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100s Cancer Prevention/Epidemiology 1559 General Poster Session (Board #4A), Sat, 1:15 PM-5:15 PM Public perception of cancer risk. Presenting Author: Lisa Burns, University College Cork, Cork, Ireland Background: The public’s knowledge of cancer risk factors has rarely been studied in Ireland. An understanding of this can help inform cancer prevention programs. Methods: An online surveywas used to assess the public’s perception of cancer risk. Results: 525 people completed the survey. Mean age was 40yrs (range:18-74), 82% were female and 36% had college degrees. 81% were concerned about developing cancer, however 20% believed if cancer was in their family there was nothing they could do about personal cancer risk. 20% did not know that cancer risk increased with age, 27% believed that �50% of cancers are inherited, and 54% believed 10-20% of cancers are inherited. The top 5 risk factors listed by respondents were: smoking 85%, diet 74%, alcohol 44%, genetics 38%, and environment 31%. Only 32% were aware that obesity is a risk factor for cancer and 33% did not think the location of fat was important for cancer prevention. When given a list of potential behaviours relevant to cancer risk 33% believed wearing a tight bra and 49% believed a blow to the breast could increase cancer risk. 87% believed genetics ‘strongly’ increased risk, 85% stress, and 86% believed cell phones increased risk. 12% believed ‘luck’ was important in avoiding cancer, 35% thought ‘detox’ diets and 61% believed organic food reduced risk. Only 33% agreed with the statement that ‘frozen vegetables/fruit are as good as fresh’, 40% were unaware of the link between red meat and cancer. The following foods were thought to increase risk: cheese (29%), soy (9%), milk chocolate (30%), red wine (25%), and eggs (11%). Aerosol use (71%), cleaning agents (73%), smoking (99%), cooking methods (68%), processed meat (86%), food irradiation (77%), and genetically modified foods (81%) were believed to increased risk. The majority were aware that berries, green tea, garlic, brassica vegetables and physical activity of 30 minutes a day can reduce cancer risk. Conclusions: There is a sizable portion of the population who are misinformed about cancer risk. Most are aware of classic risk factors (e.g. smoking, poor diet). Many overestimate risk attributable to genetics, environment, stress, and underestimate age, obesity and sunlight. One in 5 believes lifetime risk of cancer is non-modifiable. 1561 General Poster Session (Board #4C), Sat, 1:15 PM-5:15 PM Clinical and genetic predictors of weight gain in patients diagnosed with breast cancer. Presenting Author: Sangeetha M. Reddy, Northwestern University Feinberg School of Medicine, Chicago, IL Background: Obesity and weight gain in breast cancer patients has been associated with decreased quality of life, decreased response to chemotherapy, increased cancer recurrence, and higher all-cause mortality. Our study was designed to identify factors that contribute to this weight gain. Methods: Chart review was conducted on 565 breast cancer patients to obtain weights and BMIs over an 18 month period from diagnosis, tumor characteristics (ER/PR/Her2 status, grade, presence of LN metastases, stage), demographics (age, race), clinical factors (menopausal status), and treatment regimens (chemotherapy, hormone therapy, radiation). Blood samples were genotyped for polymorphisms in FTO (fat mass and obesityassociated protein) and the adiponectin pathway, two pathways found to be associated with obesity and breast cancer risk. Results: See table. For genetic analysis, one statistically significant epistatic and three gene x environmental interactions were detected for adiponectin SNPs: rs822396d x BMI at diagnosis (effect size 8.65), rs2232853a x age (2.75), rs1501299a x BMI at diagnosis (3.63), and rs266729d x rs7539542d (6.40). Conclusions: We have identified multiple clinical and genetic variables that are likely predictors of weight gain in breast cancer patients. We are conducting a prospective study of 200 breast cancer patients to validate the findings of this retrospective study. By identifying a high risk patient population, we hope to target them for aggressive lifestyle interventions to prevent weight gain and thereby improve their mortality and morbidity. OR for statistically significant clinical variables. Univariate analysis Multivariate Variable 6 mo 1 yr 18 mo analysis Chemotherapy 0.75** 0.88** 0.88** Hormone therapy 1.28** 1.18** 1.18** 1.20** Stage (3 or 4) 0.78** 0.86** 0.87** 0.85** Postmenopausal status at diagnosis 0.87* 0.91** LN metastases 0.84** 0.91* 0.91** ER status 1.37** 1.18** 1.18** 1.22** PR status 1.23** 1.11* 1.13** Grade (2 or 3) 0.80* 0.87* 0.89** African American vs. white 0.88* 0.90** Hispanic vs. white 1.43* 1.17* Asian vs. white *p � 0.05 ** p � 0.01 0.79* 0.87* 1560 General Poster Session (Board #4B), Sat, 1:15 PM-5:15 PM The effects of BR-DIM (BioResponse 3, 3’-Diindolylmethane) administered pre-prostatectomy on the androgen receptor (AR). Presenting Author: Elisabeth I. Heath, Karmanos Cancer Institute, Wayne State University, Detroit, MI Background: Consumption of cruciferous vegetables is associated with decreased risk of prostate cancer (PCa). 