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

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288s Genitourinary Cancer 4544^ Poster Discussion Session (Board #23), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Phase II trial of RAD001 in renal cell carcinoma patients with non-clear cell histology. Presenting Author: Youngil Koh, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea Background: In non-clear cell renal cell carcinoma (ncRCC), the efficacy of VEGF tyrosine kinase inhibitor (TKI) is controversial. In the while, a mTOR inhibitor, temsirolimus showed a promising efficacy in ncRCC patients in ARCC trial. Hence, we investigated the role of everolimus in ncRCC with this phase II trial. Methods: ncRCC patients received everolimus 10 mg once daily until disease progression or unacceptable toxicity. We included patients who had received VEGF TKI previously, while excluded patients who received previous mTOR inhibitor. The primary end point was progression free survival (PFS). Results: A total of 49 patients were enrolled from 5 centers. Their median age was 57 years (range 24-75 years) and male to female ratio was 37:12. Histology of the patients included papillary (n�29), chromophobe (n�8), collecting duct (n�2), sarcomatoid (n�4), and unclassifiable (n�6) RCC. Twenty-three patients had been treated with VEGF-TKI prior to the study enrollment. Among 49 patients, 46 patients underwent radiologic response assessment after everolimus treatment. Partial response was observed in 5 patients (10.2%) and stable disease in 25 patients (51.0%). Diseases of 16 patients (32.7%) progressed despite of everolimus administration. Histology of 5 patients who showed objective response to everolimus included chromophobe carcinoma (n�2), papillary carcinoma (n�2) and unclassifiable carcinoma (n�1). During the study period, 34 patients experienced PFS events and median PFS was 5.2 months. Patients with chromophobe histology showed longer PFS than patients with the other histologies (median PFS 18.8 months vs. 3.5 months, p�0.027). Estimated median PFS were not significantly different between patients VEGF-TKI treatment and patients without previous VEGF-TKI treatment (median PFS 7.1 vs. 3.7 months, p�0.110). Toxicity profiles were commensurable with previous reports. Conclusions: Everolimus shows considerable efficacy in ncRCC. Patients with chromophobe histology might earn benefit from everolimus treatment especially. Previous treatment with VEGF-TKI seems not to significantly influence outcome of everolimus therapy in these patients. (ClinicalTrials.gov number, NCT00830895) 4546 Poster Discussion Session (Board #25), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Phase III AXIS trial of axitinib versus sorafenib in metastatic renal cell carcinoma: Updated results among cytokine-treated patients. Presenting Author: M. Dror Michaelson, Massachusetts General Hospital Cancer Center, Boston, MA Background: Axitinib, a potent and selective second-generation inhibitor of vascular endothelial growth factor receptors, improved progression-free survival (PFS) compared to sorafenib in patients with metastatic renal cell carcinoma (mRCC) in the phase III AXIS trial. In patients previously treated with cytokines, median PFS (mPFS) was 12.1 mo. In a prior phase II study of axitinib for cytokine-refractory mRCC, mPFS was 13.7 mo and the 5-yr overall survival (OS) rate was 20.6%. We report updated PFS and OS for cytokine-treated patients from the AXIS trial. Methods: 723 patients with clear-cell mRCC and progressive disease after 1 systemic therapy were enrolled, of whom 251 received prior interleukin-2 (IL-2) or interferon-� (IFN-�). Patients were randomized 1:1 to axitinib (5 mg twice daily [BID] starting dose) or sorafenib (400 mg BID). Results: As of Jun 3, 2011, mPFS (95% confidence interval [CI]) for cytokine-treated patients was 12.0 mo (10.1, 13.9) with axitinib (n�126) vs 6.6 mo (6.4, 8.3) with sorafenib (n�125): hazard ratio [HR] (95% CI) 0.519 (0.375, 0.720); p�0.0001. For those treated with an IL-2-containing regimen, mPFS (95% CI) was 15.7 mo (8.3, 19.4) with axitinib (n�37) vs 8.3 mo (4.7, 