bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 181: Biological and clinical relevance of quantitative global methylation in repetitive DNA sequences in B-cell chronic lymphocytic leukemia
Authors: Bollati Valentina , Fabris Sonia , Morabito Fortunato , Agnelli Luca , Motta Valeria , Cutrona Giovanna , Gentile Massimo , Deliliers Giorgio Lambertenghi , Bertazzi Pier Alberto , Ferrarini Manlio , Neri Antonino , Baccarelli Andrea 
Published: February 2011

Abstract
Background: B-cell chronic lymphocytic leukemia (B-CLL) is characterized by highly clinical heterogeneity; the identification of reliable prognostic factors useful in predicting patient outcome and planning therapeutic strategies represent a crucial task. Global DNA hypomethylation affecting repeat sequences, such as long interspersed nuclear elements-1 (LINE-1), Alu and satellite α DNA (SAT-α DNA), has been reported in different cancer types and associated with chromosomal instability.
Aim: In order to investigate the role of global DNA methylation in B-CLL we quantified the methylation levels of Alu, LINE-1 and SAT-α repetitive in B-CLL patients and correlated them with the major cytogenetic and molecular features and clinical relevance in predicting therapy-free survival (TFS).
Patients and methods: A quantitative bisulfite-PCR Pyrosequencing method was used to evaluate methylation of Alu, LINE-1, and SAT-α in a panel of highly purified (&gt;90%) peripheral mononuclear CD19+ cells from 7 healthy donors and 77 B-CLL untreated well-characterized patients in early stage disease (Binet stage A).
Results: Forty-eight patients had unmutated IgVH genes; ZAP-70 and CD38 were positive in 28 and 35 cases, respectively; 13q14.3 deletion was present as a sole abnormality in 21/33 patients while in the remaining cases it was combined with 17p13.1 (4 pts) or 11q22.3 deletions (7 pts) or both (1 pt). The 11q22.3 and 17p13.1 deletions were detected as sole abnormality in 6 and 7 patients, respectively. Trisomy 12 occurred in 17 patients, as a sole abnormality in all cases.
Methylation levels (median %5mC) were lower in B-CLLs compared with controls (21.4 vs. 25.9; 66.8 vs. 85.7; and 84.0, vs. 88.2; for Alu, LINE-1 and SAT-α, respectively). A significant association was observed with 17p13.1 deletion (15.4 vs. 22.4; 42.9 vs. 68.5; 32.7 vs. 85.0, for Alu, LINE-1 and SAT-α) but not with other major genetic lesions, IgVH mutation status, CD38 or ZAP-70 expression. Notably, lower SAT-α methylation levels appeared to be an independent prognostic marker significantly associated with a shorter TFS.
Conclusion: Our study extended limited evidence in methylation of repetitive sequences in B-CLL suggesting an important biological and clinical relevance in the disease.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 181.
Abstract 1814: Waldenström macroglobulinemia and lymphoplasmacytic lymphoma: incidence and demographic patterns in the United States, 1988 – 2006
Authors: McMaster Mary L. , Rosenberg Phillip 
Published: February 2011

Abstract
Background: Waldenström macroglobulinemia (WM) is a clinicopathological syndrome that typically presents with bone marrow involvement by a lymphoproliferative process that produces monoclonal IgM. WM shares clinicopathological features with lymphoplasmacytic lymphoma (LPL) and has been characterized as a bone marrow-based subset of LPL to define specific patient populations for inclusion in clinical trials. However, previous epidemiologic studies of WM did not include LPL, and the extent to which the two disorders overlap is unknown. Methods: We estimated age-adjusted incidence rates (IRs) of WM and LPL in the population-based Surveillance, Epidemiology and End Results Program in the United States to analyze patterns of WM and LPL separately and jointly by age, gender, and race. We applied generalized linear regression models to test for interaction between the age-specific curves for each disorder. Results: Overall standardized IRs were 3.22 per 1 000 000 person-years for WM (n = 2 230) and 2.21 for extra-medullary LPL (EM-LPL; n = 1 547) during 1988 – 2006. Incidence of WM/LPL combined was 65% higher among males compared to females, and the male: female IR ratio was significantly higher for WM (2.20) than for EM-LPL (1.50). WM/LPL IRs were 40% lower among blacks compared to whites; this difference was due to a black: white IR ratio that was significantly decreased for WM (0.39), but not for EM-LPL (0.94). Racial differences could not be explained solely by covariates reflecting differential access to care. WM and EM-LPL had significantly different age-at-onset curves after adjusting for period effects, and IRs increased with age in both disorders. Conclusions: Epidemiological patterns for WM and EM-LPL appear to suggest disease heterogeneity. Future studies should include assessment of disease classification in reporting to cancer registries; exploration of race, gender, and age effects, with application of additional area-level measures associated with access to care, in epidemiological studies; and clinical and genetic studies to identify unique pathobiological determinants underlying each disease.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1814.
