bluuebunny/crossref_metadata_2025_split huggingface dataset:
IGF1 (CA)19 Repeat and IGFBP3 -202 A/C Genotypes and the Risk of Prostate Cancer in Black and White Men
Authors: Schildkraut Joellen M. , Demark-Wahnefried Wendy , Wenham Robert M. , Grubber Janet , Jeffreys Amy S. , Grambow Steven C. , Marks Jeffrey R. , Moorman Patricia G. , Hoyo Cathrine , Ali Shazia , Walther Philip J. 
Published: September 2005

Abstract
We investigated the relationship between the insulin-like growth factor-1 (IGF1) cytosine-adenine repeat (CA)19 polymorphism located upstream of the gene's transcription start site, the insulin-like growth factor binding protein-3 (IGFBP3) −202 A/C promoter region polymorphism, and prostate cancer risk in Black and White men. Study subjects were U.S. veterans ages 41 to 75 years identified at the Durham Veterans Administration Medical Center over a 2.5-year period. Controls (n = 93) were frequency matched to cases (n = 100) based on race (Black or White) and age. Multivariable unconditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI) for the associations between the polymorphisms and prostate cancer risk. For Blacks and Whites combined, an inverse association between prostate cancer and being homozygous for the most common IGF1 repeat allele, (CA)19, (adjusted OR, 0.3; 95% CI, 0.1-0.7) was observed. Similar associations were noted for both Blacks (OR, 0.2; 95% CI, 0.0-0.8) and Whites (OR, 0.4; 95% CI, 0.1-1.6) separately. No statistically significant associations between the IGFBP3 C allele and prostate cancer were noted for Blacks (adjusted OR, 2.3; 95% CI, 0.8-6.2) or Whites (OR, 1.0; 95% CI, 0.3-3.1). The prevalence of the homozygous IGF1 (CA)19 genotype was much lower in Black controls (21%) than White controls (46%), which may, in part, explain the increased prostate cancer incidence in Black versus White men. Further research is needed to confirm these findings.
Detection of Alkaline Sphingomyelinase Activity in Human Stool: Proposed Role as a New Diagnostic and Prognostic Marker of Colorectal Cancer
Authors: Di Marzio Luisa , Di Leo Alfredo , Cinque Benedetta , Fanini Donatella , Agnifili Alessio , Berloco Pasquale , Linsalata Michele , Lorusso Dionigi , Barone Michele , De Simone Claudio , Cifone Maria Grazia 
Published: September 2005

Abstract
Objectives: Intestinal alkaline sphingomyelinase, by exerting a major role in dietary sphingomyelin digestion, is responsible for the generation of messengers able to trigger the rapid turnover and apoptosis in intestinal epithelial cells. Markedly reduced mucosal alkaline sphingomyelinase activity has been associated with human colorectal neoplasms. The aim of this study was to analyze the alkaline sphingomyelinase activity in feces from healthy subjects and colorectal adenocarcinoma patients and to correlate it with the enzyme activity in intestinal tissues.
Materials and Methods: The enzyme activity was measured both in the intestinal samples from 12 healthy controls and 51 patients with colorectal adenocarcinoma (tumoral and paratumoral tissue) and in the fecal samples of 34 healthy subjects and 29 patients with adenocarcinoma. The relation between sphingomyelinase activity and Dukes' stage, cell differentiation degree, age, and gender was also analyzed.
Results: Alkaline sphingomyelinase was significantly decreased (P &lt; 0.001; mean reduction &gt;90%) in tumoral intestinal mucosa of patients compared with controls independently of Dukes' stage and tumor differentiation grade. Interestingly, the enzyme activity in histologically normal paratumoral tissues was statistically lower than control samples (P &lt; 0.001). As occurs in neoplastic tissues, a relevant mean reduction (P &lt; 0.0001; almost 90%) of alkaline sphingomyelinase was revealed in stool samples from tumor patients when compared with controls.
Conclusion: These findings may have implications for cancer biology and perhaps also for the design of clinical test, thus suggesting that the fecal sphingomyelinase activity could really reflect the human intestinal mucosa enzyme level and could represent a new marker for human colorectal adenocarcinoma, mainly taking into account its early appearance in intestinal neoplasms.
Antibody Responses to Simian Virus 40 T Antigen: A Case-Control Study of Non-Hodgkin Lymphoma
Authors: Engels Eric A. , Chen Jinbo , Hartge Patricia , Cerhan James R. , Davis Scott , Severson Richard K. , Cozen Wendy , Viscidi Raphael P. 
Published: September 2005

Abstract
A possible role for SV40, a macaque polyomavirus, in non-Hodgkin lymphoma (NHL) in humans was raised recently by the reported detection of SV40 DNA in tumor tissue. Animals with SV40-induced tumors frequently produce high-level antibodies against T antigen, the SV40 oncoprotein. In this study, we assessed whether SV40 T antibody measured in humans supported a relationship between SV40 and NHL. Subjects were sampled from a U.S. population-based case-control study of NHL, according to presence of antibodies against capsids of SV40 and BK, a related human polyomavirus (n = 85 cases, n = 95 controls). T antibody was measured by enzyme immunoassay. We also evaluated serum specimens from SV40-infected and SV40-uninfected macaques (n = 19 and n = 8, respectively), SV40-uninfected hamsters (n = 5), and hamsters with SV40-induced tumors (n = 10). Hamsters with SV40-induced tumors all produced robust SV40 T antibody [median absorbance, 0.99), whereas SV40-uninfected hamsters and macaques had much lower levels (median absorbance, 0.05 and 0.04, respectively). NHL cases, controls, and SV40-infected macaques resembled these latter two groups, generally showing only low-level T antibody (median absorbance, 0.03, 0.04, and 0.04, respectively). Overall, only five cases (6%) and five controls (5%) had T antibody responses classified as seropositive (odds ratio, 1.2; 95% confidence interval, 0.3-4.6). Interestingly, all 10 humans with T antibody responses also showed antibody responses to BK capsid. We found no association between the presence of T antibody and NHL, arguing against SV40 as a cause of NHL. Infrequent and low-level T antibody responses among humans could represent cross-reactivity to BK virus T antigen.
DNA Damage from Polycyclic Aromatic Hydrocarbons Measured by Benzo[a]pyrene-DNA Adducts in Mothers and Newborns from Northern Manhattan, The World Trade Center Area, Poland, and China
Authors: Perera Frederica , Tang Deliang , Whyatt Robin , Lederman Sally Ann , Jedrychowski Wieslaw 
Published: September 2005

