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

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448s Leukemia, Myelodysplasia, and Transplantation 6628 General Poster Session (Board #27A), Mon, 1:15 PM-5:15 PM Regional variation in treatment costs and survival for elderly patients with myelodysplastic syndromes. Presenting Author: Xiaomei Ma, Yale University School of Medicine, New Haven, CT Background: Myelodysplastic syndromes (MDS) occur primarily in the elderly (�65 years). The expected 5-year cost for an elderly MDS patient tops $63,200 in 2009 US$. This study assessed regional variation in the cost of care and survival for elderly MDS patients. Methods: Using the Surveillance Epidemiology and End Results–Medicare data, we identified primary MDS patients aged 66-99 years diagnosed from 2001-2007, had continuous fee-for-service coverage for Parts A and B, and had no history of other cancer. We assigned patients to Dartmouth Atlas of Health Care Hospital Referral Regions (HRRs) based on their residence at time of diagnosis. We also selected controls from a 5% sample of Medicare beneficiaries without cancer and matched controls 1:1 to patients by HRR, age, sex, pre-diagnosis cost and comorbidity. All Medicare claims through 2009 were tallied, and MDS-related costs were defined as the difference between the payments for a patient and a matched control. Results: With 6244 patients in 73 HRRs, the average 3-year MDS-related cost varied across HRRs, ranging from $12,900 to $83,600 (2009 US$). Patients in high-spending regions had more comorbidities and higher Medicare costs before diagnosis and were more likely to be racial minorities and live in lower-income areas. Three-year survival ranged from 13.0% to 62.1%. However, there was no significant correlation between 3-year costs and 3-year survival (��-0.06, p�0.61). The hazard ratios (HR) for higher spending regions compared to the lowest-expenditure region were near 1, after controlling for covariates including MDS subtype (2nd quartile: HR�1.03, 95% CI: 0.94-1.12; 2nd quartile: HR�1.04, 95% CI: 0.95- 1.14; 4th quartile: HR�0.98, 95% CI: 0.90-1.08). Conclusions: We observed considerable regional variation in Medicare expenditure on elderly MDS patients during the first 3 years post-diagnosis. However, patients in higher cost regions had similar 3-year survival to patients in lower cost regions. Given the substantial economic burden of MDS and Medicare’s current fiscal challenges, it is important to further assess the factors associated with higher regional costs and to improve the care of MDS patients in a cost-efficient way. 6630 General Poster Session (Board #27C), Mon, 1:15 PM-5:15 PM Preliminary safety and efficacy of ruxolitinib in patients (pts) with primary and secondary myelofibrosis (MF) with platelet counts (PC) of 50– 100x109 /L. Presenting Author: Moshe Talpaz, Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI Background: Ruxolitinib (RUX) has demonstrated clinical benefit as therapy for MF. This study explores the safety and efficacy of RUX in pts with MF and low PC, where clinical data are limited. Methods: In this phase II study, pts with intermediate-1 to high-risk MF, and PC of 50–100x109 /L started RUX at 5 mg BID. Doses could be increased in 5 mg QD increments every 4 weeks (wks) beginning at wk 4. Doses were decreased or held for PC �35x109 /L and �25x109 /L respectively. Assessments: Total Symptom Score (TSS, using the modified MF Symptom Assessment Form v2.0, and comprised of scores from 0�absent to 10�worst imaginable for night sweats, itching, bone/muscle pain, early satiety, abdominal discomfort and pain under left ribs); Patient Global Impression of Change (PGIC, a 7-point scale ranging from “very much improved” to “very much worse”); spleen size by palpation and by MRI (data not yet available); and safety. Results: At the time of analysis, 23 pts had completed �4 wks on study. At baseline: mean PC�72x109 /L; high (4%), intermediate-2 (52%) and intermediate-1 (44%) risk group; mean spleen length�16.6 cm; mean TSS�25.5. At the time of analysis, 4%, 40%, 26%, 