Abstract 1816: Attributable risks for hepatocellular carcinoma in the United States
Authors: McGlynn Katherine A. , Quraishi Sabah , Welzel Tania M. , Davila Jessica A. , El-Serag Hashem B. , Graubard Barry I. 
Published: February 2011

Abstract
In the United States, known risk factors for hepatocellular carcinoma (HCC) include infection with the hepatitis B virus (HBV), infection with the hepatitis C virus (HCV), excess alcohol consumption, diabetes, obesity and several rare metabolic disorders (hemochromatosis, α-1 antitrypsin deficiency, porphyrias). The proportion of risk in the U.S. attributable to each factor separately, and to all factors together, however, is not well understood. To better quantify the risk attributable to these factors, logistic regression analysis was conducted using data from the SEER-Medicare linked database. All persons diagnosed with HCC (n=5,607), with at least 3 pre-diagnostic years of Medicare coverage between 1994 and 2005, were included as cases. A 5% random sample of persons residing in SEER locations (n=190,782) were included as controls. For each risk factor, odds ratios (OR) with their 95% confidence intervals (95%CI), and attributable risks (AR) with their 95%CI were calculated. In addition to calculating overall risks, risks were calculated after stratifying on race/ethnicity, gender and time period of HCC diagnosis. Among all individuals, the AR of all factors together was 63.3%. The AR among males, however, was higher than the AR among females (64.6% vs. 60.7%, respectively). By race/ethnicity, the AR of all factors together was highest among Asians (67.9%). This AR was followed by that among Hispanics (64.9%), then whites (63.3%) and finally, blacks (53.0%). Among specific factors, diabetes had the greatest AR at 34%, followed by alcohol-related conditions at 24.0%, HCV at 20.7%, HBV at 5.7%, metabolic disorders at 3.1% and obesity at 2.0%. These findings differed by gender and race/ethnicity, however. While diabetes had the highest AR among both males and females, the factor with the second highest AR among males was alcohol-related diseases, while among females; the factor with the second highest AR was HCV. The factors with the highest AR among each race/ethnic group were: whites - diabetes (36.4%) and alcohol-related disease (23.5%), blacks - HCV (31.9%) and alcohol-related disease (20.3%), Hispanics - alcohol-related disease (29.9%) and diabetes (28.0%), and Asians - HCV (31.7%) and diabetes (26.5%). These findings indicate that the current increase in incidence of HCC in the U.S. may be fueled by different factors in different racial/ethnic and gender groups. Overall, controlling diabetes might have a greater impact than any other single factor on reducing the incidence of HCC in the U.S.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1816.
Abstract 1817: Sex disparities in colorectal cancer incidence by anatomic subsite, race and age
Authors: Murphy Gwen A. , Devesa Susan S. , Inskip Peter D. , McGlynn Katherine A. , Cook Michael B. 
