bluuebunny/crossref_metadata_2025_split huggingface dataset:
No Association Between EGF Gene Polymorphism and Gastric Cancer
Authors: Goto Yasuyuki , Ando Takafumi , Goto Hidemi , Hamajima Nobuyuki 
Published: March 2006

Abstract
The etiology of gastric cancer is not well-understood. Epidermal growth factor (EGF) transduces growth signals to mitogen-activated protein kinase via RAS and BRAF, and EGF/EGF receptor interaction is important for tumor growth and progression. Previous studies have reported that the EGF +61 (A/G) single nucleotide polymorphism in the 5′-untranslated region of the EGF gene is functional, and is associated with gastric cancer and various malignancy. Individuals with the EGF A/A genotype produce less EGF than individuals with G/G or G/A. We investigated a single nucleotide polymorphism at exon 1 of EGF, named rs4444903 in NCI dbSNP, in 454 Japanese subjects undergoing a health checkup and 202 patients with gastric cancer. Genotype was determined by PCR with confronting two-pair primers. Results showed that EGF polymorphism was not associated with gastric cancer but that the EGF A/A genotype showed a protective effect (odds ratios, 0.58; 95% confidence interval, 0.29-1.17 relative to G/G). Furthermore, when we divided cases into two groups, a differentiated type and an undifferentiated type, the A/A and G/A combined was found to be lower frequency in the latter type than in the former type without significance (OR, 0.81; 95% confidence interval, 0.44-1.49 relative to G/G). As is the case with any malignancy, other factors are involved, including environmental and host factors. The present results show that although EGF is necessary for cancer, it is not sufficient. We also found ethnic heterogeneity in the functional EGF polymorphism. Because the relationship between EGF polymorphism and malignancy remains inconsistent, confirmation of the role of EGF polymorphism in gastric cancer requires a much larger study.
Fertility Among Brothers of Patients with Testicular Cancer
Authors: Richiardi Lorenzo , Akre Olof 
Published: March 2006

AbstractObjective: Patients with testicular cancer have decreased fertility prior to the diagnosis of cancer, although it is not clear whether the subfertility is the result of an emerging tumor, or whether subfertility and testicular cancer share causes. To test if they share causes, we assessed fertility among brothers of patients with testicular cancer.Methods: We compared 5,613 siblings (2,878 brothers) of patients with germ-cell testicular cancer, diagnosed in Sweden from 1960 to 2002, with 6,151 population controls (3,202 men). Using the Swedish Multi-Generation Register, we obtained information on the number of children born (until December 2003) from cases (n = 9,480) and controls (n = 10,739). Fertility was measured using two indicators, (a) offspring twinning rates, as dizygotic twinning is reduced by male subfertility, and (b) number of children. We used unconditional logistic regression, and analyzed brothers and sisters separately. Analyses on the number of children were restricted to subjects (39%) born prior to 1954, for whom information on reproductive life until age 50 was available.Results: Brothers, but not sisters, of patients with testicular cancer were less likely to have unlike-sex twins than controls (for unlike-sex twins, the odds ratio for the father being a sibling of testicular cancer patient was 0.53; 95% confidence interval, 0.26-1.09). The likelihood of being a brother of a patient with testicular cancer decreased monotonically with increasing number of children (P = 0.05), whereas no association was observed for the sisters.Conclusion: The decreased fertility found among brothers of patients with testicular cancer argues in favor of shared causes between cancer-associated subfertility and testicular cancer. Genetic links and shared environment could explain the association.
Nipple Fluid Basic Fibroblast Growth Factor in Patients with Breast Cancer
Authors: Sartippour Maryam R. , Zhang Liping , Lu Ming , Wang He-Jing , Brooks Mai N. 
Published: March 2006

