bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1749: Role of eIF3a in DNA repair and lung cancer chemo sensitivity
Authors: Yin Jiye , Dong Zizheng , Liu Zhaoqian , Zhang Jianting 
Published: July 2012

Abstract
Drug resistance is one of the major obstacles in successful chemotherapy of lung cancers. However, the mechanism of resistance is not yet clearly understood. Recently, eIF3a that plays an important role in translational control and regulation of gene expression was found to correlate negatively with prognosis in human cervical and esophageal cancers. We, thus, hypothesize that eIF3a may be an important factor in lung cancer response to chemotherapy by regulating the expression DNA repair proteins. Examination of 211 lung cancer tissue samples revealed that eIF3a expression negatively correlates with responses of the patients to cisplatin treatment. Ectopic over-expression or knockdown of eIF3a reduced or increased cellular resistance, respectively, to cisplatin, doxorubicine, and etoposide (VP-16) in cell lines as determined using MTT assay. Altering eIF3a expression also changed DNA repair activity as well as the expression of DNA repair proteins. We conclude that eIF3a possibly suppresses the synthesis of DNA repair proteins via translational control, which in turn contributes to the increased sensitivity to DNA-damaging anticancer drugs.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1749. doi:10.1158/1538-7445.AM2011-1749
Abstract 1888: HPV viral load and alcohol synergize to increase the risk of cervical intraepithelial neoplasia (CIN)1 in HPV positive women: Korean HPV Cohort Study
Authors: Kim Mi Kyung , Lee Sang Hoon , Min Kyung-Jin , Lee Jae Kwan 
Published: July 2012

Abstract
Purpose: To investigate the associations between alcohol and the risk of cervical intraepithelial neoplasia (CIN) and cervical cancer in women with high risk HPV-positive in the Korean HPV cohort study (KHPV).
Subjects and Methods: The KHPV recruited 1,243 women, aged 18-65 from March 2006 up to December 2009, including HPV-positive women with normal cytology (n=147), CIN1 (n=164), CIN2/3 (n=161) and cervical cancer (n=202). Detailed information on consumption of alcoholic beverages at baseline and on other lifestyle factors during lifetime was collected from questionnaires. Multinomial logistic analysis estimated the multivariate-adjusted odds ratio.
Results: Drinkers had an increased risk of CIN1 (OR = 2.16; 95% CI: 1.26 – 3.72) compared to nondrinkers, after adjusting for potential confounders. The amount of alcohol consumption (p for trend = 0.027), and the frequency of alcohol consumption (p for trend = 0.037) were significantly associated with the risk of CIN1. In addition, alcohol drinking had significant effects on the risk of CIN1 in the analyses adjusted for multivariables (OR=19.1, 95% CI=6.60-55.3, interaction p &lt;0.001). The relative excess risk due to interaction was 15.7, and the attributable proportion due to the interaction and synergy index were 0.71, and 3.89, respectively. No associations were found between alcohol drinking and CIN2/3 and cervical cancer.
Conclusion: Our data showed HPV and alcohol synergize to increase the risk of CIN1 among high-risk HPV-positive women.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1888. doi:10.1158/1538-7445.AM2011-1888
Abstract 1889: Helicobacter pylori seropositivity and risk of lung cancer
Authors: Koshiol Jill , Flores Roberto , Lam Tram , Taylor Philip R. , Weinstein Stephanie , Virtamo Jarmo , Albanes Demetrius , Perez-Perez Guillermo , Caporaso Neil E. , Blaser Martin J. 
Published: July 2012

