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360s Head and Neck Cancer 5516^ Poster Discussion Session (Board #6), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Cilengitide with cetuximab, cisplatin, and 5-FU in recurrent and/or metastatic squamous cell cancer of the head and neck: The ADVANTAGE phase II trial. Presenting Author: Jan Baptist Vermorken, Department of Medical Oncology, Antwerp University Hospital, Edegem, Belgium Background: Prognosis for patients with recurrent and/or metastatic squamous cell cancer of the head and neck (R/M-SCCHN) is very poor. �v�5 integrin is overexpressed in SCCHN and selective integrin blockade is being investigated as a treatment strategy. Methods: ADVANTAGE was a phase I/II study evaluating cilengitide with cetuximab and platinum-based chemotherapy. Eligible patients were �18 years with �1 measurable lesion, Karnofski performance status �70%, and confirmed R/M-SCCHN. The phase II part reported herein was an open-label, randomized, controlled trial investigating progression-free survival (PFS) in patients treated with 2 cilengitide 2000 mg regimens: once weekly (CIL1W) and twice weekly (CIL2W) administration combined with cisplatin, 5-FU, and cetuximab (PFE) as compared with PFE alone (control). Secondary objectives included overall survival (OS) and objective response (OR). Treatment-emergent adverse events (TEAEs) were monitored. Results: 184 eligible patients were enrolled. Overall, patient characteristics were similar across arms. Median duration of treatments was shorter in the CIL2W arm compared with the CIL1W arm (cilengitide: 16.1 vs 23.4 wk, cetuximab: 16.0 vs 22.6 wk, platinum: 16.0 vs 18.0 wk, and 5-FU: 14.6 vs 18.0 wk). Median PFS was 6.4 months in the CIL1W group, 5.6 months in the CIL2W group and 5.7 months in the control group, with CIL1W and CIL2W having HRs of 1.03 (95% CI: 0.67–1.59) and 1.55 (95% CI: 0.99–2.43) vs control. The latter HR was possibly due to less compliance in the CIL2W arm. Median OS was 12.4, 10.6, and 11.6 months in the CIL1W, CIL2W, and control groups, respectively. ORs were observed in 46.8%, 26.7%, and 35.5% of patients in the CIL1W, CIL2W, and control arms, respectively. Most common (�15%) grade 3/4 TEAEs were neutropenia, hypokalemia, leukopenia, stomatitis, and fatigue. No safety differences were noted between treatment arms. Overall, there were 7 drug-related TEAEs (2 in CIL1W, 2 in CIL2W, and 3 in control) leading to death. Conclusions: In this population, neither of the cilengitide-containing regimens was able to demonstrate a PFS benefit over PFE alone. 5518 Poster Discussion Session (Board #8), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Lenvatinib treatment of advanced RAI-refractory differentiated thyroid cancer (DTC): Cytokine and angiogenic factor (CAF) profiling in combination with tumor genetic analysis to identify markers associated with response. Presenting Author: Douglas Wilmot Ball, The Johns Hopkins University School of Medicine, Baltimore, MD Background: Lenvatinib is an oral tyrosine kinase inhibitor targeting VEGFR1-3, FGFR1-4, RET, KIT and PDGFR�. In a phase II study of lenvatinib, 58 patients (pts) with DTC were enrolled and a response rate of 50% was observed (Sherman, ASCO 2011). Methods: Pts received lenvatinib at a starting dose of 24 mg oral once daily in 28-day cycles. Serum was collected at baseline (BL), on day 8 and on day 36 and concentrations of 47 CAFs were measured using multiplex bead arrays and enzyme-linked immunosorbent assay (ELISA). 33 genes (443 mutations) were examined in archival tumor tissues (n�25). Association of baseline CAF, changes in CAF levels upon treatment and gene mutation status with treatment outcomes was investigated. Results: Combination of low baseline VEGF and ANG-2 (p�0.02 and HR�0.386) correlated with longer PFS. Both baseline and changes in CAF levels demonstrated an association with gene mutation status. High baseline levels of VEGF were observed in pts with wild type RAS and BRAF (p�0.035) whereas high baseline sTIE-2 levels associated with RAS mutation (p�0.023). Supporting pre-clinical mouse xenograft tumor model developed using ANG2-overexpressing human thyroid cancer cell line FTC-286 demonstrated reduced sensitivity to lenvatinib treatment. Increased levels of IL-10 and FGF-2 8-day posttreatment (8d post-tx) significantly