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

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242s Gastrointestinal (Noncolorectal) Cancer 4012 Poster Discussion Session (Board #4), Mon, 1:15 PM-5:15 PM and 4:45 PM-5:45 PM Impact of insulin-like growth factor 1 receptor (IGF1R) and amphiregulin (AREG) expressions on survival in patients with stage II/III gastric cancer enrolled in the ACTS-GC study. Presenting Author: Wataru Ichikawa, National Defense Medical College, Tokorozawa, Japan Background: Exploratory biomarker analysis was conducted to identify factors related to outcomes of patients enrolled in the ACTS-GC study, a randomized controlled trial comparing adjuvant S-1 administration with surgery alone in 1,059 patients with stage II/III gastric cancer. Methods: Formalin-fixed paraffin-embedded surgical specimens were retrospectively examined in 829 patients (78.3%), and 63 genes involved in pyrimidine metabolic pathway, growth factor signaling pathway, apoptosis, DNA repair, etc., were analyzed by quantitative real-time RT-PCR after TaqMan assay-based pre-amplification. Gene expression levels were normalized to the geometric mean expressions of GAPDH, ACTB, and RPLP0, used as reference genes. The expression of each gene was categorized into low and high values at those median. The impacts of gene expression on survival were analyzed using the 5-year survival data of the ACTS-GC. The Benjamini and Hochberg procedure was used to control the false discovery rate (FDR). Results: Among 63 screened genes, IGF1R and AREG most strongly correlated with overall survival (OS), with FDR of 0.0048 and 0.018, respectively. OS was significantly worse in IGF1R high patients than in IGF1R low patients, but better in AREG high patients than in AREG low patients. The hazard ratio (HR) for death in the analysis of OS (S-1 vs. surgery alone) was lower in the high IGF1R group (HR, 0.55; 95%CI, 0.40-0.76) than in the low IGF1R group (HR, 0.72; 95%CI, 0.49-1.06). Likewise, the HR for death in the analysis of OS (S-1 vs. surgery alone) was much smaller in the low AREG group (HR, 0.57; 95%CI, 0.41-0.79) than in the high AREG group (HR, 0.74; 95%CI, 0.51-1.08). Interactions were not statistically significant. Conclusions: IGFR1 gene expression was associated with poor outcomes after curative resection of stage II/III gastric cancer, whereas AREG gene expression was associated with good outcomes. No interaction for survival was evident between S-1 and these gene expressions. 4014 Poster Discussion Session (Board #6), Mon, 1:15 PM-5:15 PM and 4:45 PM-5:45 PM Multivariate analysis including biomarkers in the phase III RADIANT-2 study of octreotide LAR plus everolimus (E�O) or placebo (P�O) among patients with advanced neuroendocrine tumors (NET). Presenting Author: James C. Yao, University of Texas M. D. Anderson Cancer Center, Houston, TX Background: In this large phase III trial, median progression-free survival (PFS) improved by 5.1 mo with E�O compared to P�O in patients (pts) with NET associated with carcinoid syndrome. Baseline imbalances including WHO performance status (PS) and primary site favoring P�O confounded primary analysis. Chromogranin A (CgA) and 5-hydroxyindoleacetic acid (5-HIAA) are important biomarkers in NET. Analyses were performed to identify prognostic factors and adjust for baseline imbalances. Methods: Pts were randomized to E�O (n�216) or P�O (n�213). Potential prognostic factors including baseline CgA (�2�ULN vs �2�ULN), baseline 5-HIAA (�median vs �median at baseline), age (�65 vs �65), gender, race, WHO PS (0 vs 1, 2), primary site (lung vs other), prior somatostatin analog use (yes vs no), duration from diagnosis (�6 mo, 6-24 mo, 2-5 yr, �5 yr), and organs involved (liver, bone) were assessed in univariate analysis using the log rank test and stepwise regression using Cox proportional hazards model. Results: Median PFS (mo) was significantly longer for pts with nonelevated CgA (27 vs 11; p�.001) and nonelevated 5-HIAA (17 vs 11; p�.001). Analyses