3,3’-diindolylmethane (DIM), an in vivo active compound formed after consumption of cruciferous vegetables, down-regulates the AR, and causes its nuclear exclusion which results in in vitro growth arrest and apoptosis of PCa cells. We conducted a biomarker trial evaluating BR-DIM in pre-prostatectomy patients with the primary objective of measuring DIM levels in prostate tissue and in plasma. Methods: Patients with organ-confined PCa who were candidates for surgery were treated with BR-DIM at a dose of 225 mg orally twice daily for a minimum of 14 days. Patients did not receive any androgen deprivation therapy. Patients received their last dose of BR-DIM the day before surgery. Blood samples for DIM levels were collected pre-treatment and just prior to surgery. DIM concentration was measured in the plasma and in prostate tissue specimens using a validated high-performance liquid chromatographic method with tandem mass spectrometric detection. AR was evaluated by immunohistochemistry (IHC). Results: 36 patients were treated at 2 institutions. The 26 evaluable patients had median age of 60 years (range 41 - 76), 14 were Caucasian, and 10 were African American. Reasons for inevaluability included change in surgery date (n�4), inadequate BR-DIM treatment (2), withdrawal from study (2), canceled surgery (1), and other (1). Toxicity was minimal; only two patients with grade 3 headache. Post dosing, DIM was found at a mean trough level of 10.2 ng/ml (range, 0.5 to 24.7) and 12.3 ng/gm of tissue (range, 0.0 to 26.8) in plasma and in prostate tissue, respectively. PSA levels had a slightly downward trend after BR-DIM treatment. In 18 of 20 evaluable PCa specimens, IHC showed nuclear exclusion of AR. Conclusions: BR-DIM was well tolerated, and DIM was detected in both plasma and prostate tissues at ~12 h post dosing. Nuclear exclusion of AR was found in 90% of PCa specimens post BR-DIM dosing, suggesting in vivo inactivation of AR activity. PSA levels were slightly reduced overall. Accrual is ongoing and nearly complete. Additional studies with BR-DIM in PCa are warranted. 1562 General Poster Session (Board #4D), Sat, 1:15 PM-5:15 PM Breast cancer risk reduction among patients with DCIS. Presenting Author: Melanie R. Palomares, City of Hope, Duarte, CA Background: The incidence of ductal carcinoma in situ (DCIS) has dramatically increased with widespread mammographic screening. Although risk of recurrence of DCIS is low, it is associated with a higher risk for subsequent contralateral breast cancer (CBC), for which preventive measures are available. We evaluated the uptake of surgical and pharmacologic interventions to reduce CBC risk at our institution and investigated factors that may influence treatment choices for DCIS. Methods: City of Hope (COH) DCIS patients were identified using two sources, the Circulating Breast Tumor Marker (BrTM) Registry and the National Comprehensive Cancer Network (NCCN) database. Datasets were linked together, and treatment variables were cross-tabulated with patient and tumor characteristics. Results: Of 782 patients with breast malignancy diagnosed since 1997, 370 were excluded due to concurrent or prior invasive disease, 8 due to suspected misclassification based on therapies received, and 4 due to treatment on protocol. Of the remaining pure DCIS patients, treatment choices were recorded for 289. Of those, 40 (14%) chose bilateral risk reduction mastectomy (BRRM), 82 (28%) unilateral mastectomy, 165 (57%) lumpectomy, and 2 had no surgery. Hormonal therapy (HT) was recorded for 215 individuals who did not pursue BRRM: 124 (57%) took tamoxifen, 3 of whom switched to raloxifene, 5 (2%) started with raloxifene, and 7 (3%) took an unspecified hormonal agent, for a total HT uptake of 55%. This included 8 of 29 women with ER-negative DCIS who chose HT for CBC risk reduction. Younger age at diagnosis was associated with BRRM (24% of women diagnosed before age 50, 10% of those diagnosed 50-64, and 5% of women 65� had BRRM, p�0.001) and HT (59% of women �65 chose HT compared to 40% of women 65�,p�0.009). Within ethnic minorities, more Asian women chose BRRM (22% vs 7% of other minorities, p�0.08). Interestingly, fewer high grade DCIS women opted for HT (39% vs 55% for low to intermediate grade, p�0.06). Conclusions: Young women tend to pursue surgical prophylaxis. Among women who keep their breasts, HT uptake was high across all age and ethnic groups, except for those older than 65 at diagnosis. It is unclear if this is due to patient choice or reflects age bias in physician recommendation. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