15.7) with sorafenib (n�38). For those treated with IFN-� alone, mPFS (95% CI) was 12.0 mo (10.0, 13.8) with axitinib (n�89) vs 6.5 mo (6.4, 8.2) with sorafenib (n�87). As of Nov 1, 2011, median OS (95% CI) in the cytokine-treated subgroup was 29.4 mo (24.5, not estimable) with axitinib vs 27.8 mo (23.1, 34.5) with sorafenib: HR (95% CI) 0.813 (0.555, 1.191); p�0.144. Adverse event (AE) profiles were similar in both arms. Few cytokine-treated patients (5.6%) discontinued axitinib due to toxicity. AEs reported in �25% of cytokine-treated patients receiving axitinib were diarrhea (49.2%), hypertension (47.6%), fatigue (35.7%), dysphonia (29.4%), and hand–foot syndrome (28.6%). Conclusions: Axitinib showed median PFS and OS of 1 and 2.5 yr, respectively, in cytokine-treated patients, confirming prior phase II study results, and was well tolerated. PFS was superior to that of sorafenib in second-line mRCC and compares favorably with historical results of other agents in second-line mRCC. 4545 Poster Discussion Session (Board #24), Sat, 8:00 AM-12:00 PM and 12:00 PM-1:00 PM Safety and efficacy of MET inhibitor tivantinib (ARQ 197) combined with sorafenib in patients (pts) with renal cell carcinoma (RCC) from a phase I study. Presenting Author: Igor Puzanov, Vanderbilt University Medical Center, Nashville, TN Background: Inhibitors of vascular endothelial growth factor (VEGF) and VEGF receptor are standard therapy for RCC, and the MET signaling pathway is implicated in tumor angiogenesis. Tivantinib is an oral, selective MET inhibitor. In several tumor models, tivantinib plus sorafenib exhibited synergistic antitumor activity vs single-agent activity. This phase I doseescalation study assessed the safety of tivantinib plus sorafenib in pts with advanced solid tumors. Methods: Endpoints were safety, the recommended phase II dose (RP2D) of tivantinib plus sorafenib, and antitumor activity. Previously, dose escalation established the RP2D as tivantinib 360 mg twice daily (BID) plus sorafenib 400 mg BID. Extension cohorts enrolled � 20 pts each with RCC or other tumors. Patients were treated until disease progression or unacceptable toxicity. Results: 20 pts (mean age, 60 yr) including 16 clear cell, 3 papillary, and 1 clear cell/chromophobe RCC pts received treatment at the RP2D (n � 19) or tivantinib 360 mg BID plus sorafenib 200 mg BID (n � 1). 4 pts are still on study. 16 pts (13 with clear cell RCC) received � 1 previous systemic therapy (median, 2; range, 0-4) including VEGF (14 pts) and/or mTOR (5 pts) inhibitors. The most common (� 25%) adverse events were rash (65%), diarrhea (45%), alopecia (40%), hypophosphatemia (35%), and fatigue, stomatitis, palmar-plantar erythrodysesthesia syndrome, and pruritus (25% each). Best response was partial response (PR) in 3 pts (all clear cell RCC pts) and stable disease (SD) in 15 pts (11 clear cell, 3 papillary, and 1 clear cell/chromophobe RCC pts). 7 pts with SD had � 10% tumor size reduction. The overall response rate (ORR) and disease control rate (DCR; PR � SD) were 15% and 90%, respectively. Median progression-free survival (mPFS) was 12.7 mo (95% CI, 7.1-14.5 mo). In 14 pts previously treated with a VEGF inhibitor, best response was 2 PR and 10 SD, the ORR and DCR were 14% and 86%, respectively, and mPFS was 12.7 mo (95% CI, 5.3-NR mo). Conclusions: Oral combination therapy with tivantinib plus sorafenib was well tolerated and exhibited preliminary anticancer activity in pts with RCC, including pts pretreated with VEGF inhibitors. 4547 Poster Discussion Session (Board #1), Mon, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM SWOG 0421: Prognostic and predictive value of bone metabolism biomarkers (BMB) in castration resistant prostate cancer (CRPC) patients (pts) with skeletal metastases treated with docetaxel (DOC) with or without atrasentan (ATR). Presenting Author: Primo Lara, University of California, Davis, Sacramento, CA Background: S0421, a phase III study of DOC �/- the endothelin antagonist ATR in CRPC pts with bone metastases, showed no overall survival (OS) benefit for DOC�ATR. While BMB may have a prognostic role in CRPC, their predictive role vis