family/friends of the patients and informed consent was obtained. GCs were collected via donor stimulation with a single subcutaneous dose of G-CSF (600 mcg). First time donors received an oral dose of dexamethasone (8 mg). GCs were harvested by Hetastarch-assisted leukapheresis 12 hours later via peripheral venous access with the continuous flow cell separator Spectra (COBE Caridian BCT, Lakewood, CO). Results: GCs were collected from 93 donors (67M: 26F; age median 40 (19-73 years) and 1½xblood volume processed median 7048 (3212-8085 mL). The pre/post wbc were median 8.1 (4.1-22.8)/ 42.7 (22.4-77.5). The volume collected was based on the post G-CSF wbc count (� 35 K/UL - 800 mL; �35 K/UL between 600-700 mL). The original yield (10 x10e) was median 9.7 (5.1-17.2 units), volume median 718 (538-860 mL) and WBC median 132.7 (84.2 -241.6 K/UL per bag). The Split GCs were median 4.48 (2.70-7.72 units), with neutrophils median 87% (54-97% per bag). GCs were transfused to 51 patients (31M: 20F; age median 58 [19-83 years]) who received median 3.5 (1-18 split units), containing wbcs median 10734.69 [5778-42 -162698.09 (x10^3/uL)/unit) and achieved a WBC increment median 0.2 (0.0-8.3K/UL). Conclusions: The GCs were split due to the primary care team’s reluctance to transfuse the entire volume of the product due to volume restrictions or for some other medical reason. The same rationale to split platelets from high yield single apheresis was used to split our GC products. We found that GCs from each donor was utilized maximally and also brought partial relief to other patients who lacked donors. We would like to make the case that when adequate numbers of GCs are collected it may be feasible to split the unit. This may offer a glimmer of hope to other patients in need of GCs who lack a donor network support. 6621 General Poster Session (Board #24H), Mon, 1:15 PM-5:15 PM Phase I dose escalation study of bortezomib in combination with lenalidomide in patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Presenting Author: Philip C. Amrein, Massachusetts General Hospital/Harvard Medical School, Boston, MA Background: Both bortezomib (Bz) and lenalidomide have clinical activity in patients with MDS and AML. We conducted a phase I dose escalation study to determine the maximal tolerated dose (MTD) of Bz in combination with lenalidomide. Methods: Patients with MDS (IPSS score � 0.5 or therapyrelated) received Bz by IV bolus on Days 1, 4, 8, and 11 and lenalidomide 10 mg/day PO on Days 1-21 in 28 day cycles for up to 9 cycles. Three doses of Bz were tested (0.7, 1.0, or 1.3 mg/m2 ). Cohorts consisted of 3-6 patients; the dose of Bz was escalated if there were � 2 dose limiting toxicities (DLTs). Growth factor support and transfusions were permitted. Dose limiting toxicities (DLTs) were assessed during the first cycle and were defined as severe neutropenia (absolute neutrophil count � 250/ul), thrombocytopenia (platelet count � 10,000/ul), grade � 2 neurotoxicity, or other grade � 3 non-hematologic toxicity. Following determination of the MTD, enrollment opened to patients with relapsed and refractory AML and those with untreated high risk disease for whom induction therapy was not indicated. Responses were assessed by IWG 2006 criteria for MDS and IWG 2003 criteria for AML. Results: 23 patients (14 men) were enrolled; one patient was inevaluable due to disease progression prior to starting protocol therapy. The median age was 73 years (range 54-87). There was 1 DLT observed, neutropenia, in 6 patients treated with 1.0 mg/m2 Bz and no DLTs at 0.7 or 1.3 mg/m2 . The median number of cycles was 2 (range 2-9). Grade � 3 toxicities possibly attributable to the treatment at any dose level were: anemia (2), thrombocytopenia (10), leukopenia (3), infection (1), rash (2), dyspnea (1), dizziness (1), hypotension (1), pneumonia (2) and neuropathy (1). Among the 14 patients with MDS, 1 patient with RARS experienced a CR and 2 with RAEB-2 experienced marrow CR (mCR). Among the 8 patients with AML, there was 1 CR. Conclusions: The maximal tested dose of Bz (1.3 mg/m2 ) in combination with lenalidomide is safe. Responses were seen in MDS and high risk AML. Future testing of this regimen is planned. 