26% and 4% of pts were receiving RUX 5 mg QD, 5 mg BID, 5 mg AM/10 mg PM, 10 mg BID, and 10 mg AM/15 mg PM, respectively. At wk 4 (all pts on 5 mg BID), mean TSS improved 14%; 13% had �50% improvement. At wk 8 (52% on 5 mg AM/10 mg PM), mean TSS improved 23%; 30% had �50% improvement. Mean spleen length reduction of 22% (wk 4) and 27% (wk 8) was observed, and PGIC scores of “much improved” or “very much improved” were reported in 35% (wk 4) and 39% (wk 8) of pts. There were no Grade 4 PC, no dose holds for AEs and no discontinuations; 1 pRBC transfusion-dependent pt had Grade 4 anemia. Three pts experienced a total of 4 SAEs (fever; hypnagogic dreams; and spleen pain/pneumonitis) which resolved while on treatment. Conclusions: Effects on spleen size, PGIC, and TSS, even over the first weeks at low doses, are superior to those observed in the placebo group in the COMFORT-I study. These preliminary findings suggest a dosing strategy starting with 5 mg BID RUX with subsequent dose optimization may be efficacious and well tolerated in MF pts who have low platelets. 6629 General Poster Session (Board #27B), Mon, 1:15 PM-5:15 PM History of autoimmunity to predict clinical response to DNA methyltransferase inhibitors (DNMTI) in myelodysplastic syndromes (MDS), and MDS-derived acute myeloid leukemias (AML). Presenting Author: Ashkan Emadi, The Johns Hopkins University, Baltimore, MD Background: MDS is comprised of a heterogeneous group of clonal myeloid disorders. Chronic immune stimulation has been reported as a trigger for the development of a subset of MDS, with increased autoreactive cytotoxic T cells present in the bone marrow. Autoimmunity has been associated with MDS and other marrow failures. DNMTIs, 5-azacytidine and decitabine, are approved for the treatment of MDS. In addition to epigenetic impacts, these agents may have immunomodulatory effects, including augmentation of MAGE-related anti-tumor response. These reports and clinical observations led us to hypothesize that MDS patients with a history of autoimmunity may be more responsive to DNMTIs. Methods: To identify patients with MDS, a retrospective database review (2007-2011) was performed at Johns Hopkins Hospital (JHH) and Massachusetts General Hospital (MGH). The MGH data also included those with AML whose disease had progressed from MDS. Past medical history of autoimmune disorders, diagnosis, blood counts, flow cytometry and cytogenetics were reviewed. Patients with aplastic anemia, paroxysmal nocturnal hemoglobinuria or non-malignant etiologies of cytopenia were excluded. Patients with MDS were further studied if they were treated with DNMTI. Results: Of 137 patients with MDS or MDS/AML, 23 had a documented history of autoimmunity in the medical record. Of these, 15 (65.2%) experienced a response to therapy as defined by the International Working Group. Of 114 patients without a documented history of autoimmunity, 34 (29.8%) achieved a response during therapy, a significantly lower percentage as compared to those with autoimmune conditions (p-value 0.002, t-test). The majority of responding patients with a history of autoimmunity displayed a normal karyotype (9 of 15 patients). Conclusions: A history or co-presence of an autoimmune disorder may predict a high likelihood of achieving a clinical response to DNMTIs. Correlative studies in this unique population of patients with MDS and MDS/AML and prospective clinical studies are needed to improve our understanding of the possible mechanism of action of DNMTIs in these patients. 