a vis bone-targeted therapy such as ATR is unknown. We prospectively assessed pre-treatment serum BMB from S0421 pts to validate their prognostic and predictive value. Methods: BMB for resorption (N-telopeptide, NTX and Pyridinoline, PYD) and formation (C-terminal collagen propeptide, CICP and bone alkaline phosphatase, BAP) were assayed [Quidel (PYD, CICP, BAP) and Wampole (NTX)]. Cox regression models for OS based on BMB adjusted for clinical variables were developed. An adjusted Cox model was fit with main effects and BMB x Treatment interaction to assess predictive value of ATR on OS. Results: Of 1,038 pts, 855 (82%) submitted baseline serum: 778 (91%) were usable and analyzable. Pt characteristics: median age � 69 years; PS 0-1 � 91%, Bisphosphonate use � 61%; Gleason �7 � 56%; median PSA � 68; and bone mets only � 45%. BMB values (median; range): NTX (14 nM; 9.3-23.9), BAP (64.7 u/L; 35-164), CICP (9.5 ng/mL; 6.5-17.4), and PYD (2.8 nmol/L; 2.2-3.9). Table below shows prognostic role of BMB. Pts with very high BMB (upper 25 %ile, n�47) not only have poor prognosis (HR � 4.3, p�0.001) but have OS benefit from ATR (HR�0.34, median OS � 13.6 vs. 6.7 months; interaction p�0.002**). Conclusions: S0421 validates the strong independent OS prognostic value of BMB in CRPC. Very high BMB levels appear to be significantly predictive of OS benefit with ATR. Further study of endothelin antagonists in CRPC should focus on this high-risk pt subset. (5R01-CA120469) Biomarker Hazard ratio (95% CI) Median survival, months ( median) p-value* BAP (u/l) 1.23 (1.14, 1.32) 22.8 vs. 15.4 �0.001 CICP (ng/ml) 1.38 (1.26, 1.51) 24.5 vs. 14.6 �0.001 NTx (nM) 1.40 (1.27, 1.54) 22.4 vs. 15.5 �0.001 PYD (nmol/l) 1.52 (1.28, 1.81) 22.0 vs. 15.3 �0.001 * Significance set at � 0.006 to control 2-sided error rate at 0.05. **Significance set at �0.01 to control overall 2-sided error rate at 0.05 (Bonferroni adjustment). Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
4548 Poster Discussion Session (Board #2), Mon, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM A phase I study of the androgen signaling inhibitor ARN-509 in patients with metastatic castration-resistant prostate cancer (mCRPC). Presenting Author: Dana E. Rathkopf, Sidney Kimmel Center for Prostate and Urologic Cancers, Memorial Sloan-Kettering Cancer Center, New York, NY Background: ARN-509 is a novel small molecule AR antagonist that impairs AR nuclear translocation and binding to DNA, inhibiting tumor growth and promoting apoptosis, with no partial agonist activity. (Clegg et al., 2012) We conducted a phase I trial to assess safety, pharmacokinetics (PK), and determine the recommended phase II dose (RP2D). Methods: Eligible patients with mCRPC received ARN-509 orally on a continuous daily dosing schedule. Seven doses (30, 60, 90, 120, 180, 240, and 300 mg) were tested using standard 3x3 dose escalation criteria. Once drug concentrations were achieved that met or exceeded optimal levels predicted preclinically, an additional 2 dose levels were tested to further confirm the safety margin of ARN-509 (390 and 480 mg). Anti-tumor activity was assessed by PSA, radiographic responses, and FDHT-PET imaging. Results: Thirty patients were enrolled. The most common grades 1-2 treatmentrelated adverse events were fatigue (38%), nausea (29%), and pain (24%). There was only 1 treatment-related grade 3 adverse event (abdominal pain) at 300 mg, possibly related to a higher pill burden. PK was shown to be linear and dose-dependent. At 12 weeks, 42% of patients have had � 50% PSA declines. Eleven (37%) patients have discontinued the study due to progression, with the longest patient still on study for more than 16 months. FDHT-PET imaging demonstrated AR blockade at 4 weeks across multiple dose levels. Conclusions: In this phase I study, ARN-509 was shown to be safe and well tolerated with linear PK. Based on promising activity across all dose levels and pharmacodynamic evidence of AR antagonism, an optimal biologic dose of 240 mg daily was selected for phase II investigation. DOD/PCF PCCTC trial sponsored by Aragon Pharmaceuticals. 