6623 General Poster Session (Board #25B), Mon, 1:15 PM-5:15 PM Novel risk factors for osteonecrosis of the jaw in multiple myeloma: A RADAR report. Presenting Author: Jaimee S. Holbrook, Department of Dermatology, Northwestern University Feinberg School of Medicine, Chicago, IL Background: Osteonecrosis of the jaw (ONJ) was identified in 2001 and is commonly seen in multiple myeloma (MM). The objective of this study is to evaluate novel risk factors in MM cases from a retrospective database. We hypothesized that ONJ may be related to stem cell transplant, chronic kidney disease and active smoking. Methods: We conducted a retrospective case-control study of 231 MM cases (from January 1, 1998 to September 30, 2010) identified from the electronic data warehouse (EDW) at Northwestern University (NU). The EDW is cross-institutional and integrates clinical data across NU. It comprises more than 2.3TB of data on roughly 2 million patients. The search terms used were: bisphosphonates, pamidronate, zoledronic acid, multiple myeloma, plasma cell disorders, osteonecrosis of the jaw, jaw abscess, dental abscess, among other terms described in literature. Data was abstracted onto a standardized form by 2 trained abstractors and validated by a clinician reviewer (BJE). Known and hypothesized new risk factors were abstracted, including duration of myeloma, treatment used, duration of bisphosphonate use, renal function indices, chemotherapy (vincristine, doxorubicin (A), dexamethasone (D) , thalidomide (T), cisplatin (P), cyclophosphamide (C), etoposide (E), novel agents [bevacizumab, sorafenib, angiostatin]) GCSF, smoking, and MM clinical stage. Analyses included T test, Wilcoxon, and log rank analysis. Results: ONJ occurring after MM diagnosis was identified in 33 cases out of a total of 233 cases of MM. ZOL, VAD, DT-PACE, and diabetes were more common in ONJ cases. Log rank analysis identified 2 risk factors for ONJ, the use of DT-PACE (p� 0.003), and complete and partial remission (p�0.007). Stem cell transplant and chronic kidney disease were not associated with ONJ. Conclusions: We identified novel risk factors for ONJ in MM, mainly partial or complete remission and use of DT-PACE. These results should prompt clinicians to heightened awareness and increased surveillance for the symptoms of ONJ for patients treated with DT-PACE. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
6624 General Poster Session (Board #25C), Mon, 1:15 PM-5:15 PM Adverse events (AEs) and the return of myelofibrosis (MF)-related symptoms after interruption or discontinuation of ruxolitinib (RUX) therapy. Presenting Author: Srdan Verstovsek, University of Texas M. D. Anderson Cancer Center, Houston, TX Background: RUX is a JAK1/JAK2 inhibitor that demonstrated significant clinical benefit in patients (pts) with MF in COMFORT-I (NCT00952289), a phase 3, randomized (1:1), double-blind, placebo (PBO)-controlled study (N�309). Methods: Pts assessed MF-related symptoms daily using the modified Myelofibrosis Symptom Assessment Form v2.0; Total Symptom Score (TSS) was calculated from individual scores for abdominal discomfort, pain under left ribs, early satiety, night sweats, itching, and bone/ muscle pain. Therapy was interrupted if platelet or absolute neutrophil count fell below 50,000/�L or 500/�L, respectively. AEs were evaluated during treatment interruption or discontinuation. The protocol suggested an optional tapering strategy and possible