bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A64: Effects of genetic polymorphisms of innate immunity genes on the noncardia gastric cancer risk
Authors: Kim Jeongseon , Cho Young Ae , Choi Il-Ju , Cho Soo-Jeong , Kim Chan Gyoo , Lee Jong Yeul , Kim Young-Woo 
Published: June 2012

Abstract
Background and Objective: Increasing evidence suggests that polymorphisms in innate immunity genes are associated with Helicobacter pylori (H. pylori)-induced inflammation and may influence susceptibility to developing noncardia gastric cancer. Therefore, we investigated the effect of polymorphisms of TLR2, TLR4, and CD14, their combination and interaction with environmental factors on the noncardia gastric cancer risk in a Korean population.
Methods: We genotyped four polymorphisms in three genes (TLR2, rs1898830 A&gt;G; TLR4, rs10759932 T&gt;C, rs10983755 A&gt;G; CD14, rs2569190 T&gt;C) in a case-control study of 487 noncardia gastric cancer patients and 487 sex- and age-matched healthy controls. Multiple logistic regression models were used to detect the effects of genetic polymorphisms and environmental factors, which was stratified by the histological type of gastric cancer.
Results: TLR4 rs10983755 variant allele carriers were found to have a higher risk of intestinal type gastric cancer than homozygous wild-type carriers (OR [95% CI] = 1.40 [1.01–1.96], P = 0.046). Other genetic variants did not show any association with noncardia gastric cancer risk. When we examined the combined effect with other polymorphisms, the increased risk of intestinal type gastric cancer among TLR4 rs10983755 variant allele carriers compared to wild-type homozygous carriers were observed only among homozygous wild-type carriers of TLR2 rs1898830 (OR [95% CI] = 1.97 [1.24–3.12], P = 0.004) or CD14 rs2569190 (OR [95% CI] = 1.95 [1.31–2.91], P = 0.001). In addition, the effect of TLR4 rs10983755 variant allele on intestinal type gastric cancer was stronger among H. pylori-positive participants who are under 55 years old, smoke tobacco and drink alcoholic beverages.
Conclusion: These results suggest that the genetic polymorphisms of these innate immunity genes are associated with the development of H. pylori-associated noncardia gastric cancer.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):A64.
Abstract B15: Distribution of HPV genotypes in cervical intraepithelial lesions and cervical cancer in Tanzanian women
Authors: Vidal Adriana , Murphy Susan K. , Hernandez Brenda , Oneko Olola , Overcash Francine , Hoyo Cathrine 
Published: June 2012

Abstract
Context: Cervical cancer incidence is four times higher in eastern and southern Africa than in North America and Europe. Infection with human papillomavirus (HPV) is associated with low-grade (LGSIL) and high-grade (HGSIL) intraepithelial lesions of the uterine cervix, and high-risk (HR) HPV DNA is detected in almost all invasive cervical cancers (ICC). Although vaccine development will rely on knowledge of HPV genotypes characteristic in HSIL, LSIL and cancer in different populations, these genotypes remain uncharacterized in African populations.
Objective: To describe HPV genotype distribution in women living in Northeastern Tanzania.
Methods: 215 study participants were recruited from the Reproductive Health Clinic at Kilimanjaro Christian Medical Center (KCMC). Cervical scrapes were used to grade cervical intraepithelial neoplasia (CIN). These specimens were used to detect HPV infection for 60 genotypes. Proportions were determined and ranked.
Results: Of 215 women identified from the KCMC, 79 (36.7%) were HPV-positive (20 had no evidence of cytological abnormality, 12 had CIN1, 14 had CIN2–3, and 33 had cervical cancer). Overall, 31 HPV genotypes were detected, and multiple HPV infections were more common than single infections in CIN and ICC. The prevalence of HPV infection increased with lesion grade (14% in controls, 66% in CIN1 cases, 87% in CIN2/3 and 89% in ICC). Whereas in ICC, the three most common genotypes were HPV16, 35/45/6, and 18/73, the most common genotypes in CIN2–3 were HPV53, 58 and 84/83, and in CIN1 they were HPV35, 45, 53/58/59. Among controls, the most prevalent genotype was HPV58 with HPV 16, 35, 52, 66 and 73 occurring equally. Restricting analyses to HIV-negative women revealed that HR-HPV genotypes are most frequent in ICC.
Conclusions: While small sample size limits interpretation, these findings suggest HPV genotypes other than 16 and 18 may drive cervical cancer risk in this region. The low frequency or absence of HPV 16 and 18 in CIN1 or CIN2–3 has implications for current cytology and HPV-based screening as well as for vaccine development for this region. Larger studies are required.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B15.
Abstract B2: Effects of individual and combined diet and exercise intervention in postmenopausal women on adiponectin and leptin
Authors: Abbenhardt Clare , Potter John D. , Mason Caitlin E. , Xiao Liren , Blackburn George L. , Bain Carolyn , Ulrich Cornelia M. , McTiernan Anne , Campbell Kristin L. , Alfano Catherine M. , Wener Mark H. , Duggan Catherine , Foster-Schubert Karen E. , Kong Angela 
Published: June 2012