Published: February 2011

Abstract
Background: Colorectal cancer remains the fourth most common cancer diagnosed and the second most common cause of cancer death in the United States. Though incidence and mortality rates have declined in recent years, the burden of disease is disproportionate; rates are higher in men than women and the male-to-female incidence rate ratio (MF IRR) increases progressively across the colon from the cecum to the rectum. Rates among races/ethnicities other than whites or blacks have not been frequently reported.
Methods: To examine colorectal cancer rates by sex across anatomic subsite, age, and racial/ethnic groups, we used the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program for cases diagnosed among residents of 13 registries during 1992-2006. Incidence rates were expressed per 100,000 person-years and age-adjusted to the 2000 US Standard Population; male-to-female incidence rate ratios (MF IRR) and 95% confidence intervals were also calculated.
Results: Among both males and females, total colorectal cancer rates were highest among Blacks (71.0 and 54.8 per 100,000 person-years, respectively) and lowest among Hispanics (47.8 and 32.4). Rates of proximal colorectal cancer were higher than distal and rectal sites for all race/ethnicities. Among each racial/ethnic group, the MF IRR increased fairly monotonically from close to unity for cecal cancers to 1.81 (Hispanics) for rectal cancers. MF IRRs increased with age most rapidly for distal colon cancers from &lt;1.0 at ages &lt;50 years to 1.4-1.9 at older ages. The MF IRR for rectal cancers also rose with age from about 1.0 to 2.0. For proximal cancer, the MF IRR was consistently &lt;1.5 and varied little with age; among American Indian/Alaska Natives it was &lt;1.0 across all ages.
Conclusion: The MF IRR for colorectal cancer varies markedly according to subsite and age but less by racial/ethnic group. These findings may reflect differing exposure to, or metabolism of, hormonal or environmental elements and may have consequences for screening messages.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1817.
Abstract 1824: Sun exposure and the risk of malignant lymphoma in an Asian population: The Singapore Lymphoma Study
Authors: Wong Kin-Yoke , Chia Sin-Eng , Kuperan Ponnudurai , Lee Khai-Mun , Lim Soon-Thye , Loong Susan , Mow Benjamin , Ng Siok-Bian , Tan Suat-Hoon , Tan Leonard , Tan Soo-Yong , Tao Miriam , Wong Alvin , Wong Gee-Chuan , Seow Adeline 
Published: February 2011

Abstract
INTRODUCTION
Recent epidemiological studies have reported an inverse association between sun exposure and Non-Hodgkin lymphoma (NHL) which may be related to vitamin D or other factors, but these studies have been conducted almost exclusively in the Western countries, and in temperate locations.
METHODS
The Singapore Lymphoma Study is a hospital-based, case-control study conducted in Singapore between Feb 2005 and Dec 2008. Singapore residents (men and women, ethnic Chinese/Malays/Indians) aged 18 to 90 formed the study population. Detailed information on outdoor activities under sun (for recreational or occupational purposes) during childhood and in adulthood, skin colour and sun sensitivity, and other information on other possible risk factors were collected in personal interviews.
A total of 543 incident malignant lymphomas including 74 Hodgkin's lymphoma (HL), 403 B-cell and 61 T and NK-cell NHL and 5 others, and 830 controls were recruited. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression analysis, adjusted for age, gender, ethnicity, and housing types as surrogate for social economic status.
RESULTS
Skin colour and sun sensitivity did not show any association with risk of malignant lymphoma, after adjusting for ethnicity. We observed a reduced overall risk of NHL (but not HL) among subjects who reported spending time outdoors regularly, especially on weekends/rest days.
A lower risk of NHL was associated with recreational sun exposure in childhood non-school days (OR 0.7, 95% CI 0.5-0.9) and in adulthood weekends/rest days (OR 0.8, 95%CI 0.6-1.0), and the observed association was significant in females when stratified by gender. In addition, occupational sun exposure in males was inversely associated with the risk of NHL (OR 0.7, 95%CI 0.5-1.0). Cumulative working time outside under sun appeared unrelated to NHL overall. The associations were more consistently observed in B-cell NHL subtypes (OR 0.6, 95%CI 0.5-0.8), in diffuse large B-cell lymphoma (OR 0.6, 95%CI 0.5-0.9) and mucosal-associated lymphoid tissue lymphoma (OR 0.5, 95%CI 0.2-1.0), than in T-cell NHL.