Abstract
Purpose: It has been shown that early detection of breast cancer could save lives. Recently, there has been increasing interest in nipple fluid as a potential supplemental avenue for breast cancer diagnosis.
Experimental Design: In this study, we determined the levels of an angiogenic factor basic fibroblast growth factor (bFGF) in the nipple fluid of healthy subjects as well as patients with benign breast conditions, those at high risk for breast cancer, and patients with active breast cancer. ELISAs were used to measure bFGF.
Results: Nipple fluid bFGF levels were as follows (mean ± SE): 158 ± 17 pg/mL from benign breasts, 561 ± 277 pg/mL from high-risk breasts, and 1,343 ± 441 pg/mL from cancerous breasts. One-way ANOVA showed that the bFGF levels from cancerous breasts were significantly higher than those from benign and high-risk breasts (P = 0.0001 and P = 0.0193, respectively). After logarithmic transformation was applied to the data, high-risk breast bFGF levels were higher than those from benign breasts (P = 0.0028). With a cutoff level of 250 pg/mL, the sensitivity was 79.2%, specificity was 82.5%, and correct diagnosis was 66.4%. The area under the receiver operating characteristic curve was 0.86.
Conclusions: We conclude that nipple fluid bFGF levels are progressively elevated in high-risk and cancerous breasts compared with benign breasts. The sensitivity and specificity of this test are promising compared with current breast cancer screening methods, and this test deserves further studies with larger clinical trials. Potential areas of usefulness include the detection of breast cancer risk or breast cancer, as well as the monitoring and/or prediction of the antiangiogenic effect of preventive therapies. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2995–8)
Regular Analgesic Use and Risk of Endometrial Cancer
Authors: Moysich Kirsten B. , Baker Julie A. , Rodabaugh Kerry J. , Villella Jeannine A. 
Published: March 2006

Abstract
Background: Analgesic use has been implicated in the chemoprevention of a number of solid tumors, but thus far, no previous research has focused on the role of aspirin in endometrial cancer etiology.
Methods: We conducted a hospital-based case-control study of 427 women with primary, incident endometrial cancer, and 427 age- and residence-matched controls without benign or malignant neoplasms. All participants received medical services at Roswell Park Cancer Institute in Buffalo, NY, and completed a comprehensive epidemiologic questionnaire. Women who reported analgesic use at least once a week for at least 6 months were classified as regular users and served as the reference group throughout the analyses. We used unconditional logistic regression analyses to compute crude and adjusted odds ratios (OR) with corresponding 95% confidence intervals (CI).
Results: Compared with nonusers, regular aspirin users were not at reduced risk of endometrial cancer (adjusted OR, 0.91; 95% CI, 0.66-1.26), nor were women with the highest frequency, duration, or cumulative lifetime aspirin use. When the sample was divided by body mass index status, regular aspirin use was not associated with risk among women classified as normal weight or overweight, but a significant risk reduction was seen for obese women (adjusted OR, 0.50; 95% CI, 0.27-0.92). Significant decreases in risk were also observed for obese women with the greatest frequency, duration, and cumulative aspirin use. No significant associations in the overall sample or among obese women were noted for acetaminophen use.
Conclusion: We observed no evidence of an overall chemoprotective effect of aspirin on endometrial cancer risk, but the significant risk reductions among obese women warrant further investigation. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2923–8)
Prevalence and Clustering Patterns of Human Papillomavirus Genotypes in Multiple Infections
Authors: Chaturvedi Anil K. , Myers Leann , Hammons Ansley F. , Clark Rebecca A. , Dunlap Kathleen , Kissinger Patricia J. , Hagensee Michael E. 
Published: March 2006

Abstract
Prevalence of multiple human papillomavirus (HPV) infections, involvement of specific HPV phylogenetic clades in multiple infections, and clustering patterns of multiple infections at the clade level were assessed in 854 HIV (−) and 275 HIV (+) women cross-sectionally. Reverse line blot assay was used to detect 27 HPV genotypes. Involvement of specific clades in coinfections and clustering patterns were assessed using HPV clade/genotype as the unit of analyses. Expected frequencies assuming independence for all possible clade combinations in two-genotype infections were derived using a multinomial expansion and comparisons of observed and expected frequencies were done using a composite goodness-of-fit test. In all, 100 two-genotype infections were detected; 61 in HIV (−) and 39 in HIV (+) women. Clade A9 (HPV types 16, 31, 33, 35, 52, and 58) was significantly less likely to be involved in multiple infections compared with all other clades (55.2% versus 64.6%; adjusted odds ratios, 0.68; 95% confidence interval, 0.48-0.95). Observed patterns for all possible clade combinations (among HPV clades A3, A5, A6, A7, A9, and A10) in two-genotype infections did not significantly differ from those expected in the entire sample, across HIV, Pap smear, and age strata (all goodness-of-fit exact P &gt; 0.20). These results indicate that clade A9 is less likely to be involved in multiple infections and that HPV genotypes predominantly establish multiple infections at random, with little positive/negative clustering for either phylogenetically related or unrelated types. The current method of analysis affords the opportunity to test clustering of a large number of HPV genotype/clade combinations at nominal alpha levels.
The Predicted Impact of Coding Single Nucleotide Polymorphisms Database
Authors: Rudd Matthew F. , Williams Richard D. , Webb Emily L. , Schmidt Steffen , Sellick Gabrielle S. , Houlston Richard S. 
Published: March 2006