Abstract
Introduction: Obesity and sedentary lifestyles are modifiable risk factors for several chronic diseases. Adiponectin and leptin play central roles in energy balance, insulin homeostasis and lipid/glucose metabolism. We examined the individual and combined effects of dietary weight loss and/or exercise on serum adiponectin and leptin concentrations.
Methods: We conducted a 12-month randomized controlled trial in 439 overweight/obese postmenopausal women to examine biomarkers of breast cancer risk. Participants were randomly assigned to dietary weight loss (D) (N=118), moderate-to-vigorous intensity aerobic exercise (E), 225 minutes/week (N=117), combined diet + exercise (D+E) (N=117), or control (N=87). Blood samples were taken at baseline and 12 months follow-up. Changes in adiponectin and leptin were measured via radioimmunoassay.
Results: Adiponectin increased significantly over the intervention period in the D+E (+6.6%; p=.0001) and D group (+9.5%; p&lt;.0001), compared to controls (−0.4%). No statistically significant adiponectin changes were observed in the E intervention. In all intervention groups leptin decreased significantly compared to controls (D+E −40.1% p&lt;.0001; D −27.1% p&lt;.0001; E −12.1% p=0.005). When stratified by baseline BMI, we observed slightly stronger increases in adiponectin among those with BMI ≥ 30kg/m2 in the D+E intervention. Changes in leptin with the intervention were equally strong independent of baseline BMI. With increasing weight loss, adiponectin increased independent of the intervention group (D, D+E or E).
Conclusion: Our study showed that a dietary weight-loss intervention had strong effects on adiponectin levels, independent of exercise. We also observed that lifestyle interventions associated with weight loss, are successful in reducing serum leptin concentrations.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B2.
Abstract B32: Interactive, automated phone outreach encourages health plan members to have recommended mammograms and leads to early breast cancer detection
Authors: Freeman Lisa , Powers Janet 
Published: June 2012

Abstract
Background: Interactive, automated phone calls let health plans have timely, relevant conversations with their members about key health topics. This channel is effective in widely reaching individuals of all ages and socio-demographic categories and can offer several language alternatives. In one program multiple goals can be achieved –sharing health information, determining planned behavior, assessing and addressing barriers, and increasing engagement.
Objective/purpose: As a way to increase key quality ratings, health plans reach out to eligible members to encourage them to have their age-appropriate screenings. This communication is designed to provide health plans with a better understanding of screening barriers and how to address these issues. A parallel goal is earlier detection of breast cancer diagnoses among members. Designed as an engaging conversation, this outreach also increases members' satisfaction and loyalty to their health plan.
Methods: This program used proprietary interactive voice recognition technology and communication expertise to develop an interaction aimed at reminding members of the importance of having their mammogram.
Results: The outreach determined that 85% (3,068) of all members contacted planned to schedule their mammogram. After conducting outcomes analysis, based on claims data, 19% (597) of the members who said that they planned to have their mammogram screened positive for breast cancer and received treatment.
Discussion/Conclusions: The ultimate goal of this outreach is to engage women in their health and increase the number who speak with their doctor and have a mammogram. While additional analysis is still being conducted, it can be determined that interactive, automated outreach is an effective method to breast cancer early detection and prevention.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B32.
Abstract B41: A mouse model for inflammation-driven lung tumorigenesis
Authors: Melkamu Tamene , Qian Xuemin , O'Sullivan Gerry , Kassie Fekadu 
Published: June 2012