addition of steroids if RUX therapy was discontinued for reasons other than thrombocytopenia. Results: In RUX-treated patients with treatment interruption, TSS gradually returned to baseline levels over approximately 1 week. The most common AE leading to treatment interruption or discontinuation in each group was thrombocytopenia (n�11, RUX) and abdominal pain (n�4, PBO). Of these, only 1 RUX pt discontinued for thrombocytopenia. A summary of new onset/worsening AE data after treatment interruption or discontinuation is presented (Table). Of 58 pts who discontinued study treatment, 23 (n�10, RUX; n�13, PBO) experienced a total of 43 SAEs (19, RUX; 24, PBO) that showed no specific pattern or difference between treatment groups. Four of 21 RUX-treated pts had dose tapering following study drug discontinuation. Conclusions: Apart from the expected return of MF-related symptoms, there was no pattern of AEs to suggest that RUX interruption or discontinuation is associated with a specific withdrawal syndrome. RUX (N�155) PBO (N�151) Treatment interruption, n 49 54 Mean duration, days 16 9 Grade >3 AEs, n 8 7 SAEs, n 3 3 Gastrointestinal hemorrhage; Anemia; pulmonary edema; fatigue and neutropenic hepatic encephalopathy fever; urosepsis and acute gout Treatment discontinuation, n 21 37 Grade >3 AEs, n 12 17 SAEs, n 10 13 6626^ General Poster Session (Board #26B), Mon, 1:15 PM-5:15 PM Health-related quality of life (HRQoL) and symptom burden in patients (Pts) with myelofibrosis (MF) in the COMFORT-II study. Presenting Author: Jean-Jacques Kiladjian, Hôpital Saint-Louis et Université Paris Diderot, Paris, France Background: Ruxolitinib has demonstrated rapid and durable reductions in splenomegaly and improved disease-related symptoms and QoL in 2 phase 3 studies (COMFORT-I and -II) in pts with primary MF (PMF), postpolycythemia vera-MF (PPV-MF), or post-essential thrombocythemia-MF (PET-MF). The prevalence of individual symptoms among these pts has not been defined. We evaluated the baseline HRQoL and symptoms among pts enrolled in COMFORT-II. Methods: COMFORT-II is a randomized, openlabel, multicenter, phase 3 study comparing ruxolitinib with best available therapy. HRQoL and symptoms were assessed at baseline using the European Organisation for the Research and Treatment of Cancer QoL Questionnaire–Core 30 (EORTC QLQ-C30) and Functional Assessment of Cancer Therapy–Lymphoma (FACT-Lym); this analysis summarizes these scores for all pts, regardless of assigned treatment. Results: In COMFORT-II (N � 219), 52% of pts were aged � 65 years and 57% were male. By IPSS criteria (Cervantes et al. 2009), 40% had intermediate-2 and 60% had high-risk MF. Mean (95% CI) EORTC global health status/QoL (53.7 [50.6-56.7]; median, 50.0) and FACT-General total scores (73.0 [70.8- 75.2]) were comparable to those for pts of similar age with other cancers (Oliva et al. 2011: median global health status score of 50 for acute myeloid leukemia [AML]). The most frequent symptoms (reported as “quite a bit” or “very much”) were fatigue (54%), dyspnea (30%), insomnia (30%), pain (29%), night sweats (23%), and itching (21%), and there were differences in baseline symptoms across MF subtypes (Table). Conclusions: This analysis shows that pts with MF experience severe disease-related symptoms and have diminished HRQoL similar to pts with AML, but because pts with MF have a longer life expectancy (an average of 2.3 to 4 years for high and intermediate-2 risk pts, respectively), they may suffer with a reduced QoL for many years. % “quite a bit” or “very much” PMF (N � 116) PPV-MF (N � 68) PET-MF (N � 35) Fatigue 59.2 46.1 53.2 Dyspnea 28.7 30.2 31.2 Insomnia 32.7 25.4 28.2 Pain 25.9 28.6 41.9 Night sweats 21.3 27.3 18.2 Itching 16.8 28.8 21.3 Weight loss 12.1 22.7 6.3 Leukemia, Myelodysplasia, and Transplantation 6625^ General