6631 General Poster Session (Board #28A), Mon, 1:15 PM-5:15 PM Correlation of TCR diversity with immune reconstitution after cord blood transplant. Presenting Author: Ryan Emerson, Adaptive Biotechnologies, Seattle, WA Background: Umbilical cord blood is an important source of hematopoietic stem cells for allogeneic transplants used to treat hematologic disorders and malignancies. Stem cells from cord blood has several advantages over other sources (peripheral blood or marrow) including reduced incidence of graft-versus-host disease (GvHD) which allows less strict donor-patient HLA-type matching requirements. However, hematopoietic recovery (both myeloid and platelet engraftment) and immune reconstitution is significantly delayed in CBT patients resulting in patients remaining at high risk of infection for an extended period of time. Though the high risk of infections to patients is well-documented and recognized, physicians lack an objective means to monitor each patient’s progress toward functional reconstitution of the adaptive immune system. Our project aims to test if our measure of TCR diversity is a better proxy of immune reconstitution in CBT patients. Methods: To do this, we compare our proposed measure of immune reconstitution, TCRB CDR3 sequence diversity and richness over time, against the observed clinical course of severe infection in patients who have received CBT. Previously, peripheral blood mononuclear cells (PBMC) were collected and cyropreserved from 35 CBT recipients at six time points, pre-transplant, and 28, 56, 100, 180, and 365 days post-transplant. Concordantly, clinical outcomes for these patients were collected for up to four years post-transplant. We use a t-test to test if size of TCR repertoire differs between CBT patients with non-relapse related mortality and all other CBT patients. Results: Our TCR sequencing method was successful at measuring immune reconstitution, and TCR diversity is predictive of subsequent mortality from severe infection by 56 days post-transplant. Conclusions: TCR repertoire sequencing is a viable method to monitor immune reconstitution. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
6632 General Poster Session (Board #28B), Mon, 1:15 PM-5:15 PM Post hoc analysis of relationship between baseline white blood cell count and renal and hepatic function and response in a randomized phase III trial of decitabine in patients age 65 or older with acute myeloid leukemia. Presenting Author: Jacques Delaunay, University of Nantes, Nantes, France Background: A phase III trial (NCT00260832) in patients (N�485) �65y with newly diagnosed acute myeloid leukemia (AML) was conducted (Kantarjian, JCO; in press). Every 4 wk, patients received decitabine (DAC) 20 mg/m 2 (1-h intravenous infusion, 5 successive days) or treatment choice (TC) with either supportive care or cytarabine (20 mg/m2 subcutaneous injection daily, 10 successive days). This post hoc analysis examined whether baseline (BL) renal and hepatic function and white blood cell (WBC) counts were associated with response to DAC or TC. Methods: For patients with available data, BL WBC count and markers of renal function (blood urea nitrogen [BUN], creatinine) and liver function (ALT, AST, albumin) were tabulated for patients with/without a response to DAC or TC. Response was defined as morphologic complete remission (CR), CR with incomplete blood count recovery (CRi), or partial remission (PR). Results: Nonresponders had a higher mean BL creatinine vs responders (86.78 vs 80.23 mmol/L, respectively; P�.005); with no differences in BL BUN levels. There were no other between-group differences. Conclusions: This analysis suggests that there is no relationship between BL WBC or hepatic function and response to treatment with DAC or TC. Although there was no difference in BL BUN, higher mean creatinine levels in nonresponders may suggest a prognostic relationship but further studies are needed to clarify. Parameter Nonresponder to DAC or TC Responder to DAC or TC (CR�CRi�PR) P value WBC (10 9 /L) n 372 101 Mean (SD) 9.25 (13.98) 7.02 (12.25) .118 Median (range) 3.72 (0.33-126.60) 2.70 (0.43-95.57) ALT (U/L) n 372 100 Mean (SD) 25.32 (35.53) 20.79 (14.53) .054 Median (range) 18 (5-614) 17 (6-103) AST (U/L) n 371 101 Mean (SD) 23.82 (15.93) 21.74 (9.84) .106 Median (range) 20 (5-203) 18 (9-65) Albumin (g/L) n 377 102 Mean (SD) 34.18 (5.47) 35.07 (5.34) .139 Median (range) 35 (19-48) 36 (16-44) BUN (mmol/L) n 377 102 Mean (SD) 6.97 (2.65) 6.48 (2.27) .064 Median (range) 6.40 (1.3-23.7) 6.15 (2.9-19.5) Creatinine (mmol/L) n 377 102 Mean (SD) 86.78 (27.08) 80.23 (18.88) .005 Median (range) 81 (38-254) 78 (44-169) TPS6634 