Abstract
The link between chronic inflammation and cancer development has lately gained extensive epidemiological and experimental support, particularly in organs like liver, stomach, colon, and lung. Although experimental models are available to study inflammation-driven tumorigenesis in the liver, stomach, and colon, no such models are available for lung cancer. Therefore, the objective of the present study is to develop a model for inflammation-driven lung tumorigenesis. A/J mice received four intraperitoneal injections (two doses/week) of the tobacco smoke carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) at a dose level of 50 mg/kg body weight. Beginning one week after the last dose of NNK, the mice were given weekly intranasal instillations of lipopolysaccharide (LPS, 10ug/mouse), a potent inflammation-inducing agent, until the end of the study at week 27. Upon termination of the study, tumors on the surface of the lung were counted, their size determined and histopathologically analyzed. Moreover, we analyzed alterations in the expression of inflammation- and tumorigenesis-related proteins and microRNAs (miRs) by Western immunoblotting and qRT-PCR, respectively. Chronic exposure NNK-treated mice to LPS increased the number and size of lung tumors (47.3 ± 11 tumors/mouse for the NNK plus LPS group versus 28 ± 8 tumors/mouse in the NNK only group).
Furthermore, lung tumors in the NNK plus LPS treated mice were significantly larger than the lung tumors of the mice challenged with NNK alone.
Multiplicities of lung tumors in LPS-treated mice were similar to those mice given the vehicle. Multiplicities of the histopathological lesions pulmonary hyperplastic foci, adenoma, adenoma with dysplasia and adenocarcinoma in the NNK only group were 3.0 ± 1.2, 7.1 ± 2.9, 1.3 ± 1.1, and 0.3 ± 0.5/mouse, respectively. The corresponding frequencies of the lesions in the NNK plus LPS group were 3.1 ± 1.8, 11.8 ± 5.2, 3.9 ± 1.8, and 0.6 ± 0.7/mouse. Western immunoblotting studies showed that LPS exposure of NNK-treated mice enhanced activation of NF-kappaB, STAT3, and Akt but caused down-regulation of the tumor suppressor protein PTEN. Further, analyses of levels of five carcinogenesis-related microRNAs (miR-21, miR-146a, miR-150, miR-155 and miR-21, and miR-181b-1) showed increases in the expressions of miR-155 and miR-21. Levels of miR-155 and miR-21 were increased by 2.3-fold and 1.9-fold, respectively, in mice treated with NNK plus LPS group as compared to mice treated with NNK. Moreover, levels of miR-155 and miR-21 were increased by 10.5-fold and 4.7-fold, respectively, in LPS treated mice compared to vehicle-treated mice. In summary, our results demonstrate that LPS-induced chronic lung inflammation enhances lung tumorigenesis. This model could be a vey useful tool to understand the role inflammation in lung tumorigenesis and for identification of anti-inflammatory and lung cancer chemopreventive agents.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B41.
Abstract B42: Lack of chemopreventive effects of metformin in azoxymethane-induced rat colon carcinogenesis
Authors: Rao Chinthalapally V. , Janakiram Naveena B. , Mohammed Altaf , Madka Venkateshwar , Qian Li , Brewer Misty , Duff Ashley , Zhang Yuting , Steele Vernon E. 
Published: June 2012