Abstract
BACKGROUND: Lung cancer is the leading cause of cancer mortality worldwide. Infections may contribute to lung carcinogenesis. Results from a few small studies have suggested that Helicobacter pylori (HP) may be a potential risk factor. However, these studies have been limited in size and in the evaluation of lung cancer histology and smoking.
METHODS: We conducted a study of 350 lung adenocarcinoma cases, 350 squamous cell carcinoma cases, and 700 controls nested within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC) cohort of male Finnish smokers. Controls were 1 to 1 matched by age (+/- 5 years) at and date (+/- 30 days) of baseline serum draw and had to be alive and cancer free at the date that the corresponding case was diagnosed. We used enzyme linked immunosorbent assays to detect immunoglobulin G antibodies against HP whole-cell and CagA antigens and calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) for associations between HP seropositivity and lung cancer risk using conditional logistic regression.
RESULTS: 79% of cases and 78% of controls were seropositive for whole cell HP, and 43% of cases and 44% of controls were seropositive for the cytotoxin-associated gene (cagA) antigen. Whole cell seropositivity was not associated with lung adenocarcinoma (OR: 1.2, 95% CI: 0.80-1.8) or squamous cell carcinoma (OR: 1.1, 95% CI: 0.73-1.6) after adjusting for age at serum draw, date of serum draw, age at smoking initiation, pack-years, and cigarettes smoked per day. Similarly, CagA seropositivity was not associated with lung adenocarcinoma (OR: 1.1, 95% CI: 0.78-1.5) or squamous cell carcinoma (OR: 0.88, 95% CI: 0.63-1.2).
CONCLUSIONS: Despite earlier small studies suggesting that HP may contribute to lung carcinogenesis, HP seropositivity does not appear to be associated with lung cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1889. doi:10.1158/1538-7445.AM2011-1889
Abstract 1908: Meta-analysis of prospective epidemiologic studies of red meat intake and colorectal cancer
Authors: Alexander Dominik D. , Cushing Colleen A. , Perez Vanessa , Weed Douglas L. 
Published: July 2012

Abstract
Background: The relationship between red meat consumption and colorectal cancer (CRC) has been the subject of scientific debate. Objective: To estimate the summary association between red meat intake and CRC and to examine sources of heterogeneity, a meta-analysis of prospective studies was conducted. Design: Thirty-four prospective studies of red meat and CRC were identified, of which, 25 represented independent non-overlapping study populations. Summary relative risk estimates (SRREs) for high vs. low intake and dose-response relationships were calculated. Results: In the high vs. low intake meta-analysis, the SRRE was 1.12 (95% CI: 1.04-1.21) with significant heterogeneity (p = 0.014). Summary associations were modified by tumor site and gender. The SRREs for colon cancer and rectal cancer were 1.11 (95% CI: 1.03-1.19) and 1.19 (95% CI: 0.97-1.46), respectively. The SRREs among men and women were 1.21 (95% CI: 1.04-1.42) and 1.01 (95% CI: 0.87-1.17), respectively. Conclusions: The available epidemiologic data are not sufficient to support an independent and unequivocal positive association between red meat intake and CRC. This conclusion is based upon summary associations that are weak in magnitude, heterogeneity across studies, inconsistent patterns of associations across the sub-group analyses, and the likely influence of confounding by other dietary and lifestyle factors.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1908. doi:10.1158/1538-7445.AM2011-1908
Abstract 1911: Dietary intake of riboflavin and risk of lung cancer among non-smokers: A prospective cohort study among Chinese women
Authors: Cai Qiuyin , Beeghly-Fadiel Alicia , Shrubsole Martha J. , Shu Xiao-Ou , Yang Gong , Ji Bu-Tian , Li Honglan , Chow Wong-Ho , Gao Yu-Tang , Zheng Wei 
Published: July 2012