AbstractNonsynonymous single nucleotide polymorphisms (nsSNP) have the potential to affect the structure or function of expressed proteins and are, therefore, likely to represent modifiers of inherited susceptibility. We have classified and catalogued the predicted functionality of nsSNPs in genes relevant to the biology of cancer to facilitate sequence-based association studies. Candidate genes were identified using targeted search terms and pathways to interrogate the Gene Ontology Consortium database, Kyoto Encyclopedia of Genes and Genomes database, Iobion's Interaction Explorer PathwayAssist Program, National Center for Biotechnology Information Entrez Gene database, and CancerGene database. A total of 9,537 validated nsSNPs located within annotated genes were retrieved from National Center for Biotechnology Information dbSNP Build 123. Filtering this list and linking it to 7,080 candidate genes yielded 3,666 validated nsSNPs with minor allele frequencies ≥0.01 in Caucasian populations. The functional effect of nsSNPs in genes with a single mRNA transcript was predicted using three computational tools—Grantham matrix, Polymorphism Phenotyping, and Sorting Intolerant from Tolerant algorithms. The resultant pool of 3,009 fully annotated nsSNPs is accessible from the Predicted Impact of Coding SNPs database at http://www.icr.ac.uk/cancgen/molgen/MolPopGen_PICS_database.htm. Predicted Impact of Coding SNPs is an ongoing project that will continue to curate and release data on the putative functionality of coding SNPs.
Estrogen and Progesterone Levels in Nipple Aspirate Fluid of Healthy Premenopausal Women: Relationship to Steroid Precursors and Response Proteins
Authors: Gann Peter H. , Geiger Angela S. , Helenowski Irene B. , Vonesh Edward F. , Chatterton Robert T. 
Published: March 2006

Abstract
Background: Concentrations of estrogen and progesterone within the breast could provide a better reflection of breast cancer risk than levels in the circulation. We developed highly sensitive immunoassays for multiple steroid hormones and proteins in the nipple aspirate fluid (NAF), which can be obtained noninvasively with a simple suction device. Previous studies showed that NAF hormone levels are strongly correlated between breasts and within a single breast over time and are predictably related to hormone replacement therapy or use of oral contraceptives. This study evaluates the relationship of NAF estrogen and progesterone levels to those in serum and saliva, the relationship of NAF estradiol to androgenic and estrogenic precursors in NAF, and the relationship of NAF hormone levels to those of response proteins such as cathepsin D and epidermal growth factor (EGF).
Methods: Normal premenopausal women collected saliva daily and donated blood and NAF in the midluteal phases of menstrual cycles at intervals of 0, 4, 12, and 15 months. Analytes were measured by immunoassays after solvent fractionation. Log-transformed values were fit to repeated measures analysis of covariance models to ascertain associations between analytes.
Results: Small nonsignificant associations were found between NAF and serum or salivary estradiol. However, progesterone in NAF was significantly associated with progesterone in serum and saliva (R = 0.18 and 0.32, respectively). Within NAF, the estradiol precursors estrone sulfate, androstenedione, and dehydroepiandrosterone were significantly associated with estradiol concentration (P &lt; 0.06), and a multiprecursor model explained the majority of variance in NAF estradiol (model R2 = 0.83). Cathepsin D and EGF in NAF could not be predicted from serum or salivary steroid measurements; however, both could be predicted from estradiol and its precursors in NAF (model R2 = 0.70 and 0.93, respectively).
Conclusions: By showing consistent associations between estradiol and its precursors and response proteins, these data provide support for the biological validity of NAF hormone measurements and for the importance of steroid interconversion by aromatase and sulfatase within the breast. The low correlation between estrogen levels in NAF and those in serum or saliva suggests that the degree of association between estrogen or its androgen precursor levels and risk of breast cancer observed in epidemiologic studies using serum estimates might be highly attenuated. (Cancer Epidemiol Biomarkers Prev 2006;15(1):39–44)
High Serum Selenium and Reduced Risk of Advanced Colorectal Adenoma in a Colorectal Cancer Early Detection Program
Authors: Peters Ulrike , Chatterjee Nilanjan , Church Timothy R. , Mayo Charlotte , Sturup Stefan , Foster Charles B. , Schatzkin Arthur , Hayes Richard B. 
Published: March 2006