associated with RAS (N- or K-) and BRAF mutation. Combination of gene mutation status with baseline CAF levels provided better prediction of longer PFS compared to gene mutation alone. Hierarchical clustering modeling using changes in CAF levels 8d post-tx with tumor shrinkage identified a set of CAFs that could predict two categories of lenvatinib response: longer PFS and greater tumor shrinkage or longer PFS in the absence of significant tumor shrinkage. Conclusions: CAF profiling identified potential predictive biomarkers of lenvatinib treatment outcomes in DTC. Combination of RAS and BRAF mutation with baseline VEGF and ANG-2 or treatment-associated changes in FGF-2 and IL-10 level correlated with lenvatinib treatment response. 5517 Poster Discussion Session (Board #7), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Genomic profiling of a clinically annotated cohort of locoregionally advanced head and neck cancers (HNC) treated with definitive chemoradiotherapy. Presenting Author: Tanguy Y. Seiwert, The University of Chicago Medical Center, Chicago, IL Background: Recent advances in genomic technology and sequencing have allowed the near comprehensive characterization of genetic abnormalities in HNC, but their correlation with clinical outcome remains to be determined. We analysed a clinically annotated cohort of locoregionally advanced HNC for copy number changes and mutations and correlated with outcome in an exploratory fashion. Methods: 120 head and neck cancers (frozen tissue) and matching normal tissues/blood from patients with locoregionally advanced HNC treated with definitive chemoradiation �/induction at the University of Chicago were obtained from our tissue bank. DNA, RNA, protein were extracted. Barcoded, multiplexed sequencing libraries for 500 head and neck cancer associated genes (Agilent capture) were built and sequenced on Illumina HiSeq next generation sequencers. 150 commonly copy number altered and HNC relevant genes were analysed for copy number alterations (CNA) using the Nanostring nCounter platform. Respective genetic aberrations in curated pathways were allocated to tumor subgroups. Exploratory analysis correlated data with induction response and progression free survival. Confirmatory HPV testing was performed using an E6, nested, multiplex PCR. Results: �80% of targeted sequences were successfully captured and sequenced. Commonly mutated genes included: TP53, CDKN2A, PIK3CA, NOTCH1. Of note PIK3CA mutations were enriched in HPV(�) tumors. Commonly copy number altered genes included amplifications of VEGF1, CCND1, MYC, EGFR, MDM4, CTTN, as well as PIK3CA, and deletions of CDKN2A, SUCLG2, FHIT, TGFBR2, PTPRD, IKBKG, TRAF6, and RASSF1. CCND1, and MYC were commonly co-amplified and correlated with poor progression free survival, representing a distinct HNC phenotype. Analysis for additional genes and influence on induction response will be presented. Conclusions: Targeted, medium throughput genomic profiling is feasible, and provides the majority of HNC specific genetic aberrations at a comparably low cost. Impact on outcome (CCND1/MYC amplification) and potential treatment targets (PIK3CA mutations in HPV(�) tumors) were identified. 5519 Poster Discussion Session (Board #9), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Safety, molecular, and imaging responses to cetuximab administered in a window pre-operative study in squamous cell carcinoma of the head and neck (SCCHN). Presenting Author: Sandra Schmitz, Department of Head and Neck Surgery, St-Luc Hospital, Catholic University of Louvain, Brussels, Belgium Background: Only a minority of SCCHN pts benefits from anti-EGFR mAbs. Trials with pre- and post-therapy tumor biopsies are crucial to better characterize the molecular pathways involved in treatment response or resistance. Targeted agents (TA) are often investigated in unselected end-stage cancer pts, making difficult optimal translational research. One way to resolve this issue is to perform “window” studies where a TA is given during the incompressible period between the diagnosis and surgery. Methods: We conducted a phase I/II study: cetuximab (C) was given pre-operatively to treatment-naïve SCCHN pts selected for primary curative surgery. C (400mg/m2 first wk followed by 250mg/m2/wk) was given during 2 wks (day -15 until day -1, 3 infusions) before surgery (day 0). Tumour biopsies, FDG/PET, and CT were performed at diagnosis and surgery. In the phase I, we investigated the safety of preoperative C by progressively reducing the delay between the last dose of C and surgery (minimum delay : 24 hrs ; 3�3 phase 1 design). The aims of the phase II were (i) safety, (ii) C activity by FDG-PET (Po�0.10, P1�0.35, a�0.05 and b� 0.10). As controls, 5 additional pts were included without C treatment but with the same requirements regarding biopsies and imaging. Results: The phase 1 study (n�18) demonstrated that C infusion given 24 hrs before surgery was safe. Safety was confirmed in the phase II (n�20). 