1563 General Poster Session (Board #4E), Sat, 1:15 PM-5:15 PM Risk perception and knowledge of breast and colon cancers in a diverse population. Presenting Author: Katherine Lang, Virginia Commonwealth University, Richmond, VA Background: The accuracy of cancer risk perception has implications for preventive behaviors. Studies show that despite receiving personalized breast and colon cancer risk information, people continue to overestimate their numeric risks. It is still not fully understood why this occurs. Breast cancer, especially, is highly visible in the media so an individual may hear more about breast cancer, increasing general knowledge but potentially inflating risk perceptions. This study explores relationships between general knowledge and numeric risk perceptions for breast cancer (BC) and colon cancer (CC) among women. We hypothesize that general knowledge of BC will be high relative to CC, but risk perception for BC will be less accurate. Methods: Data was obtained from the first 369 (final N�490) patients recruited for the Kin Fact study from a Women’s Health Clinic. Kin Fact is a randomized controlled trial examining effects of an intervention to increase cancer risk communication in families. Women complete baseline surveys including knowledge and numeric risk perception measures for BC and CC. We use CA Gene software to calculate actual lifetime risk for BC and CC. Correlations, t-tests and linear regressions were used for the analysis. Results: Women averaged 33 years old, and 58% were African American. Average lifetime risk was 3% for CC and 11% for BC. Women overestimated their numeric risk for both BC and CC, but the mean overestimation for BC (24%) was significantly larger than for CC (19%) (p�0.001). Average scores for BC knowledge were also significantly higher than for CC (p�0.001). Compared to knowledge about CC, women who had greater knowledge of BC also were more inaccurate in terms of their perceived numeric risk (r� -0.131, p�0.016). This finding remained significant controlling for age, race and genetic literacy. Conclusions: Results endorse an apparently paradoxical effect that compared with CC, women with increased knowledge of BC have less accurate risk perception for BC. Inaccuracies in perceived risk can affect psychosocial well-being and adherence to screening and prevention recommendations. Findings reveal a need for increasing knowledge about cancer without adversely impacting the accuracy of risk perceptions. 1565 General Poster Session (Board #4G), Sat, 1:15 PM-5:15 PM Factors and trends in cancer screening in the United States from 2004 to 2010. Presenting Author: Thanyanan Reungwetwattana, Mayo Clinic, Rochester, MN Background: Understanding the prevalence of cancer screening in the US and the factors associated with its accessibility is important for public health promotion. Methods: The 2004 and 2010 Behavioral Risk Factor Surveillance Systems were used to ascertain cancer screening rates among populations indicated for each test by age, gender, and the American Cancer Society recommendation for cancer screenings [fecal occult blood test (FOBT) or endoscopy for colorectal cancer (CRC) screening, digital rectal examination (DRE) or prostate specific antigen (PSA) for prostate cancer screening, clinical breast examination (CBE) or mammogram for breast cancer screening, and Papanicolaou (Pap) test for cervical cancer screening]. Results: Over this period, CRC and breast cancer screening rates significantly increased (15.9%, 13.9%) while prostate and cervical cancer screening rates significantly decreased (1.2%, 5.2%). Race/ethnicity might be an influence in CRC and cervical cancer screening accessibility. Prostate cancer screening accessibility might be influenced by education and income. The older-aged populations (70-79, �79) had high prevalence of CRC, prostate and breast cancer screenings even though there is insufficient evidence for the benefits and harms of screenings in the older-aged group. Conclusions: The disparities in age, race/ethnicity, health insurance, education, employment, and income for the accession to cancer screening of the US population have decreased since 2004. The trajectory of increasing rates of CRC and breast cancer screenings should be maintained. To reverse the trend, the causes of the decreased rate of cervical cancer screening and the high rates of screenings in older-aged populations should, however, be further explored. Proportion of cancer screenings in year 2004 and 2010 (weighted %). Screenings 2004 2010 Absolute difference P value CRC FOBT 17.52 18.25 �0.73 0.001 Sigmoidoscope/colonoscope 49.66 59.90 �10.24 0.000 Total 49.74 65.62 �15.88 0.000 Prostate cancer DRE 64.35 59.89 -4.46 0.000 PSA 65.87 66.71 �0.84 0.080 Total 77.40 76.24 -1.16 0.008 Breast cancer CBE 63.26 82.99 �19.73 0.000 Mammogram 74.06 74.88 �0.82 0.004 Total 74.06 87.94 �13.88 0.000 Cervical cancer Pap 76.06 70.83 -5.23 0.000 Cancer Prevention/Epidemiology 101s 1564 General Poster Session (Board #4F), Sat, 1:15 PM-5:15 PM First report on screening an asymptomatic population for cancer: The yield of an integrated cancer prevention center. Presenting Author: Tal Sella, Sheba Medical Center, Ramat Gan, Israel Background: Cancer is a leading cause of mortality worldwide. Screening is a key strategy for reducing cancer morbidity and mortality. We aimed to evaluate the utility of cancer screening in an asymptomatic population at an integrated cancer prevention