also indicated age (14 vs 12; p�.01), WHO PS (17 vs 11; p�.004), liver involvement (14 vs not reached; p�.02), bone metastases (8 vs 15; p�.001), and lung as primary site (11 vs 14; p�.06) as potentially prognostic. Multivariate analysis indicated that significant prognostic factors for PFS included baseline CgA (HR, 0.47; CI, 0.34-0.65; p�.001), WHO PS (HR, 0.69; CI, 0.52-0.90; p�.006), bone involvement (HR, 1.52; CI, 1.06-2.18; p�.02), and lung as primary site (HR, 1.55; CI, 1.01-2.36; p�.04). Adjusted for covariates, a 38% reduction in risk of progression was observed for E�O (HR, 0.62; 95% CI, 0.51-0.87; p�.003). Conclusions: In the phase III RADIANT-2 trial, baseline CgA levels, WHO PS, lung as primary site, and bone involvement were important prognostic factors. Exploratory analysis adjusted for these prognostic factors indicated significant benefit of everolimus therapy. 4013 Poster Discussion Session (Board #5), Mon, 1:15 PM-5:15 PM and 4:45 PM-5:45 PM Actionable targets in pancreatic cancer detected by immunohistochemistry (IHC), microarray (MA) fluorescent in situ hybridization (FISH), and mutational analysis. Presenting Author: Daniel D. Von Hoff, Virginia G. Piper Cancer Center at Scottsdale Healthcare/TGen, Scottsdale, AZ Background: A great need exists for new therapeutic approaches for patients with pancreatic cancer. Methods: The study cohort included 1029 patients analyzedfor a.) up to 29 different immunohistochemical biomarkers – (e.g., COX-2, MGMT, PGP, RRM1, TOPOI, TOPOII, SPARC etc.)b.); in up to 450 patients’ specimens a whole genome expression analysis was performed using HumanHT-12 v4 beadChips ( Illumina Inc.,San Diego, CA) c.) in up to 695 patients FISH for c-Myc, EGFR, HER2 and TOPO2A gene copy amplifications; and d.) in up to 783 patients sequencing for KRAS, EGFR, PI3CA and BRAF, was performed. Results: IHC identified actionable targets included; 74% high COX-2; 57% negative ERCC1; 8% negative MGMT; 22% negative MRP1; 47% negative PGP; 77% low RRM1, 44% high SPARC; 30% high TOPO2A; 61% high TOPOI and 73% negative TS. Other biologically important findings by IHC for possible new therapeutics included 27% negative PTEN; and 20% high PDGFR. Microarray results presented multiple overexpressed targets for consideration including 36% of specimens with overexpressed adenosine deaminase; 28% asparagine synthase; 17% BCL2; 20% survivin; 23% carboxylesterase; 67% DNMT1; 40% thymidine phosphatase; 49% EPHA2 (and others in the src family of kinases); 57% FOLR2; 41% HDAC1; 62% HiF1�; 23% IL2RA (CD25); 46% NFkB1; 48% OGFR; 32% RARA; 26% VEGFR; and 43% vitamin D receptor. FISH yielded 2% amplified EGFR and 10% amplified Her2neu. Sequencing noted 73% mutated KRAS and 3% mutated PIK3CA. Conclusions: Examining actionable targets in patients’ pancreatic cancers (a)reiterates the commonality and importance of KRAS mutations in this disease (needs renewed targeting effort) (b)suggests that TOPO2 inhibitors (particularly if transport into tumor can be improved) should be examined in this disease (c)suggests other pathways to target including DNA repair, epigenetic, Src and inflammation (d) suggests protein turnover, amino acid targets and folate receptor2 as fresh areas to explore against the disease. Supported in part by a Stand Up To Cancer Dream Team Award. 4015 Poster Discussion Session (Board #7), Mon, 1:15 PM-5:15 PM and 4:45 PM-5:45 PM Predictive and prognostic factors for treatment and survival in 305 patients with advanced gastrointestinal poorly differentiated neuroendocrine carcinoma: The NORDIC NEC study. Presenting Author: Halfdan Sorbye, Haukeland University Hospital, Bergen, Norway Background: Gastrointestinal poorly differentiated neuroendocrine carcinoma (GI-NEC) are aggressive tumors with Ki-67�20% and usually metastatic at diagnosis. Knowledge about GI-NEC is limited. We retrospectively reviewed clinical data to identify predictive and prognostic markers for advanced GI-NEC patients. Methods: Epidemiological, biochemical, histopathological, treatment