General Poster Session (Board #29A), Mon, 1:15 PM-5:15 PM Dasatinib plus SMO antagonist versus dasatinib alone for treating patients (pts) with newly diagnosed Philadelphia chromosome-positive (Ph�) chronic myeloid leukemia in chronic phase (CML-CP): Design of CA180-363, a phase II, open-label randomized trial. Presenting Author: Geralyn C. Trudel, Bristol-Myers Squibb, Montreal, QC, Canada Background: Dasatinib 100 mg once daily (QD) is approved as first-line therapy for pts with newly diagnosed Ph� CML-CP and those who are resistant or intolerant to prior therapy, including imatinib, based on demonstrated efficacy and tolerability. BMS-833923 (SMO antagonist), selectively blocks hedgehog (Hh) pathway signaling by binding to and antagonizing Smoothened (SMO), preventing downstream signaling and activation of target genes. In preclinical studies, SMO loss or inhibition reduces hematopoietic stem cell renewal, induces CML stem cell depletion, and inhibits imatinib-resistant CML cell growth (Dierks, Cancer Cell 2008; Zhao, Nature 2009). In pts with CML, Hh signaling genes (Sonic hedgehog, SMO, and Gli1) are significantly upregulated compared with control pts (Long, J Exp Clin Cancer Res 2011), suggesting that drug resistance and disease recurrence may be overcome by targeting the Hh signaling pathway. Methods: CA180-363 is a phase 2 trial to assess dasatinib activity with or without SMO antagonist in pts with newly diagnosed Ph� CML-CP. Pts receive dasatinib 100 mg QD for 12 months and are then randomized 1:1 to continuing dasatinib 100 mg QD with or without SMO antagonist up to 24 months, followed by dasatinib 100 mg QD alone until end of study (60 months). Randomization is stratified by Sokal score at diagnosis and major molecular response (MMR) at 12 months (yes/no). Eligible pts are aged �18 years, have an Eastern Cooperative Group (ECOG) performance status of 0-2, and previously untreated Ph� CML-CP diagnosed within 6 months of enrollment. Primary endpoint (evaluated in pts who do not achieve MMR prior to randomization) is comparison of MMR rates for dasatinib alone vs dasatinib plus SMO antagonist. Other endpoints (evaluated in all pts) are complete molecular response, progression-free survival, event-free survival, transformation-free survival, and safety of the combination regimen. Recruitment started in September 2011 (14 pts enrolled to date); estimated primary completion date is November 2014. ClinicalTrials.gov ID: NCT01357655. Leukemia, Myelodysplasia, and Transplantation 449s 6633 General Poster Session (Board #28C), Mon, 1:15 PM-5:15 PM Phase II study of short CHOP-rituximab combination with early consolidation with ibritumomab-tiuxetan-Y90 (IT-Y90 ) in non-pretreated patients age 65 to 80 with CD20� diffuse large B-cell lymphoma (DLBCL). Presenting Author: Frederic Peyrade, Anticancer Center, Centre Antoine-Lacassagne, Nice, France Background: IT-Y90was approved in follicular lymphoma, and some data indicates that it could be used in DLBCL. It has been reported that early TEP-TDM negativity is associated with a longer survival in DLBCL, which suggest that these patients could benefit of a less intensive protocol. Methods: We conducted an international, open-label, phase II nonrandomised study, in patients aged between 65 and 80 with age-adjusted (aa) IPI score of 0 and 1 and CD20� DLBCL. The primary objective was to evaluate the efficacy of 3 cycles of RCHOP14 followed by, in case of complete response (CR), an injection of IT-Y90 . Results: Thirty patients (M/F� 1) were included. Median age was 72.6 years (range 65 - 80). Patients had a stage III/IV, elevated LDH and IPI�1 in 38%, 16.6 and 57% respectively. 25 patients received the full treatment. Five obtained an uncomplete FDG-PET response and were excluded after 2 RCHOP cycles. 