Abstract
Lung cancer is the leading cause of cancer death in the United States and many other countries. A significant subset of lung cancers is not associated with smoking, and risk factors for these cancers remain unclear. Riboflavin (vitamin B2), a water-soluble vitamin, is involved in vital metabolic processes and is necessary for normal cell function, growth, and energy production. Riboflavin is the central component of the flavin mononucleotide (FMN) and flavin dinucleotide (FAD), coenzymes for a wide variety of oxidative enzymes. We prospectively examined the association of dietary intake of riboflavin with lung cancer risk in the Shanghai Women's Health Study cohort. A total of 73,237 women aged 40-70 years and free of cancer at enrollment were included in this analysis. Usual dietary intake was assessed at baseline (1997-2000) through in-person interviews by using a validated food-frequency questionnaire. We used Cox proportional hazards regression to estimate the relative risks (RR) and 95% confidence intervals (CI) for the association of lung cancer risk with dietary riboflavin consumption. In 665,554 person-years of follow-up, we identified 328 lung cancer cases, of which 303 were non-smokers. Dietary intake of riboflavin was inversely associated with lung cancer risk. The RRs (95% CI) of developing lung cancer among non-smokers decreased with increasing quintiles of riboflavin intake (P for trend = 0.007) from 1.0 to 1.01 (0.73-1.42), 0.77 (0.53-1.13), 0.81 (0.55-1.20), and 0.51 (0.31-0.83) for the lowest to highest quintiles. Exclusion of 51 cases diagnosed within two years of follow-up did not change the HR estimations appreciably. Further, adjusting for dietary intakes of other B vitamins (B1, B6, B12, niacin, and folate) and methionine did not meaningfully affect the HR estimates. No statistically significant associations were found for other B vitamins. In summary, our findings among non-smoking Chinese women suggest that dietary intake of riboflavin may reduce the risk of lung cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1911. doi:10.1158/1538-7445.AM2011-1911
Abstract 1914: Consumption of Lake Ontario sport fish and prostate cancer incidence in the New York State Angler Cohort Study (NYSACS)
Authors: Green Joseph W. , Mu Lina , Swanson Mya , Mix Jacqueline , Bonner Matthew R. 
Published: July 2012

Abstract
Fish from the Great Lakes are an important source of exposure to persistent organic pollutants, including polychlorinated biphenyls (PCBs) and organochlorine pesticides (e.g., Mirex and DDT). Some of these pollutants are hypothesized to be hormonally active and therefore may increase the risk of prostate cancer. Conversely, fish are also a source of micro- and macro-nutrients hypothesized to have chemopreventive properties. We investigated the consumption of sport-caught fish from Lake Ontario and the incidence of prostate cancer in the NYSACS, a prospective cohort of 17,110 anglers and their spouses aged 18 to 40 years old at enrollment. Participants completed a mailed self-administered questionnaire upon enrollment in 1991. Demographic factors, smoking history and selected potential confounders were ascertained. The questionnaire also queried for the number of years that fish from Lakes Ontario and Erie were consumed as well as the preparation and cooking practices for sport caught fish. As of December 31, 2008 fifty-eight first primary incident prostate cancers were identified via the New York State Cancer Registry. Vital status was determined by linkage with the Social Security Administration Death file. Of the 10,436 males enrolled at baseline, 10% (n=1,075) were lost to follow-up. Fish consumption was dichotomized into never vs. ever. Duration of consumption was categorized into tertiles based on the distribution among the cases who reported eating L Ontario sport caught fish. Poisson regression was used to calculate rate ratios (RR) and 95% confidence intervals, adjusting for age, education and pack-years of smoking. Ever eating Lake Ontario fish was inversely associated with prostate cancer incidence (RRadjusted=0.5 (95% CI=0.3-0.9)) compared with never consumers. In addition, we found a suggestion of an inverse association with increasing duration of L. Ontario fish consumption (non-eaters RR = 1.0 (ref); 1st tertile RR = 0.6 (95% CI = 0.3-1.3); 2nd tertile RR = 0.4 (95% CI = 0.2-1.0); 3rd tertile RR = 0.5 (95% CI = 0.2-1.0); although the exposure-response gradient was neither monotonic nor significant (ptrend = 0.157). The exposure-response gradients were similar when consumption was lagged 5- and 10-years (5-year lag ptrend = 0.289; 10-year ptrend = 0.269). While interpretation is complicated by a lack of information on family history of prostate cancer, and a small number of cases, these preliminary results are suggestive of an inverse association between Lake Ontario fish consumption and prostate cancer risk.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1914. doi:10.1158/1538-7445.AM2011-1914
Abstract 1918: Type 2 diabetes mellitus and colorectal neoplasia risk in Puerto Rican Hispanics: A case-control study
Authors: Diaz-Algorri Yaritza , Gonzalez Dilka , Lozada Maria E. , Hernandez Jessica , Pedrosa Carmen , Toro Doris H. , Cruz-Correa Marcia 
Published: July 2012