4550 Poster Discussion Session (Board #4), Mon, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Tasquinimod and survival in men with metastatic castration-resistant prostate cancer: Results of long-term follow-up of a randomized phase II placebo-controlled trial. Presenting Author: Andrew J. Armstrong, Duke Cancer Institute, Durham, NC Background: Tasquinimod (T) is an oral quinoline-3-carboxamide derivative that binds S100A9 protein and has preclinical anti-angiogenic and anti-tumor activity. Between 12/07-6/09, 201 (134 T, 67 Placebo (P)) men with metastatic CRPC were randomized and received treatment once-daily at an initial dose of 0.25 mg/day escalated to 1.0 mg/day over 4 weeks. Placebo patients could cross over to T after 6 months or at disease progression. The primary endpoint of improved PCWG2 criteria-defined progression at 6 months was met (69 vs. 37% of patients (T/P) were progression free) with PFS of 7.6 vs. 3.3 months for pts on T vs. P1 with acceptable toxicity. This abstract provides the first analysis on symptomatic progression, overall survival (OS) as well as a multivariate analysis for PFS and OS. Methods: Survival data were collected between June 2011 and January 2012 with a median time to censoring of 32 months. Survival data was also evaluated in an exploratory multivariate model of known prognostic factors in CRPC. Results: An imbalance of several baseline prognostic criteria favored placebo (e.g. baseline PSA of 29 vs. 19 (T/P)) (JCO 2011;20:4022). Time to symptomatic progression was longer in T treated patients (p�0.039, HR�0.42). Record of death (97 events) or survival �13 months was documented in 182 patients. Median time to death was 34.2 vs. 30.2 months (T/P). Median time to death in the PCWG2 bone-metastatic subgroup (N�92/44) was 34.2 vs. 25.6 months. A multivariate analysis of known prognostic factors including PSA, LDH, PSA kinetics, and hemoglobin demonstrated an adjusted HR for PFS of 0.54 (95% CI 0.37,0.81) and OS of 0.72 (95% CI 0.46,1.12) in the total population and 0.63 (95% CI 0.37,1.07, n�136) in the bone-metastatic group. Conclusions: OS observed after tasquinimod treatment is longer than previously reported in this patient population. The current exploratory data indicates that the prolongation in PFS observed with tasquinimod treatment may lead to a survival advantage in men with metastatic CRPC. A phase III placebo-controlled study (NCT01234311) is ongoing in men with bone-metastatic CRPC powered to detect an OS improvement. Genitourinary Cancer 289s 4549 Poster Discussion Session (Board #3), Mon, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Safety and activity of the investigational agent orteronel (ortl) without prednisone in men with nonmetastatic castration-resistant prostate cancer (nmCRPC) and rising prostate-specific antigen (PSA): Updated results of a phase II study. Presenting Author: Daniel J. George, Duke University Medical Center, Durham, NC Background: Ortl is an investigational, oral, non-steroidal selective 17,20lyase inhibitor that suppresses androgen production. Ortl affects cortisol synthesis less than similar agents due to limited inhibition of 17�hydroxylase, and may permit steroid-free dosing. Ortl 300 mg BID was examined in patients (pts) with nmCRPC and rising PSA. Methods: Eligible pts had nmCRPC with PSA �2 ng/mL (PSA �8 ng/mL if doubling time �8 mo), and surgical/medical castration, with testosterone (T) �50 ng/dL. Prior chemotherapy, ketoconazole, or concomitant corticosteroids were excluded. Starting dose of ortl was 300 mg BID and continued until PSA progression, metastases, or unacceptable toxicity. The primary endpoint was the percentage of pts with PSA �0.2 ng/mL after 3 mo. Secondary endpoints included safety, PSA kinetics, time to metastases, changes in endocrine markers and circulating tumor cells (CTCs). Results: 39 pts were enrolled with baseline demographics including median age 71 y, ECOG PS �1, median PSA 12.1 ng/mL (range 2.6-67.8), T 7.9 ng/dL (1.4–17.3), and ACTH 19 ng/L (n�33; 0-47); 3 pts had dose reduction due to adverse events (AEs). Gr �3 AEs occurred in 16 pts (drug-related in 14); Gr �3 AEs �5% were dyspnea (8%), hypertension (13%), fatigue, hypokalemia, pneumonitis (5% ea). 