23 patients received the full IT-Y90 dosage (0.4mCi/Kg) and two received the attenuated dosage (0.3mCi/Kg). Mean treatment time was 54 days (median 52; min 48-max 69). The CR rate after RCHOP treatment was 85% [95% CI: 65-94]. No treatment-related deaths occurred. Grade III-IV neutropenia and thrombocytopenia was observed in 45% and 4%, respectively. Five patients experienced at least one febrile neutropenia. After IT-Y90 , mean duration time for platelets �50G/l was 2.08 weeks (median 2; min 0-max 5). Two patients required platelet transfusion. With a median follow-up of 29.5 months [95% CI: 23-39], the estimated 3-year PFS was 90% [95% CI: 80-100] and the 3-year OS was 100% [95% CI: 100-100]. Among patients treated with 90Y-IT, only 3 relapsed were recorded (at 6, 16 and 24 months). Conclusions: this study suggested the feasibility, and efficacy of a short regimen including one injection of IT-Y90for selected DLBCL in complete response after 3 cycles of RCHOP14. This results need to be confirmed by further studies. TPS6635 General Poster Session (Board #29B), Mon, 1:15 PM-5:15 PM Targeting microenvironment-mediated resistance in leukemias: Phase I trial of mobilization and elimination of FLT3-ITD� acute myelogenous leukemia (AML) stem/progenitor cells by plerixafor/g-CSF/sorafenib. Presenting Author: Michael Andreeff, University of Texas M. D. Anderson Cancer Center, Houston, TX Background: FLT3-ITD AML are associated with poor prognosis. We identified Sorafenib (S) as potent inhibitor of FLT3-ITD (Zhang W, JNCI, 2008; Borthakur G., Haematologica, 2010). FLT3-ITD is associated with overexpression of chemokine receptor CXCR4 and we found increased in vivo activity of S combined with CXCR4 inhibitor Plerixafor (P) and G-CSF (G) (Zeng Z et.al. Blood 2009). Here we report first data testing this concept in patients with R/R FLT3-ITD AML. Methods: G (10 ug/kg) and P(240 ug/kg) were given s.c. QOD on days 1 – 13, S (400-600mg), S on d 1 - 28(one cycle). G/P was held when blasts � 5x104/ uL. CD34, 38, 123, CXCR4 (1D9, 12G5), VLA4, CD44 and phospho-proteins were measured by flow cytometry. Results: 10 patients have been treated so far : 2 achieved CRp, 4 PR and 4 failed (NR), for an overall response rate of 6/10; 3/6 responders and 4/4 NR were previously treated with FLT3 inhibitors. 4/10 pts. developed hyperleukocytosis (and missed 1 to 5 doses of G/P), 6 skin rash and 3 hypertension. Analysis of cells mobilized in 22 cycles revealed a 29-fold increase in WBC, 41-fold in absolute blasts, 77-fold in granulocytes. Increase in circulating stem/progenitor cells was as follows: CD34�: 231-fold, CD34�/38- : 90-, CD34�/38-/123�(LSC) : 148-, CXCR4�: 139-, VLA-4� : 68- and CD44�: 82-fold. Increase in LSC was correlated with baseline blasts and VLA4, not with CXCR4. FISH confirmed mobilization of leukemic cells. Increased levels of pERK and pAKT were observed in mobilized cells. Conclusion: The combination of G-CSF�Plerixafor appears superior in increasing circulating leukemic blasts and stem/progenitor cells in FLT3-ITD AML, as compared to Plerixafor alone in R/R AML(blast increase 2.1-fold; Uy et al. Blood, in press). Treatment resulted in 2/10 CRp and 4/10 PRs. Mobilized stem/progenitor cells displayed increased MAPK/AKT signaling and increased CXCR4 expression. This is the first clinical report of G-CSF/Plerixafor for the “mobilization” of AML cells, aimed at removing them from their protective bone marrow microenvironment. The initial results are providing proof-of–principle of this concept. 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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Author Index Note: Numerals refer t
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Alexanian, Raymond 8093 Alexeev, Bo
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Arkenau, Hendrik-Tobias 2540, 3000,
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Ballen, Karen K. 6606, 6617, 6618,
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Ben-Aharon, Irit 548, 2556, e13080
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Blancas, Isabel e11535, e11545, e21
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Brandes, Johann Christoph 7048, 106
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Cakir, Betul 9567 Calabek, Bernadet
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Ceraulo, Domenica 4017 Cerbone, Lin