Abstract
Background: Epidemiological studies have provided inconclusive evidence regarding the potential link between type 2 diabetes mellitus (DM) and colorectal cancer (CRC).The association between type 2 DM and colorectal neoplasia (colorectal cancer and/or adenomas) has not been well studied in Hispanics, an ethnic minority at high risk for type 2 DM.
Objective: To evaluate the association between type 2 DM and colorectal neoplasia (CRN) in Puerto Rican Hispanic adults enrolled in the studies Epidemiology of Loss of Imprinting in Colorectal Cancer, Familial Colorectal Cancer Registry and the Type 2 diabetes mellitus and colorectal neoplasia risk in Hispanics: A case-control study at the VA Caribbean Healthcare System.
Methods: The case-control study included patients with incident CRN and controls with negative colonoscopy and without previous history of CRC or adenomas evaluated from January 1, 2005 to December 31, 2009. Diagnosis of type 2 DM was established by previous medical diagnosis and/or anti-diabetic medications use. Unconditional logistic regression was employed to estimate the odds ratio (OR) between type 2 DM and CRN using STATA 10.0.
Results: A total of 422 participants (mean age 60.8 ± 12.1 yrs., 61.1% males), prevalence of type 2 DM was 26.3%. 276 patients with CRN and 146 controls were evaluated. In the cases, the prevalence of colorectal adenomas was 25.4% (70/276) and the prevalence of colorectal cancer was 74.6% (206/276). Colorectal neoplasia were mostly adenocarcinomas (60.4%), located in the distal colon (37.3%), and with TNM stage III (21.4%). Cases were mostly men (p=0.01), had lower education (p&lt;0.001) and reported lower use of aspirin (p=0.02) compared to the controls. Cases and controls did not differ by median age (p=0.52), first degree of family history of CRC (p=0.27), first degree of family history of DM (p=0.33) or obesity (p=0.73). There were no statistical significant associations between DM and CRN (OR=1.41; 95% CI: 0.74-2.68), DM and CRC (OR=1.70; 95% CI: 0.74-3.87) or DM and colorectal adenomas (OR=1.04; 95% CI: 0.45-2.42) after adjusting for gender, age, education, aspirin use, obesity and study center.
Conclusion: We did not observe a statistical significant association between type 2 DM and CRN. Nonetheless, a tendency towards an increase risk of colorectal neoplasia was observed among type 2 DM patients on adjusted analysis. Possible explanation for our lack of association may be related to high prevalence of type 2 DM in cases and controls and/or the high prevalence of obesity in the study sample.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1918. doi:10.1158/1538-7445.AM2011-1918
Abstract 1921: Body fatness and sex steroid hormone concentrations in US men – Results from NHANES III
Authors: Rohrmann Sabine , Shiels Meredith S. , Lopez David S. , Rifai Nader , Nelson William G. , Kanarek Norma , Guallar Eliseo , Menke Andy , Joshu Corinne E. , Feinlieb Manning , Sutcliffe Siobhan , Platz Elizabeth A. 
Published: July 2012

Abstract
Background: Obesity is associated with a variety of chronic diseases, including cancer, which may partly be explained by its influence on sex steroid hormone concentrations. However, different measures of obesity are not equally strongly associated with the risk of these diseases, and, thus, might also differently influence circulating levels of sex steroid hormones.
Objective: To estimate and compare the associations of body mass index (BMI), waist circumference, and percent body fat with circulating sex steroid hormone levels.
Methods: In our analysis, we included 1,256 men, aged 20+ years, who attended the morning examination session of the Third National Health and Nutrition Examination Survey (NHANES III; 1988-1991). Serum hormones were measured by immunoassay. Weight, height, and waist circumference were measured by trained staff. Percent body fat was estimated from bioelectrical impedance. Linear regression was used to estimate associations between body fatness measures and hormone levels adjusting for age, race/ethnicity, previously identified correlates of hormone levels, and the other hormones.
Results. Total and free testosterone and sex hormone binding globulin (SHBG) concentrations decreased with increasing BMI, waist circumference, and percent body fat (all p-trend &lt;0.05), whereas total and free estradiol increased with increasing measures of body fatness (all p-trend &lt;0.05). The magnitude of change in any one of these hormones was similar for a one quartile increase in each body fatness measure.
Conclusions: Measured BMI, waist circumference, and percent body fat led to similar inferences about the association between body fatness and hormone levels in men.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1921. doi:10.1158/1538-7445.AM2011-1921
Abstract 2003: Role of de novo DNMTs in carcinogen induced transformation of human bronchial epithelial cells
Authors: Teneng Ivo , Tellez Carmen S. , Belinsky Steven A. 
Published: July 2012