and survival data were registered for advanced GI-NEC patients diagnosed during 2000-2009 at 12 Nordic university hospitals. Results: 305 patients were included. Palliative chemotherapy was given to 252 patients, median survival was 11 months. Response rate to 1st-line chemotherapy was 31%, 33% had stable disease. Ki-67�55% was by ROC analyses the best cut-off value concerning correlation to response rate. Response rate to platinum-based chemotherapy was lower in patients with Ki-67�55% (14% vs.44%, p�0.001). Response rate for 84 patients given 2nd-line chemotherapy was 18%, whereas 33% achieved SD. The most important negative prognostic factors for survival were poor performance status, primary colorectal tumors, and elevated baseline platelets or lactate dehydrogenase (LDH) levels. Patients with Ki-67�55% had longer median survival (15 months) than patients with Ki-67�55% (10 months) (p�0.001). Survival and response rates did not differ between the different platinum chemotherapy schedules (cisplatin-based vs. carboplatin-based) or morphology subtypes. 53 patients received best supportive care only with a median survival of 1 month. Conclusions: This is, to our knowledge, the largest study reporting patient and tumor characteristics, treatment and survival in advanced GI-NEC. Performance status, location of primary tumor and blood levels of platelets and LDH were the strongest prognostic factors for survival. Patients with Ki-67�55% had significantly longer survival than patients with higher Ki-67, but were less responsive to platinum-based chemotherapy. Our data indicate that to consider all GI-NEC as one single disease entity may not be correct. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
4017 Poster Discussion Session (Board #9), Mon, 1:15 PM-5:15 PM and 4:45 PM-5:45 PM Maintenance sunitinib (MS) or observation (O) in metastatic pancreatic adenocarcinoma (MPA): Clinical and translational results of a phase II randomized trial (NCT00967603). Presenting Author: Michele Reni, San Raffaele Scientific Institute, Milan, Italy Background: Combination chemotherapy (CT) prolonged progression-free survival at 6 months (PFS6) of patients (pts) with MPA from �20% with gemcitabine (GEM) to �50%. To prolong CT over 6 months has unproven benefit and is hampered by cumulative toxicity. This open-label, randomised, multi-centre phase II trial explored the role of MS in pts with MPA without progressive disease (PD) after CT, using an O group as calibration arm. The role of circulating endothelial cells (CEC) as biomarker of MS activity was explored. Methods: Adult pts with pathologic diagnosis of MPA, performance status (PS) �50%, without radiological PD or CA19.9 raise �20% after 6 months of CT were stratified based on PS and previous CT and randomized to O (arm A) or MS at 37.5 mg daily until PD or a maximum of 6 months (arm B). Primary endpoint was PFS6. Sample size (H0 10%; H1 30%; a .10; b .10) was 26 pts per arm and MS had to be considered of interest with �5 pts PFS6. CEC were evaluated by flow cytofluorometry on a baseline peripheral blood sample. Results: 56 pts (29 arm A; 27 arm B) were enrolled. One arm B pt had kidney cancer and was excluded. Pts characteristics were (A/B): median age 64/61 years; median PS 90/100; median CA19.9 45/32; previous CT: GEM 3/3; combination CT 26/22. Main grade 3-4 toxicity in arm B was 15% neutropenia; 12% thrombocytopenia and hand-foot syndrome, 8% diarrhea. Second line CT was given to 76% of pts in both arms. One arm A (3%) and 6 arm B pts (23%; p�.01) were PFS6; 2y overall survival (OS) was 4% and 25% (p�.09). Blood sample for CEC analysis was available for 46 of 55 pts (84%). In arm A, median PFS was longer for pts with CEC number �30 (lower terzile group) when compared to �30 (2.9 versus 1.9 months; p.08). MS significantly increased PFS in CEC �30 group (3.4 months; p�.01). No PFS difference between arms was observed in �30 group (2.3 months). Conclusions: This is the first randomized trial on