CONCLUSION As the first case-control lymphoma study in Asia, our data are consistent with an inverse association between intermittent sun exposure and NHL in this study population.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1824.
Abstract 1826: Anthropometric characteristics, physical activity and risk of lymphoid neoplasms in a large US cohort
Authors: Patel Alpa V. , Diver William Ryan , Birmann Brenda M. , Gapstur Susan M. 
Published: February 2011

Abstract
Body size, height, and physical inactivity are known to alter immune function and have been hypothesized to increase risk of non-Hodgkin lymphoma (NHL). However, results of other studies are inconsistent and whether these relationships vary by histologic subtypes of NHL is not well-documented. Therefore, we examined measures of body size (BMI, adult weight gain, and BMI at age 18), height, physical activity, and sitting time in relation to risk of NHL overall and within the major subtypes (diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), and B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), and multiple myeloma (MM)) in the American Cancer Society Cancer Prevention Study II (CPS-II) Nutrition Cohort, a prospective study of cancer incidence and mortality, using information obtained at baseline in 1992. From 1992-2007, 2000 incident NHL cases were identified among 150,189 men and women who were cancer-free at enrollment. Cox proportional hazards modeling was used to compute hazard rate ratios (RR) while adjusting for potential confounders. Obese men and women (BMI &gt; 30) had a 20% higher incidence of all NHL (95% confidence interval (CI) 1.05-1.37) compared to normal weight individuals (BMI 18.5-&lt;25). BMI at age 18 and BMI measured 10-years prior to baseline (in 1982) were also associated with NHL risk (trend p=0.008 and p=0.0003, respectively) in men and women, even after adjustment for baseline BMI. Height was positively associated with overall risk (RR=1.25, 95% CI 1.10-1.43 for sex-specific quintile 5 vs. 1). Associations were similar across all subtypes of NHL examined. Measures of physical activity and sitting time were not associated with risk of NHL or within any specific subtype. These findings suggest that obesity throughout adulthood and greater height may play a role in the etiology of NHL. While more recent obesity may impact immune function or levels of various hormones, height and BMI at age 18 may reflect early-life consequences of nutrition or exposure to growth hormones.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1826.
Abstract 1827: Ethnic differences in the association between body mass and risk of colorectal cancer in the multiethnic cohort
Authors: Lim Unhee , Nomura Abraham M. Y. , Wilkens Lynne R. , Marchand Loic Le , Monroe Kristine R. , Murphy Suzanne P. , Albright Cheryl L. , Henderson Brian E. , Kolonel Laurence N. 
Published: February 2011

Abstract
Introduction. Higher body mass has been associated with elevated risk of developing colorectal cancer. However, limited prospective data are available as to whether the association differs among ethnic groups with varying degrees of susceptibility for central obesity and obesity-related metabolic diseases. We investigated potential ethnic heterogeneity in the body mass-colorectal cancer association in the Multiethnic Cohort.
Methods. Baseline self-reported data were obtained on height, weight, physical activity, diet, and other risk factors from a population-based sample of over 96,810 men and 118,441 women in Hawaii and Los Angeles who were of Caucasian, African, Japanese, Latino, and Native Hawaiian ancestry and were 45-75 years old in 1993. By December 2006, 1,575 male and 1,316 female incident colorectal cancer cases were ascertained from linkage with SEER registries. The associations of interest were estimated by multivariable-adjusted Cox proportional hazards models with age as the time metric.