Abstract
Malignant tumors and cell lines are characterized by increased expression of DNMT3a and 3b. While evidence suggests that DNMT1, 3a and 3b co-operate in methylation and gene silencing during carcinogenesis, very little is known about targets for DNMT3a and 3b or their impact on the development of adenocarcinoma. We developed an in vitro model using human telomerase /cyclin dependent kinase 4 -immortalized human bronchial epithelial cell lines (HBECs) to identify key molecular changes that drive transformation and clonal outgrowth of preneoplastic lung epithelial cells during exposure to tobacco carcinogens. Carcinogen exposure (0.5µM MNU and 0.05µM BPDE) for 12 weeks induced transformation of HBEC1 and HBEC2 cells and transformation efficiency was associated with DNA repair capacity. A significant increase in DNMT1 protein was observed during carcinogen exposure while moderate increases in DNMT3a and 3b were observed in transformed cells. Increased DNMT3a and 3b levels have been reported in several cancers. We observed 5-20 fold increased expression of DNMT3a and 3b in tumor derived lung cancer cell lines. Therefore we tested the hypothesis that over expressing DNMT3a and 3b would accelerate transformation by targeting specific genes for methylation and promote full malignancy in carcinogen-treated HBECs. HBEC1 and HBEC2 clones that expressed DNMT3a or 3b at levels comparable to those observed in tumor derived cell lines were isolated, expanded and characterized. Over expression of DNMT3a or 3b had no effect on DNA repair capacity, did not affect DNMT1 expression and was not sufficient to drive transformation as evidenced by inability to form colonies on soft agar. Two clones from each cell line over expressing DNMT3a or 3b were treated with carcinogen for one hour, once a week for 12 weeks and analyzed for transformation on soft agar. Studies completed for HBEC1 indicate that expression of DNMT3b increases transformation efficiency. Soft agar analyses for HBEC2 clones are on going. Further studies will characterize the mechanism for increased transformation by examining reprogramming of the epigenome and tumorigenicity of transformed cells in xenografts
This study was supported by R01 ES008801.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2003. doi:10.1158/1538-7445.AM2011-2003
Abstract 202: Endogenous c-jun inhibits mammary epithelial cellular apoptosis in vivo
Authors: Katiyar Sanjay , Casimiro Mathew , Dettin Luis , Ju Xiaoming , Wagner Erwin , Tanaka Hirokazu , Pestell Richard 
Published: July 2012

Abstract
c-jun, which is overexpressed in a number of human cancers encodes a critical component of the AP-1 complex. c-jun has been shown to either induce or inhibit cellular apoptosis. Germ line deletion of both c-jun alleles is embryonically lethal. To determine the role of the endogenous c-jun gene in apoptosis, we performed mammary epithelial cell-targeted somatic deletion using floxed c-jun (c-jun f/f) conditional knockout mice. Laser capture microdissection demonstrated endogenous c-jun inhibits expression of apoptosis inducing genes and reactive oxygen species (ROS)-reducing genes (MnSOD, catalase). ROS have been implicated in apoptosis and undergo enzymatic elimination via MnSOD and CuZnSOD with further detoxification via catalase. c-jun-mediated survival was in part dependent on ROS production. c-jun-mediated repression of MnSOD and catalase occurred via mitochondrial complex I and NOX I. Collectively, these studies define a pivotal role of endogenous c-jun in promoting cell survival via maintaining mitochondrial integrity and expression of the key regulators of ROS production.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 202. doi:10.1158/1538-7445.AM2011-202