center. Methods: One-thousand consecutive asymptomatic, apparently healthy adults, aged 20-80 years, were screened for early detection of 11 common cancers by routine screening tests. Results: Malignant and benign lesions were found in 2.4% and 7.1% of the screenees, respectively. The most common malignant lesions were in the gastrointestinal tract and breast followed by gynecological and skin. The compliance rate for the different screening procedures was considerably higher than the general Israeli population – 78% compared to 60% for mammography (p�0.001) and 39% compared to 16% for colonoscopy (p�0.001). Advanced age, family history and certain lifestyle parameters were associated with increased risk for cancer. Moreover, polymorphisms in the APC and CD24 genes indicated high cancer risk. When two of the polymorphisms existed in an individual, the risk for a neoplastic lesion was extremely high (OR 2.3 [95% CI 0.94-5.9]). Conclusions: A significant number of neoplastic lesions were diagnosed at an early stage. Polymorphisms in the APC and CD24 genes may identify individuals at an increased risk for cancer. Cancer may be diagnosed at an early stage using the screening facilities of a multidisciplinary outpatient clinic. 1566 General Poster Session (Board #4H), Sat, 1:15 PM-5:15 PM Sun exposure profile in the French population: Results of the EDIFICE melanoma survey. Presenting Author: Bruno Sassolas, CHRU Brest, Brest, France Background: The main environmental risk factor for melanoma is related to UV-exposure. Our objective was to evaluate in a survey the profile of sun exposition in the French population as well as the level of knowledge about UV risk and UV protection. Methods: “Edifice Melanoma” a nationwide observational survey was conducted in France via phone interviews among a representative sample of 1502 subjects aged � 18, using the quota method. The survey took place shortly after the summer (September 28th to October 20th , 2011). Results: From the total population of 1502 subjects, 330 (22%) denied any sun exposition. Among those declaring being exposed to the sun (1172), 62% affirmed using a photoprotection method (clothes, sun protective cream). The opportunities for sun exposure arose during holidays (85%), sport (79%) or professional activities (23%), with an annual average exposure of 113 days. 902 subjects (77%) declared avoiding sun exposure between 12 and 4 PM. The main sociodemographic characteristics of subjects exposed to the sun, compared to non-exposed ones are as followed (p�0,05): men, aged �40, with no children or with children aged �15, from high social and occupational group, with at least a 2-years university degree. The analysis of sociodemographic characteristics of subjects declaring to use sun protective measures are (p�0,05): women from high social and occupational group, with at least a 2-years university degree, with high income levels. We explored additional risk behavior in the population studied. Subjects who declared having sun exposure were more likely (p�0,05) to be : smokers, alcohol users and/or alcoholic, tanning bed users before the age of 30, and have a high number of nevi (�50). On the other hand, prior history of cancer was associated with a non-exposure behavior. Conclusions: These data provide important new information about sun behavior in the French population and might give important clues in the field of public health and education to increase the effectiveness of melanoma primary prevention campaigns. A better knowledge of the target to improve would provide better results for public health benefit. 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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ASCO Conflict of Interest Policy an
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2s Special Awards also “normalize
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2012 ASCO Annual Meeting Proceeding
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500 Oral Abstract Session, Sun, 8:0
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508 Clinical Science Symposium, Sat
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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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Chinen, Ludmilla T.D. e16046 Chinen
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Come, Steven E. 9071, 9100 Comis, S
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Dahlheimer, Tambra 2546 Dahmane, El
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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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Foroni, Chiara e11546 Foroni, Letiz
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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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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,
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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
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Zhang, Xinmin e16022 Zhang, Xu Dong
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