90 % had a FDG-PET partial response (PR) (EORTC guideline) in the C group and 0% in the controls. 52% had a �SUVmax decrease of �50%. 2 pts evaluable by CT/MRI had a PR (RECIST). Then, we compared the pre-and post treatment biopsies by immunochemistry. For the whole group, C did not reduce Ki67 (p�0.1) and did not seem to induce apoptosis (caspase). However, for pts with �SUVmax decrease � 25% or � 50%, Ki67 was decreased (p�0.04 and 0.006). C induced downregulation of pEGFR (p�0.0004) and pERK (p�0.007) but not pAKT/AKT (Histoscore). Conclusions: Pre-operative study with C is safe. Our findings suggest that the main downstream molecular pathway blocked by C in SCCHN is the RAS/RAF/ERK. Further analyses are ongoing to better characterize molecular response and escape mechanisms. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
5520 Poster Discussion Session (Board #10), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Role of c-MET pathway in the outcome prediction of cetuximab-based therapy in patients with recurrent or metastatic squamous cell carcinoma of the head and neck. Presenting Author: Victoria Casado, Oncology Department. Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Madrid, Spain Background: Activation of the c-MET oncogene promotes tumor growth, invasion and metastasis in several tumor types. In addition, c-MET has been reported in consort with EGFR and/or be activated as a compensatory pathway in the presence of EGFR blockade resulting a mechanism of acquired resistance to EGFR inhibitors in lung and colorectal carcinoma. We investigated the impact on cetuximab sensitivity of HGF, c-MET, c-MET activation and c-MET gene status in recurrent or metastatic squamous cell carcinoma of the head and neck (HNSCC) patients. Methods: A singleinstitution retrospective analysis including 50 HNSCC patients was carried out. For each case, formalin-fixed tumor specimens were assayed for HGF, total and phosphorylated Y1234/35 c-MET (p-c-MET) by immunohistochemistry and c-MET gene by FISH. Overexpression criteria were defined by ROC curves for each protein and amplification was defined by �2 copies in at least two of the three studied tumor areas. Results were analyzed for association with clinico-pathological features and survival outcomes for cetuximab-treated patients (median follow-up 75 months). Results: c-MET overexpression was detected in 26 (52%) of patients, c-MET amplification in 15 (30%) and p-c-MET in 12 (24%). Amplification was associated with c-MET overexpression (p�0.004). HGF overexpression was observed in 8 (12%) associated with c-MET phosphorylation (p�0.001), suggesting a paracrine activation of receptor. No significant association with clinicopathological parameters was detected. Log-rank test showed significantly worse outcome in c-MET overexpressing patients for progression-free (PFS) (p�0.002) and overall survival (OS) (p�0.045); p-c-MET was correlated with worse PFS (p�0.014) and OS (p�0.001). In multivariate logistic regression analysis, p-c-MET was an independent prognostic factor for PFS (HR 6.5; 95% CI 1.5-8.9). Conclusions: HGF/c-MET pathway correlated with worse outcome in cetuximab-based regimen treated HNSCC patients, acting as a resistance mechanism for EGFR inhibitors and supporting a dual blocking HGF/c-MET and EGFR pathways for treatment of these patients. 