maintenance therapy in MPA. In arm B, the primary endpoint was fulfilled and 2y OS was remarkably high, suggesting that MS may have a role in pts with MPA. The number of CEC may be useful to predict benefit from MS. 4019 Poster Discussion Session (Board #11), Mon, 1:15 PM-5:15 PM and 4:45 PM-5:45 PM Dual blockade of epidermal growth factor receptor (EGFR) and insulin-like growth factor receptor-1 (IGF-1R) signaling in metastatic pancreatic cancer: Phase I/randomized phase II trial of gemcitabine, erlotinib, and cixutumumab versus gemcitabine plus erlotinib (SWOG-0727). Presenting Author: Philip Agop Philip, Karmanos Cancer Institute, Wayne State University, Detroit, MI Background: Targeting a single pathway in pancreatic adenocarcinoma (PAC) is unlikely to impact its natural history. EGFR targeting with erlotinib added to gemcitabine (G) marginally improved the outcome of patients with advanced disease. We tested the hypothesis that if the EGFR and IGF-1R pathways are simultaneously blocked then progression free survival (PFS) would be significantly improved by abrogating reciprocal signaling that leads to resistance to either drug. Methods: This was a phase I/randomized phase II (RP2) study testing the anti-IGF-1R monoclonal antibody cixutumumab combined with erlotinib and G in patients with metastatic PAC. The control arm was erlotinib plus G. The primary endpoint of the RP2 portion of the study was PFS. Eligibility included patients with untreated metastatic disease, performance status 0/1, fasting blood glucose less than institutional upper limit of normal, and willingness to provide tissue and blood specimens for correlative studies. Results: In phase I portion (n�10) safety of cixutumumab 6 mg/kg IV/wk, erlotinib 100 mg/day orally and G 1000 mg/m2 IV D 1, 8, and 15 of a 28-day cycle was established. In the RP2 portion (n�124) 114 eligible patients (median age 63) were included. On the cixutumumab arm, 59% of patients were female vs. 40% on control arm. Median PFS and overall survival were 3.7 and 6.7 months, respectively, in both arms of the study. Major grade 3 and 4 toxicities were (cixutumumab/control) elevation of transaminases (12%/6%), fatigue (16%/12%), gastrointestinal (35%/28%), neutropenia (21%/10%), and thrombocytopenia (16%/7%). Grade 3/4 hyperglycemia was seen in 16% of patients on cixutumumab. Grade 3 or 4 kin toxicity was similar in both arms of the study (� 5%). Five treatment-related deaths were reported: 2 cardiac on each arm, 1 pulmonary on cixutumumab. Conclusions: IGF-1R inhibitor cixutumumab did not improve the progression free or overall survival of patients with metastatic PAC treated with erlotinib and G in a molecularly unselected population. Gastrointestinal (Noncolorectal) Cancer 243s 4018 Poster Discussion Session (Board #10), Mon, 1:15 PM-5:15 PM and 4:45 PM-5:45 PM FOLFIRI.3 (CPT-11 plus folinic acid plus 5-FU) alternating with gemcitabine or gemcitabine (G) alone in patients (pts) with previously untreated metastatic pancreatic adenocarcinoma (MPA): Results of the randomized multicenter AGEO phase II trial FIRGEM. Presenting Author: Isabelle Trouilloud, Hôpital Européen Georges Pompidou, Paris, France Background: CPT-11 showed modest activity and tolerability in MPA. We developed a new strategy to improve efficacy and tolerability of CPT-11 based regimen in MPA pts. Methods: Chemotherapy-naive pts with histologically proven MPA, bilirubin levels � 1.5 ULN and performance status (PS) 0-1 were randomized in a phase II trial to receive either FOLFIRI.3 (CPT-11 90 mg/m2 as a 60-min infusion on day (D) 1, leucovorin 400 mg/m2 as a 2-hr infusion on day 1, followed by 5-FU 2000 mg/m2 as a 46-hr infusion and CPT-11 90 mg/m2 , repeated on D3, at the end of the 5-FU infusion, every 2 weeks) for 2 months alternarting with G (1000 mg/m² at a fixed dose rate of 10 mg/m²/min on D1, D8, D15, D29, D36 and D43) for 2 months (arm A) or G alone (arm B). Using Fleming design the primary end point was rate of progression free survival (PFS) at 