Results. Prevalence of obesity at baseline (body mass index (BMI) ≥ 30) ranged from 8% in Japanese to 36% in Native Hawaiian men and from 6% in Japanese to 35-37% in African American and Native Hawaiian women. Baseline BMI was positively associated with colorectal cancer risk in men (hazard ratio (HR) for BMI ≥ 30 compared with 18.5-22.9 = 1.50 (95% confidence interval: 1.32, 1.70)) and women (HR = 1.50 (1.33, 1.70)). When examined by sex and ethnicity, men of Caucasian (HR = 1.80 (1.36, 2.39)), African (HR = 2.17 (1.48, 3.16)), and Japanese (HR = 1.80 (1.44, 2.25)) ancestry showed a positive association, whereas Latino and Native Hawaiian men showed a null association (p-interaction = 0.11). In women, the association was strongest among Native Hawaiians (HR = 2.39 (1.24, 4.60)) and Japanese Americans (HR = 2.21 (1.75, 2.79)), followed by Latinas (HR = 1.67 (1.15, 2.41)) and Caucasians (HR = 1.38 (1.07, 1.77)), while it was null among African Americans (p-interaction = 0.12).
Conclusions. These findings from a large follow-up study of diverse ethnic make-up suggest sex- and ethnicity-related heterogeneity in the body mass-colorectal cancer association, which would be important to consider for understanding the etiology and identifying higher-risk groups for intervention.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1827.
Abstract 1835: Life Raft Group registry: An observational registry of gastrointestinal stromal tumor (GIST) patients
Authors: Call Jerry W. , Josephy P. D. , Eickhoff Jens , Pazmino Roberto , Sarnas Magda , Scherzer Norman J. 
Published: February 2011

Abstract
We report on an international observational registry of patients with Gastrointestinal Stromal Tumors (GIST). The Life Raft Group (LRG) registry contains information provided by its members since May 8, 2000. As participation is primarily via the internet some selection bias may occur, e.g., participation by younger patients may be higher. The median current age is 56.2 for females and 57.8 for males. The registry includes 1106 GIST patients, 536 females and 570 males. Mutational status was reported by 268 patients as follows. KIT: exon 11 = 156 pts (58%), exon 9 = 37 pts (14%), exon 13 = 4 (1.5%), unspecified exon = 2 (.7%); PDGFRA: unspecified exon = 1 (.4%), exon 12 = 2 (.7%), exon 14 = 1 (.4%); exon 18 = 12 (4.5%); wild-type = 49 (18%); SDH mutations = 4 (1.5%). Pediatric patients represented 2.6% of the registry. Wild-type patients had a lower median age at diagnosis (29.5 years) than other types, representing a high percentage of pediatric-type GIST patients in this series. Overall, 74% (199) of patients had a KIT mutation, 6% (16) had a PDGFRA mutation, 18% (49) were wild-type and 1.5% (4) had SDH mutations. The age at diagnosis distribution was different between males and females with a higher ratio of females to males diagnosed prior to age 35 (2.02 to 1), a lower ratio between age 35 to 70 (0.81 to 1) and about the same ratio in older patients, 70 and older (1.09 to 1). Overall, the ratio of females to males was 0.94 to 1. The median overall survival for all patients was 14.5 years for females and 8.8 years for males. A multivariate Cox proportional hazard model was used to evaluate the association between gender and overall survival. Age was included as a covariate. For age at diagnosis, the hazard ratio was 1.025 (P = &lt;0.001); for gender, the hazard ratio was 0.642 (P = &lt;0.001). In this observational registry, significant differences were noted between females and males; the ratio of females to males varied with age at diagnosis category and females had a significantly longer overall survival than males.Age at diagnosisAge CategoryFMGrand TotalF/M Ratio5-15166222.6715-20115162.2020-25136192.1725-302412362.0030-353118491.7235-403339720.8540-4552681200.7645-5070751450.9350-5576951710.8055-6069791480.8760-6547721190.6565-703947860.8370-751917361.1275-80811190.7380-856392.0085-90101 90-951121.00Unknown2016361.25Grand Total53657011060.94
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1835.