5522 Poster Discussion Session (Board #12), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Exploratory pharmacodynamics (PD) trial to investigate the mechanism of action of RG7160 (GA201), a novel dual-acting, monoclonal antibody (mAb) designed to enhance antibody-dependent cellular cytotoxicity (ADCC), compared with cetuximab (C) in neoadjuvant head and neck squamous cell carcinoma (HNSCC). Presenting Author: Stéphane Temam, Institut Gustave Roussy, Villejuif, France Background: GA201 efficacy was superior to C in orthotopic xenograft models in terms of activity and PD. In a phase I study, objective responses and long lasting stable disease were observed in heavily pre-treated patients (pts). Methods: HNSCC pts (T2-4, any N, M0) received i.v. neo-adjuvant 700/1400 mg GA201 or C (as per SPC), on D1 and 8. Tumor biopsies were taken at baseline (BL) and pre-surgery. The primary objective was determination of changes in tumor immune cell infiltration after treatment. Peripheral CD3�, CD16�, CD56� cells, plasma cytokines, tumor EGFR and 18F-FDG-PET avidity were also studied. Results: To date, 39 pts (15/10 vs 14 pts for 700/1400 GA201 vs C, respectively) were evaluable for the primary objective and 4 pts are on-going. Patient characteristics at BL were as follows: median age, 57/62 vs 62 years; gender, 11/10 vs 12 male; tumor size � 4 cm, 7/3 vs 3 pts. A greater proportion of pts receiving GA201 compared to C had metabolic tumor reduction (� 25% of SUVmax) (10/15 at 700 mg [1 pathological CR], 7/10 at 1400 mg GA201 vs 7/14 C pts) and symptomatic relief (6/12 at 700 mg, 6/7 at 1,400 mg GA201 vs 2/10 C pts). Table shows changes in PD markers. Conclusions: GA201 treatment, compared to C, exhibited more extensive tumor immune cell infiltration and a greater metabolic response. Consistent with the proposed mechanism of action of GA201, peripheral NK cells dropped and a unique cytokine profile was observed. The data support the immunomodulatory superiority of GA201 - a mAb designed to enhance ADCC compared to C. Median change from BL (range) GA201 C ‡ 700 mg* 1,400 mg † Tumor biopsy 1 CD3� (cells/mm 2 ) 396 (–987, 2336) 205 134 (–45, 722) EGFR (intensity 3; %) –14 (–83, 25) – –5.5 (–65, 43) Peripheral blood CD16� and/or CD56�/CD3– % –97 (–100, –92) –98 (–100, –97) –1 (–71, 59) CD3� % –89 (–98, –73) –93 (–96, –78) –59 (–86, 178) IL-15 % 946 (0, 2113) 695 (649, 742) 0 (–53, 7) IL-1RA % 6,950 (706, 21,933) 1,201 (873, 1,529) –16 (–70, 19) *n� 14-15; † n � 1-2; ‡ n � 8-12 for paired samples. 1 Correlations with SUVmax are being investigated. Head and Neck Cancer 361s 5521 Poster Discussion Session (Board #11), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Differential expression of EGFR, HER2, P16, and high-risk (hr) HPV status in oropharyngeal (Or) and oral cavity (OC) squamous cell carcinoma (SCC). Presenting Author: Anne Sudaka, Centre Antoine Lacassagne, Nice, France Background: We aimed to better characterize the expression of epidermal growth factor receptors family in Or and OC SCC and correlate it to hr HPV status and anatomoclinical features. Methods: In formalin fixed paraffin embedded tumor tissues, chromogenic in situ hybridization (CISH) was performed to detect hr HPV and immunohistochemistry to evaluate EGFR (positive score: 4 to 6), HER2 (0�negative, 1�positive) and P16 (positive score:�70% labeled cells) expression. Baseline data were collected and analyze will be used. Results: Among 128 pts, 69 were tobacco users and 58 male. Median age at diagnosis was 61 y [23-95]. EGFR, Her2, P16 expression and hrHPV positivity were seen in 84 (65%), 12 (9%), 47 (37%) and 47 (37%) respectively. P16 signal was linked with absence of tobacco (31% vs. 72%, Pearson chi2 test: p�10-3 ), absence of alcohol (48% vs. 83%, p�10-3 ), Or site (53% vs. 76%, p�0.005), T1 (34% vs. 19%, p�0.06), N0 (52% vs. 23%, p�0.003), absence of nodal capsular rupture (85% vs. 68%, p�0.02), WHO grade 3 (37% vs. 68%, p�0.001), hr HPV detection (17% vs. 70%, p�10-3 ). Multivariate analysis confirmed the link between P16 expression and hr HPV CISH positivity (OR�0.05, CI 95% [0.01-0.21], p�10-3 ) , absence of tobacco (OR�9.2, CI 95% [2.1-40.7], p�0.03) and N0 (OR�0.2, CI 95% [0.04- 0.75], p�0.02). EGFR signal was linked with tobacco (31% vs 78%,p�10-3 ), alcohol (57% vs 81%, p�0.02), OC localization (77% vs 58%, p�0.03), well differentiated SCC (73% WHO grade 1-2 vs 56% grade 3, p�0.04), absence of hr HPV detection (74% vs 52%, p�0.01) and absence of P16 labeling (78% vs 44%, p�10-3 ). Multivariate analysis confirmed the link between EGFR positivity and tobacco (OR�0.32, CI 95% [0.1-0.9], p�0.03), alcohol (OR�9.5, CI 95% [1.2- 72.8], p�0.03) and OC localization (OR�0.3, CI 95% [0.1-1], p�0.05). HER2 signal was linked with alcohol (5% vs 18%, p�0.04), history of tobacco associated neoplasia (10% vs 0%, p�0.02), Or site (14% vs 2%, p�0.03) and who grade 3 (5% vs 14%, p�0.06). Her2 labeling was not associated with tobacco, sex, hr HPV detection, P16 positivity or EGFR one. Conclusions: Hr HPV associated SCC have a low expression of EGFR and are not associated with HER2 labeling. 