Abstract
Metformin, an insulin-lowering agent, has been associated with decreased cancer risk in epidemiologic studies in diabetic patients. Short-term preclinical and clinical observations also supported inhibition of colonic precancerous lesions. However, recent meta-analysis studies show that metformin or related drugs may reduce risk of pancreatic and hepatocellular carcinoma but a non-significant inverse correlation with colon cancer risk. The present study explores a systematic analysis of chemopreventive efficacies of metformin on a well established model of colon carcinogenesis, using colonic preneoplastic lesions and adenocarcinomas as end points. Effect of dietary metformin (100 ppm, 400 ppm, 800 ppm to 1,600 ppm) on AOM-induced aberrant crypt foci (ACF) development; and a dietary metformin (500 ppm and 1,000 ppm) on AOM-induced colon adenocarcinoma was studied in F344 rats. ACF and tumor efficacy endpoints were carried out on AOM-treated 8-week-old rats (48 per group) fed the control AIN-76A diet. Either three days (ACF Study) or 4 weeks (adenocarcinoma study) after carcinogen treatment, rats were fed the diets containing different doses of metformin. ACF and colon adenocarcinomas were determined at 8 and 48 weeks after AOM-treatment, respectively. Dietary metformin at 100 and 400 ppm had no significant effect on the colonic ACF formation; whereas at higher doses a significant increase was observed in the total ACF (37%) and multicrypt ACF by 43%. In long term bioassay, dietary metformin at 500 and 1,000 ppm had no significant effect on adenocarcinoma incidence. With regard to colon adenocarcinoma multiplicity, metformin at both dose levels failed to provide any inhibitory effect, albeit, modest increase (∼20%) in adenocarcinoma multiplicity at high dose level was seen. Similarly, dietary metformin fail to show any inhibitory effect on colon tumor volume. Rats that were fed with metformin fail to show significant effects on markers of cell proliferation and apoptosis in colonic tumors. These observations show, for the first time, that metformin tested at different dose levels does not provide chemopreventive effects at the preneoplastic lesion stage or at adenocarcinoma stages in a well-established rat colon cancer model. Further studies are warranted to understand the discrepancies between preclinical models and more so in human clinical observations on the potential beneficial effects of metformin for colon cancer risk.
{This work is supported by NCI-N01 CN-53300}
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B42.
Abstract B51: Genetic variation in nucleotide excision repair pathway genes, pesticide exposure, and prostate cancer risk
Authors: Barry Kathryn Hughes , Zheng Tongzhang , Alavanja Michael CR , Berndt Sonja I. , Koutros Stella , Andreotti Gabriella , Sandler Dale P. , Burdette Laurie A. , Yeager Meredith , Freeman Laura E. Beane , Lubin Jay H. , Ma Xiaomei 
Published: June 2012

Abstract
Introduction: Previous research has demonstrated increased prostate cancer risk for pesticide applicators and pesticide manufacturing workers. Although underlying mechanisms are unknown, human biomonitoring studies indicate increased genetic damage with pesticide exposure. Given that the nucleotide excision repair (NER) pathway repairs a broad range of DNA damage, we evaluated interactions between pesticide use and 324 single nucleotide polymorphisms (SNPs) tagging 27 NER genes among 776 prostate cancer cases and 1,444 male controls in a nested case-control study of white pesticide applicators in the Agricultural Health Study, a prospective cohort of pesticide applicators in Iowa and North Carolina.
Methods: We used likelihood ratio tests from logistic regression models to determine P-values for interactions between three-level pesticide variables (none/low/high) based on lifetime days of use weighted to an intensity score and SNPs (assuming a dominant model). We employed the False Discovery Rate (FDR) method to adjust for multiple comparisons.
Results: Of the seventeen interactions that met FDR&lt;0.2, three also displayed a monotonic increase in prostate cancer risk with increasing pesticide use in one genotype group and no significant association in the other group. Men carrying the variant A allele at ERCC1 rs2298881 exhibited increased prostate cancer risk with high versus no fonofos use (Odds Ratio (OR): 2.98; 95% Confidence Interval (CI): 1.65–5.39; Pinteract=3.6×10–4; FDR-adjusted P=0.11). Men carrying the homozygous wild-type TT genotype at two correlated CDK7 SNPs, rs11744596 and rs2932778 (r2=1.0), exhibited increased prostate cancer risk with high versus no carbofuran use (OR: 2.01; 95% CI: 1.31–3.10 for rs11744596; Pinteract=7.2×10–4; FDR-adjusted P=0.09). In contrast, we did not observe associations with prostate cancer among men with other genotypes at these loci.
Conclusions: While requiring replication, our findings suggest a role for NER genetic variation in pesticide-associated prostate cancer risk.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B51.
Abstract B54: Reproductive status at first diagnosis influences risk of radiation-induced second primary contralateral breast cancer in The WECARE Study
Authors: Brooks Jennifer D. , Thomas Duncan C. , Haile Robert W. , Smith Susan A. , Capanu Marinela , Bernstein Jonine L. , Shore Roy E. , Boice John D. , Stovall Marilyn , Reiner Anne S. , Bernstein Leslie , John Esther M. , Lynch Charles F. , Mellemkjaer Lene , Knight Julia A. 
Published: June 2012