Poster Session (Board #26A), Mon, 1:15 PM-5:15 PM Association of cytokine levels and reductions in spleen size in COMFORT- II, a phase III study comparing ruxolitinib to best available therapy (BAT). Presenting Author: Claire N. Harrison, Guy’s and St. Thomas’ NHS Foundation Trust, London, United Kingdom Background: Ruxolitinib is a potent and selective oral JAK1/2 inhibitor that has been approved for the treatment of myelofibrosis (MF). Ruxolitinib has demonstrated rapid and durable reductions in splenomegaly and improved disease-related symptoms and quality of life (QoL) in 2 phase 3 studies (COMFORT-I and –II) in patients (pts) with primary MF (PMF), postpolycythemia vera-MF (PPV-MF), or post-essential thrombocythemia-MF (PET-MF). This analysis evaluated associations between cytokine levels and spleen size reductions in the COMFORT-II study. Methods: COM- FORT-II is a randomized (2:1), open-label, phase 3 study comparing the safety and efficacy of ruxolitinib with BAT. Spleen volume was measured by MRI every 12 weeks and spleen length by palpation at each study visit. Plasma samples were analyzed using Rules Based Medicines Human MAP v1.6; 89 cytokines were measured at BL and wks 4, 24, and 48. Simple linear regression was used to evaluate the correlation between BL or change from BL in cytokine levels with % change of spleen size. Results: In the ruxolitinib arm, association was found between changes in TNF-� and leptin levels and % spleen volume reduction at wk 24 (TNF-�: N� 93; correlation coefficient [R] � 0.43; false discovery rate adjusted P value [P] � .01; leptin: N � 96; R � -0.28; P � .09) and wk 48 (TNF-�:N� 86; R � 0.43; P � .01; leptin: N � 87; R � -0.34; P � .02) that was not observed with BAT and was independent of JAK2V617F status. For ruxolitinib-treated JAK2V617F� pts, higher leptin levels at BL were associated with greater % spleen length reductions at wk 48 (N � 45; R � -0.44; P � .11). A clear trend was observed for increased leptin levels that preceded weight gain on ruxolitinib treatment. For ruxolitinib-treated JAK2V617F� pts, decreased IL-8 at wk 4 was associated with % spleen volume reductions at wk 24 (N � 68; R � 0.28; P � .24) and wk 48 (N � 60; R � 0.38; P � .15). Conclusions: This analysis has shown statistically significant associations between changes in cytokine levels and spleen size reductions. Further analysis is in progress to determine associations between cytokine levels and QoL or symptoms and to confirm these observations in an independent data set. 6627 General Poster Session (Board #26C), Mon, 1:15 PM-5:15 PM Post hoc analysis of association between treatment response and various indicators of efficacy and safety in a randomized phase III trial of decitabine in older patients with acute myeloid leukemia. Presenting Author: Mark D. Minden, Princess Margaret Hospital, Toronto, ON, Canada Background: In a recent, large phase III trial (NCT00260832; Kantarjian, JCO; in press), 485 patients �65y with newly diagnosed acute myeloid leukemia (AML) received, every 4 wks, treatment choice (TC) of either supportive care or cytarabine (20 mg/m 2 subcutaneous injection, 10 consecutive days) or decitabine (DAC) 20 mg/m2 (1-h intravenous [IV] infusion, 5 consecutive days). This post hoc analysis investigated relationships between response to treatment and indicators of efficacy and safety. Methods: Response was defined as morphologic complete remission (CR), or CR with incomplete blood count recovery (CRi) or partial response (PR). Transfusions (red blood cell [RBC] or platelets [PLT]), IV antibiotic use, and dose modifications were tabulated for responders and nonresponders to DAC or TC during the treatment period. Results: Fewer responders than nonresponders had dose modifications (30.4% vs 64.5%, respectively; P�.0001). Antibiotic use and transfusions