7 pts (18%) had serious AEs; most common was pneumonitis (2�Gr 3, 1�Gr 2). 8 pts discontinued due to AEs; 2 pts required corticosteroids. At 3 mo, 6 pts (16%) achieved PSA �0.2 ng/mL; PSA50 and PSA90 rates were 76% and 32%, respectively; median PSA declined by 83% (n�34); median T declined by 89% to 0.78 ng/dL (n�31), and median ACTH increased by 171% to 43 ng/L; median cortisol declined by 21%. At 6 mo, PSA50 and PSA90 rates were 45% and 21%, respectively. Median time to PSA progression was 14.8 mo. 17 pts (44%) were on treatment �6 mo. Of 37 pts with baseline CTC/7.5 mL assessed, only 1 had CTC �5 and converted to �5; 6 had 1–4 CTCs at baseline, none converted to �5 during treatment. Conclusions: Ortl without steroids produces marked and durable declines in T and PSA, has manageable toxicities, and is feasible in men with nmCRPC. 4551 Poster Discussion Session (Board #5), Mon, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Radium-223 chloride (Ra-223) impact on skeletal-related events (SREs) and ECOG performance status (PS) in patients with castration-resistant prostate cancer (CRPC) with bone metastases: Interim results of a phase III trial (ALSYMPCA). Presenting Author: A. Oliver Sartor, Tulane Cancer Center, New Orleans, LA Background: Ra-223, a 1st-in-class alpha-pharmaceutical, targets bone metastases (mets) with high-energy alpha-particles of short range (�100 �m). ALSYMPCA, a phase III, double-blind, randomized, multinational study, compared Ra-223 plus best standard of care (BSC) v placebo (pbo) plus BSC in patients (pts) with bone mets in CRPC. The primary endpoint was OS; secondary endpoints included SREs and ECOG PS. Methods: Eligible pts had progressive, symptomatic CRPC with � 2 bone mets on scintigraphy and no known visceral mets; were receiving BSC; and either previously received docetaxel, were docetaxel ineligible, or refused docetaxel. Pts were randomized 2:1 to 6 injections of Ra-223 (50 kBq/kg IV) q4 wks or matching pbo and stratified by prior docetaxel use, baseline ALP level, and current bisphosphonate use. Results: 921 pts were randomized from 6/2008-2/2011. In a planned interim analysis (n � 809), Ra-223 significantly improved OS v pbo (median OS 14.0 v 11.2 mo, respectively; two-sided P � .00185; HR � .695; 95% CI, .552-.875).SREs were lower in the Ra-223 v pbo group, and time to 1st SRE was significantly delayed (median time to SRE 13.6 mo v 8.4 mo, respectively; P � .00046; HR � .610; 95% CI, .461-.807). The proportion of pts with ECOG PS deterioration (� 2 points) was less in Ra-223 v pbo group at Wk 12 and Wk 24 (4%, 15/389 v 9%, 16/180 and 7%, 16/236 v 12%, 10/83, respectively). Time to ECOG PS deterioration (� 2 points) was significantly delayed by Ra-223 v pbo (P � .003; HR � .62; 95% CI, .46-.85). Conclusions: Ra-233 significantly delayed time to 1st SRE and SRE components, notably SCC. Fewer pts in the Ra-223 group had ECOG PS deterioration. Ra-223 improves OS with excellent safety and may provide a new standard of care for CRPC pts with bone mets. Time to 1st event No. (%) of patients (Ra-223 vs Pbo) Ra-223 Pbo HR SRE component n � 541 n � 268 p value* (95%CI) External beam radiotherapy 122 (23) 72 (27) .0038 .65 (.48-.87) Spinal cord compression 17 (3) 16 (6) .016 .44 (.22-.88) Pathologic bone fracture 20 (4) 18 (7) .013 .45 (.24-.86) Surgical intervention 9 (2) 5 (2) .69 .80 (.27-2.4) *Not adjusted for multiplicity. 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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Page 693 and 694:
Page 695 and 696:
Page 697 and 698:
Page 699 and 700:
Page 701:
TPS10634 General Poster Session (Bo
Page 704 and 705:
Author Index Note: Numerals refer t
Page 706 and 707:
Alexanian, Raymond 8093 Alexeev, Bo
Page 708 and 709:
Arkenau, Hendrik-Tobias 2540, 3000,
Page 710 and 711:
Ballen, Karen K. 6606, 6617, 6618,
Page 712 and 713:
Ben-Aharon, Irit 548, 2556, e13080
Page 714 and 715:
Blancas, Isabel e11535, e11545, e21
Page 716 and 717:
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,
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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