Abstract
Background: Epidemiologic and animal studies suggest that selenium may reduce risk of colorectal cancer. However, the epidemiologic data is mainly from relatively small investigations, limiting their interpretation. Although substantial evidence suggests that smoking is a strong effect modifier for other antioxidative nutrients, little is known about smoking-selenium interactions in colorectal tumors.
Methods: We studied the association of serum selenium and advanced colorectal adenoma, a cancer precursor, in 758 cases and 767 sex- and race-matched controls, randomly selected from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Cases had at least one verified advanced adenoma (≥1 cm or villous elements, or high-grade dysplasia) of the distal colon, and controls had a negative sigmoidoscopy.
Results: The multivariable odds ratio (OR) comparing participants in the highest quintile of serum selenium with those in the lowest quintile was 0.76 [95% confidence interval (95% CI), 0.53-1.10; Ptrend = 0.01]. The inverse association between serum selenium and advanced colorectal adenoma was significant among recent smokers (OR, 0.53; 95% CI, 0.27-1.01 for highest versus lowest tertile; Ptrend = 0.008). Serum selenium was unrelated to adenoma risk in nonsmokers and former smokers who quit smoking ≥10 years ago.
Conclusion: Selenium may reduce the risk of developing advanced colorectal adenoma, particularly among the high-risk group of recent smokers. (Cancer Epidemiol Biomarkers Prev 2006;15(2):315–20)
Sun-Protective Behavior among Individuals with a Family History of Melanoma
Authors: Azzarello Lora M. , Dessureault Sophie , Jacobsen Paul B. 
Published: March 2006

Abstract
Routine sun protection is recommended to prevent skin cancer. Skin cancer prevention may be particularly important for individuals at greater risk, such as those with a family history of melanoma. Our aims were to examine the prevalence of sun-protective behavior (SPB) in unaffected first-degree relatives (FDR) of individuals diagnosed with melanoma and to examine the relationship between protection motivation theory (PMT) variables (i.e., perceived risk, perceived severity, self-efficacy, response efficacy) and SPB. FDRs (n = 100), who were nominated by melanoma patients, completed a standardized, self-report questionnaire measuring demographic characteristics, melanoma risk factors, PMT variables, and SPB. The results indicated that less than one-third of FDRs used sunscreen routinely when in the sun and fewer stayed in the shade or used protective clothing on a frequent basis. FDRs with a college education and with more melanoma risk factors reported higher levels of SPB. Of the four PMT variables, greater perceived risk and greater self-efficacy were significantly correlated with higher levels of SPB. Furthermore, results of multiple regression analyses suggest that perceived risk mediated the relationship between education and SPB and between melanoma risk factors and SPB. These findings suggest that interventions to increase the frequency of SPB in at-risk individuals should highlight risk information as well as methods to improve individuals' confidence in their abilities to engage in SPB. (Cancer Epidemiol Biomarkers Prev 2006;15(1):142–5)
Association of Energy Intake and Energy Balance with Postmenopausal Breast Cancer in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial
Authors: Chang Shih-Chen , Ziegler Regina G. , Dunn Barbara , Stolzenberg-Solomon Rachael , Lacey James V. , Huang Wen-Yi , Schatzkin Arthur , Reding Douglas , Hoover Robert N. , Hartge Patricia , Leitzmann Michael F. 
Published: March 2006