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Come, Steven E. 9071, 9100 Comis, S
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DeLacure, Mark D. e16052 Delage, Ju
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Domingo, Gelenis 6568, 6575, 6588 D
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El Sherbeiny, Esam e15129 El-Deiry,
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Fayad, Luis 6501, 8067 Fayette, Jer
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Gang, Wu 7091, e14511 Gangaram, Anj
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Gimenez Capitan, Ana 4068, 10596, e
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Granowetter, Linda 9537 Grant, Barb
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Hainsworth, John D. 618, 1018, 1086
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Heerschap, Arend e13111 Heersink, M
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Hong, Seung-Mo 3568 Hong, Sook Hee
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Im, Young-Hyuck 598^, 644, TPS649,
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Ji, Yongling e17527 Jia, Jingquan e
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Kaparelou, Maria 583 Kapaun, Christ
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Kim, Chan Kyu e14688 Kim, Chang Won
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Komatsu, Yoshihiro e14689 Komatsu,
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Laack, Nadia N. 2032, e14507 Laadem
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Lee, Ji-Hyun TPS3114, 6100 Lee, Jih
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Lim, Kian-Huat e14584 Lim, Kiat Hon
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Loupakis, Fotios 3518, 3540, 3546,
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Man, Shan e11061, e15177^ Manaloor,
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Mathieu-Nicot, Florence e19623 Math
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Mergenthaler, Hans-Guenther e15026
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Molero, Xavier e21035 Moles-Moreau,
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Munoz-Sanchez, MM e19590 Munsell, M
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Ng, Daniel e15050 Ng, Dawn Marie e1
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Oguri, Senri 5556 Oh, Do Youn 1003
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Palassini, Elena 10026, 10053, 1006
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Peisker, Uwe 10600 Peker, Deniz e18
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Piwnica-Worms, Helen 3047 Pizzo, Fa
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Rabinowits, Guilherme 5501, 5582, 9
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Reyes-Rivera, Irmarie CRA3503 Reyna
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Rose, Steven C. 3590 Rosell, Rafael
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Sakata, Shinya e18059 Sakata, Yuh 3
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Schenkein, David P. 6606 Schepp, Wo
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Sha, Dan 3564 Sha, Huifang e13528 S
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Silva, Jose D. 5567 Silva, Milton J
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Sousa, Carlos Eduardo Pires 643 Sou
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Su, Xinying 4124 Su, Yu-Chieh e1600
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Tan, Chee Seng 1064, e19523 Tan, Ch
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Tillmanns, Todd D. 5014, e15514 Til
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Uchiyama, Tomotaka e21108 Udovitsa,
Page 812 and 813:
Videtic, Gregory M.M. e14611, e1466
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Wang, Yuan e15124 Wang, Yunfei 547
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Wischnewsky, Manfred 1078 Wischnik,
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Yasuda, Hiromi e14029 Yasuda, Hiroy
Page 820:
Zhang, Xinmin e16022 Zhang, Xu Dong
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