6 months from (H0) 25% over (H1) 45% needing to include 49 pts/arm. Results: Between 2007 and 2011, 98 pts were enrolled (males: 59, median age: 62 years, PS 0: 32%). Median follow-up was 23 months. Grade 3-4 toxicities per pts (%) in arm A/B were diarrhea 13/0, nausea-vomiting 11/4, neutropenia 51/25 and febrile neutropenia 4/0. No toxic death occurred. Response rate were 40 and 11% as disease control rate (CR�PR�SD) were 73 and 52% in arm A and B, respectively. The primary endpoint of the trial was met with rate of PFS at 6 months of 48% (95% CI: 33-63) in arm A while in arm B PFS was 30% (95% CI: 17 - 44). One year PFS was 23% (95%CI: 11.5-36) and 11% (95%CI: 4-21), respectively. Conclusions: FIRGEM strategy is feasible and efficient with a manageable toxicity profile in good condition pts with MPA. A phase III trial comparing this strategy with the FOLFIRINOX triplet therapy focusing on quality of life should now be performed. 4020 Poster Discussion Session (Board #12), Mon, 1:15 PM-5:15 PM and 4:45 PM-5:45 PM Long-term survival in patients with pancreatic cancer: Relevant factors in CONKO-001. Presenting Author: Marianne Sinn, Medical Department, Division of Hematology, Oncology and Tumor Immunology Charité - Universitätsmedizin Berlin, Berlin, Germany Background: Long-term survival (LTS) in patients with pancreatic cancer is still rare, even in resectable and potentially curative stages. Few prospective data are available to identify predictive factors. The CONKO-001 study establishing adjuvant gemcitabine (GEM) may provide data to answer this question. Methods: CONKO-001 patients (pts) with an overall survival � 5 years were included in this analysis and compared to those with � 5 years. Central re-evaluation of the primary histology was done to confirm the diagnosis of pancreatic adenocarcinoma. Univariate analysis with the x²-test identified qualifying factors (p�0.10). Logistic regression with a stepwise selection process was used to investigate the influence of these covariates on LTS. Results: Of the 354 pts included in the intention-to-treat analysis of CONKO-001, 53 (15%) pts with an overall survival of more than 5 years could be identified, for 39 (74%) tumor specimens could be obtained. In 38 (97% of pts with LTS) the diagnosis of adenocarcinoma was confirmed, 1 showed a high-grade neuroendocrine tumor. Relevant factors for all 53 pts with LTS compared to remaining 301 non-LTS pts in univariate analysis were active treatment (GEM) (68% in LTS pts vs 48% in non-LTS pts; p�0.006), tumor grading (G1 17% vs 3%, G2 64% vs 55%, G3 17% vs 40%; p�0.000), tumor-size (T2 15% vs 9%, T3 74% vs 84%; p�0.004) and lymph nodes (N0 47% vs 25% N1 53% vs 74%; p�0.003. Significance could not be demonstrated for resection margin (R0 vs R1), sex, age, Karnofsky performance status (�80% vs 80% vs �80%) and CA 19-9 (40-100 U/ml vs �40 U/ml) at study entry. In the multivariate analysis tumor grading (gr) (odds ratio gr 3 vs gr 1�0.07; gr 3 vs gr 2� 0.38; p�0.017) and active treatment (odds ratio GEM vs observation�0.38; p�0.004) were the only independent prognostic factors. Conclusions: Long-term survival can be achieved in adenocarcinoma of the pancreas. In pts with completely resected pancreatic cancer, tumor grading and active treatment with GEM were the only predictive factor for LTS. 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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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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Chinen, Ludmilla T.D. e16046 Chinen
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Come, Steven E. 9071, 9100 Comis, S
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Domingo, Gelenis 6568, 6575, 6588 D
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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
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
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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