Abstract
Energy restriction remains one of the most effective ways known to prevent breast cancer in animal models. However, energy intake has not been consistently associated with risk of breast cancer in humans. In a prospective study, we assessed whether energy intake, body size, and physical activity each independently influence breast cancer risk in postmenopausal women and estimated the joint effect of combinations of these individual factors. As part of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, 38,660 women, ages 55 to 74 years and recruited from 10 centers in the United States during 1993 to 2001, were randomized to the screening arm of the trial. At baseline, the women completed a self-administered questionnaire, including a food frequency questionnaire. During follow-up from 1993 to 2003, 764 incident breast cancer cases were ascertained. Women in the highest quartile of energy intake (≥2,084 kcal/d) compared with those in the lowest quartile (&lt;1,316 kcal/d) had a significantly increased risk for breast cancer [multivariate relative risk (RR), 1.25; 95% confidence interval (95% CI), 1.02-1.53; Ptrend continuous = 0.03]. Current body mass index (BMI) was also positively and significantly associated with risk (multivariate RR comparing &gt;30 kg/m2 with &lt;22.5 kg/m2, 1.35; 95% CI, 1.06-1.70; Ptrend = 0.01). Women with ≥4 hours/wk of vigorous recreational physical activity had a significantly reduced risk of breast cancer compared with those who reported no recreational physical activity (multivariate RR, 0.78; 95% CI, 0.60-0.99; Ptrend = 0.15). None of these associations with individual energy balance measures was substantially confounded by the other two measures. When we estimated the joint effect of all three variables, women with the most unfavorable energy balance (the highest energy intake, highest BMI, and least physical activity) had twice the risk (RR, 2.10; 95% CI, 1.27-3.45) of women with the most favorable energy balance (the lowest energy intake, lowest BMI, and most physical activity). Although our estimates of absolute energy intake, based on a food frequency questionnaire, are imperfect, these results suggest that energy intake, in addition to BMI and physical activity may be independently associated with breast cancer risk. In addition, these three aspects of energy balance may act jointly in determining breast cancer risk. (Cancer Epidemiol Prev 2006;15(2):334–41)
Inflammation and Endometrial Cancer: A Hypothesis
Authors: Modugno Francesmary , Ness Roberta B. , Chen Chu , Weiss Noel S. 
Published: March 2006

AbstractEndometrial cancer is the most common gynecologic malignancy in the United States. Substantial epidemiologic data implicate an imbalance of estrogens and progestogens in the etiology of this disease. We propose that inflammation also plays a role in endometrial cancer development. Emerging laboratory data suggest that elevated levels of prostaglandin E2 may underlie the transformation of normal endometrium to neoplastic tissue and that in vitro nonsteroidal anti-inflammatory drugs may inhibit endometrial cancer cell growth. In this review, we suggest that the risk factors for endometrial cancer—unopposed estrogens, anovulation, polycystic ovary syndrome, excessive menstruation, early menarche, and late menopause—may be viewed as factors increasing the exposure of the endometrium to inflammation, whereas pregnancy and smoking, two likely protective factors, have the opposite effect. Chronic inflammation can induce rapid cell division, increasing the possibility for replication error, ineffective DNA repair, and subsequent mutations. A proinflammatory milieu can also directly increase estrogen production. Hence, inflammation may work in conjunction with or in addition to estrogen exposure in the development of endometrial cancer. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2840–7)
Sun Protection and the Development of Melanocytic Nevi in Children
Authors: English Dallas R. , Milne Elizabeth , Simpson Julie A. 
Published: March 2006

Abstract
Childhood sun exposure causes nevi (and melanoma), but there is little evidence regarding the effectiveness of sun protection strategies on the number of nevi. We previously found that boys but not girls receiving a school-based sun protection program had fewer nevi on their backs than controls. Here, we investigated whether specific program components (encouraging children to stay indoors in the middle of the day during summer, to wear clothing while outdoors, and to use sunscreen) were associated with fewer nevi. An observational analysis was done on data from a sun protection trial in 1,623 children in Perth, Australia. The outcome was number of nevi on the back 6 years after baseline, when the children were 12 years old. Information on sun protection was obtained by questionnaires 4 and 6 years after baseline. The data were analyzed by mixed-effects linear regression. The time spent outdoors between 11 a.m. and 2 p.m. and the proportion of total time outdoors that was between these hours were positively associated with number of nevi. Ratios of mean counts for doubling the respective measures were 1.09 [95% confidence interval (95% CI), 1.05-1.12] and 1.10 (95% CI, 1.05-1.14). Children whose backs were covered &lt;70% of the time while outdoors had 1.53 (95% CI, 1.34-1.75) times more nevi than children whose backs were always covered. Using sunscreen on the back when it was uncovered was not associated with number of nevi (P = 0.59). Children who stayed indoors in the middle of the day and wore clothing while outdoors had fewer nevi. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2873–6)