5523 Poster Discussion Session (Board #13), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Differences in biomarker expression in HNSCC according to p53 status. Presenting Author: Rebecca Anne Feldman-Moreno, Caris Life Sciences, Phoenix, AZ Background: Patients with p53 wildtype head and neck squamous cell carcinoma (HNSCC) tend to be HPV-positive, which associates with better prognosis. The purpose of this study was to explore biomarker expression profiles for insight into molecular differences in HNSCC patients based on p53 status. Methods: TP53 gene sequencing using the AmpliChip p53 microarray (Roche Molecular Systems, Inc.) was attempted on 61 HNSCC patients previously tested with Caris Target Now tumor profiling service. DNA was extracted from a FFPE sample, amplified and processed on the AmpliChip p53 microarray to detect single base pair substitution and deletion mutations in exons 2-11andtheir flanking splice sites in the TP53 gene (GenBank X54156). EGFR FISH , HER2 IHC and 22 other predictive biomarkers, e.g. TS, TOPO2A, MGMT, etc., were assayed and retrospectively analyzed. All tests were performed in a CLIA-certified lab and interpreted by board-certified pathologists or cytogeneticists. Statistical analysis was performed using SPSS (PASW statistics17) for parametric and non-parametric tests of independence. Results: 52 cases provided sufficient quality DNA for p53 analysis and results revealed a mutation rate of 25% in HNSCC patients. Interestingly, only EGFR FISH and HER2 IHC (p�.002 and p�.004, respectively) were differentially expressed in wildtype vs. mutated p53. Matched-pair analysis in the p53 mutated subgroup (n�13) showed no significant trend regarding EGFR status (p�.763) but a slight trend towards HER-2 negativity (p�.020). In the p53 wildtype subgroup (n�39), a strong association with EGFR FISH nonamplification (n�28, 71.8%, p�.001) as well as HER-2 negativity (n�38, 97.4%, p�.001) was shown. Conclusions: To our knowledge, this is the first analysis of differential biomarker expression profiles in HNSCC based on p53 status. We hypothesize that the absence of EGFR amplification in the p53 wildtype cancers may be a contributing factor to the improved prognosis observed in HPV-positive HNSCC. Additionally, the strong association between p53 wildtype HNSCC patients and EGFR nonamplification suggests EGFR-targeted therapies like cetuximab would likely fail in p53 wildtype patients. 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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Brandes, Johann Christoph 7048, 106
Page 718 and 719:
Cakir, Betul 9567 Calabek, Bernadet
Page 720 and 721:
Ceraulo, Domenica 4017 Cerbone, Lin
Page 722 and 723:
Chinen, Ludmilla T.D. e16046 Chinen
Page 724 and 725:
Come, Steven E. 9071, 9100 Comis, S
Page 726 and 727:
Dahlheimer, Tambra 2546 Dahmane, El
Page 728 and 729:
DeLacure, Mark D. e16052 Delage, Ju
Page 730 and 731:
Domingo, Gelenis 6568, 6575, 6588 D
Page 732 and 733:
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,
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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,
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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
Page 782 and 783:
Palassini, Elena 10026, 10053, 1006
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Peisker, Uwe 10600 Peker, Deniz e18
Page 786 and 787:
Piwnica-Worms, Helen 3047 Pizzo, Fa
Page 788 and 789:
Rabinowits, Guilherme 5501, 5582, 9
Page 790 and 791:
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
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Tillmanns, Todd D. 5014, e15514 Til
Page 810 and 811:
Uchiyama, Tomotaka e21108 Udovitsa,
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Videtic, Gregory M.M. e14611, e1466
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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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