were similar in both groups. Overall survival for responders was 16.1–18.5 mo vs 4.2–4.9 mo for nonresponders. Conclusions: These data suggest that response to DAC or TC treatment predicts clinically relevant benefits, with fewer dose modifications in older patients with newly diagnosed AML. The number of transfusions and antibiotic use was impacted by the longer survival time of responders vs nonresponders. Data on the impact of early response are being analyzed. Parameter* Nonresponders (n�383) 447s CR�CRi�PR responders (n�102) p value † Overall survival, median, mo IV antibiotic use 4.2–4.9 16.1–18.5 – Number of patients 383 102 Yes, n (%) PLT transfusions 77 (20.1) 14 (13.7) .143 Number of patients 279 75 Mean (SD) 11.64 (14.7) 13.67 (21.7) .447 Median (range) RBC transfusions 7 (1–110) 7 (1–136) Number of patients 342 97 Mean (SD) 10.68 (12.2) 14.38 (14.5) .023 Median (range) Dose modifications 7 (1–102) 11 (1–89) Number of patients 383 102 Yes, n (%) 247 (64.5) 31 (30.4) �.0001 *All patients who had both response and parameter data. † Based on 2 sample t test to compare means; 2 proportion Z test to compare proportions. 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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Blancas, Isabel e11535, e11545, e21
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El Sherbeiny, Esam e15129 El-Deiry,
Page 734 and 735:
Fayad, Luis 6501, 8067 Fayette, Jer
Page 736 and 737:
Foroni, Chiara e11546 Foroni, Letiz
Page 738 and 739:
Gang, Wu 7091, e14511 Gangaram, Anj
Page 740 and 741:
Gimenez Capitan, Ana 4068, 10596, e
Page 742 and 743:
Granowetter, Linda 9537 Grant, Barb
Page 744 and 745:
Hainsworth, John D. 618, 1018, 1086
Page 746 and 747:
Heerschap, Arend e13111 Heersink, M
Page 748 and 749:
Hong, Seung-Mo 3568 Hong, Sook Hee
Page 750 and 751:
Im, Young-Hyuck 598^, 644, TPS649,
Page 752 and 753:
Ji, Yongling e17527 Jia, Jingquan e
Page 754 and 755:
Kaparelou, Maria 583 Kapaun, Christ
Page 756 and 757:
Kim, Chan Kyu e14688 Kim, Chang Won
Page 758 and 759:
Komatsu, Yoshihiro e14689 Komatsu,
Page 760 and 761:
Laack, Nadia N. 2032, e14507 Laadem
Page 762 and 763:
Lee, Ji-Hyun TPS3114, 6100 Lee, Jih
Page 764 and 765:
Lim, Kian-Huat e14584 Lim, Kiat Hon
Page 766 and 767:
Loupakis, Fotios 3518, 3540, 3546,
Page 768 and 769:
Man, Shan e11061, e15177^ Manaloor,
Page 770 and 771:
Mathieu-Nicot, Florence e19623 Math
Page 772 and 773:
Mergenthaler, Hans-Guenther e15026
Page 774 and 775:
Molero, Xavier e21035 Moles-Moreau,
Page 776 and 777:
Munoz-Sanchez, MM e19590 Munsell, M
Page 778 and 779:
Ng, Daniel e15050 Ng, Dawn Marie e1
Page 780 and 781:
Oguri, Senri 5556 Oh, Do Youn 1003
Page 782 and 783:
Palassini, Elena 10026, 10053, 1006
Page 784 and 785:
Peisker, Uwe 10600 Peker, Deniz e18
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Piwnica-Worms, Helen 3047 Pizzo, Fa
Page 788 and 789:
Rabinowits, Guilherme 5501, 5582, 9
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Reyes-Rivera, Irmarie CRA3503 Reyna
Page 792 and 793:
Rose, Steven C. 3590 Rosell, Rafael
Page 794 and 795:
Sakata, Shinya e18059 Sakata, Yuh 3
Page 796 and 797:
Schenkein, David P. 6606 Schepp, Wo
Page 798 and 799:
Sha, Dan 3564 Sha, Huifang e13528 S
Page 800 and 801:
Silva, Jose D. 5567 Silva, Milton J
Page 802 and 803:
Sousa, Carlos Eduardo Pires 643 Sou
Page 804 and 805:
Su, Xinying 4124 Su, Yu-Chieh e1600
Page 806 and 807:
Tan, Chee Seng 1064, e19523 Tan, Ch
Page 808 and 809:
Tillmanns, Todd D. 5014, e15514 Til
Page 810 and 811:
Uchiyama, Tomotaka e21108 Udovitsa,
Page 812 and 813:
Videtic, Gregory M.M. e14611, e1466
Page 814 and 815:
Wang, Yuan e15124 Wang, Yunfei 547
Page 816 and 817:
Wischnewsky, Manfred 1078 Wischnik,
Page 818 and 819:
Yasuda, Hiromi e14029 Yasuda, Hiroy
Page 820:
Zhang, Xinmin e16022 Zhang, Xu Dong
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