Abstract
The breast undergoes changes in composition, function and hormonal milieu during puberty, pregnancy, lactation and postmenopausal involution. These changes may influence the susceptibility of the breast to carcinogens, including exposure to ionizing radiation.
The Women's Environmental, Cancer and Radiation Epidemiology (WECARE) Study is a multi-center, population-based, case-control study of 708 women (cases) with asynchronous contralateral breast cancer (CBC) and 1,399 women (controls) with unilateral breast cancer (UBC). Radiation therapy (RT) records were used to reconstruct the radiation dose to the location in the contralateral breast where the second cancer arose (or to the equivalent breast location for UBC controls). Rate ratios (RR) and 95% confidence intervals (CI) were computed to assess the relationship between reproductive status at first breast cancer diagnosis, RT and risk of CBC, adjusting for known breast cancer risk factors: age at (first) diagnosis, menopausal status/age at menopause at first diagnosis, age at menarche, number of full-term pregnancies, first degree family history of breast cancer, histology and stage of first primary breast cancer, and treatment (chemotherapy/hormonal therapy).
Women who were nulliparous at first diagnosis and exposed to ≥1 gray (Gy) to the contralateral breast, had a higher risk of CBC than unexposed nulliparous women (RR=2.2, 95% CI 1.2–4.0). An increased risk was not seen in RT exposed parous women (RR=1.1, 95% CI 0.8–1.4). Women treated with RT who later became pregnant had a greater risk of CBC compared with unexposed women who also became pregnant (RR=6.0, 95% CI 1.3, 28.4), though these results were based on small numbers. The effect of radiation on risk of CBC did not vary by number of pregnancies, history of breast feeding or menopausal status at the time of first breast cancer diagnosis.
These results suggest that RT may be associated with an increased risk of developing a second breast cancer in nulliparous but not parous women.
Women who become pregnant after first breast cancer diagnosis may also be at an increased risk of CBC. It is possible that RT could be the initiating event, leading to preneoplastic cellular changes that are then promoted by the hormonal changes of a subsequent pregnancy.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B54.
Abstract B62: Differential influence of vitamin D on the tumor promoting eicosanoid PGE 2
Authors: Qin Wenyi , Dahlman Julie , Rebecca Lessard , Sauter Edward 
Published: June 2012

Abstract
Numerous lines of evidence point to the tumor promoting properties of prostaglandin (PG)E2. Preclinical studies have demonstrated the ability of both vitamin D (vitD) and celecoxib to downregulate the ecisanoid. We hypothesized that the two agents would work synergistically. The purpose of the study was to determine the dose dependent effects of vitD, with or without celecoxib. 24 women were prospectively enrolled and randomized in double blind fashion for one month (postmenopausal) or one menstrual cycle (premenopausal) to one of four daily treatment regimens: placebo, 400 IU vitD, 2000 IU vitD, or 2000 IU vitD + 400 mg celecoxib. Breast nipple aspirate fluid (NAF) and serum were collected. Both breast specific and systemic levels of PGE2 were measured. There was a significant dose dependent increase in 25(OH)D levels (p&lt;.01). The post-treatment levels of NAF (but not serum) PGE2 were lower and the decrease greater in the 2000 IU vitD than in the other groups (p&lt;.05) of normal risk women. A similar effect was not observed in women at increased breast cancer risk, nor in women receiving vitD + celecoxib. These findings suggest the potential of vitamin D, given in adequate dose, at lowering a key cancer promoting enzyme in women of normal breast cancer risk.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):B62.