AbstractPolycyclic aromatic hydrocarbons (PAH), of which benzo[a]pyrene is a representative member, are combustion-related environmental pollutants and include known carcinogens. Laboratory animal studies indicate that the dose of PAHs to the fetus is on the order of a 10th that to the mother and that there is heightened susceptibility to PAH-induced carcinogenesis during the fetal and infancy periods. Carcinogen-DNA adducts, a measure of procarcinogenic genetic damage, are considered a biomarker of increased cancer risk. Here we compare the levels of benzo[a]pyrene-DNA adducts as a proxy for PAH-DNA damage measured in maternal blood and newborn cord blood obtained at delivery in four different populations of mothers (total of 867) and newborns (total of 822), representing a 30-fold range of exposure to ambient PAHs. The populations include residents in Northern Manhattan, participants in a study of the effects of the World Trade Center disaster, residents in Krakow, Poland, and residents in Tongliang, China. Mean adduct concentrations in both maternal and cord blood and the proportion of samples with detectable adducts, increased across the populations [Northern Manhattan &lt; World Trade Center (WTC) &lt; Krakow &lt; Tongliang], consistent with the trend in estimated ambient exposure to PAHs (P &lt; 0.001). For mothers, the means in the respective populations were Northern Manhattan (0.21 adducts per 108 nucleotides), WTC (0.23 adducts per 108 nucleotides), Krakow (0.28 adducts per 108 nucleotides), Tongliang (0.31 adducts per 108 nucleotides); the corresponding means in the newborns were Northern Manhattan (0.23), WTC (0.24), Krakow (0.29), Tongliang (0.31). The percentage of mothers with detectable levels of adducts in the respective populations were Northern Manhattan (36.8%), WTC (57.5%), Krakow (72.9%), Tongliang (73.4%); the corresponding percentages among the newborns were Northern Manhattan (42.4%), WTC (60.6%), Krakow (71.1%), Tongliang (79.5%). Despite the estimated 10-fold lower PAH dose to the fetus based on laboratory animal experiments, the adduct levels in the newborns were similar to or higher than in the mothers. This study suggests that the fetus may be 10-fold more susceptible to DNA damage than the mother and that in utero exposure to polycyclic aromatic hydrocarbons may disproportionately increase carcinogenic risk. The data support preventive policies to limit PAH exposure to pregnant women and children.
Does Health Insurance Coverage of Office Visits Influence Colorectal Cancer Testing?
Authors: Varghese Reuben K. , Friedman Carol , Ahmed Faruque , Franks Adele L. , Manning Marsha , Seeff Laura C. 
Published: September 2005

Abstract
Objective: To assess the effect of differing health insurance coverage of physician office visits on the use of colorectal cancer (CRC) tests among an employed and insured population.
Method: Cohort study of persons ages 50 to 64 years enrolled in fee-for-service (FFS) or preferred provider organization (PPO) health plans, where FFS plan enrollees bear disproportionate share of office visit coverage, for the period 1995 through 1999.
Results: Compared with FFS plans, enrollees in PPO plans were significantly more likely to obtain CRC tests [adjusted relative risk (RRa), 1.27; 95% confidence intervals (CI), 1.21-1.24]. The association was more pronounced among hourly individuals (RRa, 1.43; 95% CI, 1.41-1.45) than among salaried individuals (RRa, 1.09; 95% CI, 1.05-1.10), consistent with a greater differential in office visit coverage among the hourly group.
Conclusions: Disproportionate cost-sharing seems to have a negative effect on the use of CRC tests most likely by discouraging nonacute care physician office visits.
Genetic Factors in Catechol Estrogen Metabolism in Relation to the Risk of Endometrial Cancer
Authors: Doherty Jennifer A. , Weiss Noel S. , Freeman Robert J. , Dightman Douglas A. , Thornton Perry J. , Houck John R. , Voigt Lynda F. , Rossing Mary Anne , Schwartz Stephen M. , Chen Chu 
Published: September 2005

Abstract2-Hydroxylated metabolites of estrogen have been shown to have antiangiogenic effects and inhibit tumor cell proliferation, whereas 4-hydroxylated metabolites have been implicated in carcinogenesis. We examined whether polymorphisms in certain genes involved in estrogen metabolism are associated with endometrial cancer risk in a population-based case-control study with 371 cases and 420 controls. Based on previously published genotype-phenotype correlation studies, we defined variant alleles thought to increase estrogen 2-hydroxylation as presumptively low-risk (CYP1A1 m1 T6235C and m2 Ile462Val) and those thought to increase estrogen 4-hydroxylation as high-risk (CYP1A1 m4 Thr461Asn, CYP1A2 A734C, and CYP1B1 Leu432Val). Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression. Carrying at least one CYP1A1 m1 or m2 variant allele was associated with a decreased risk of endometrial cancer [ORs (95% CIs), 0.64 (0.44-0.93) and 0.54 (0.30-0.99), respectively]. No strong alteration in risk was observed among women with any of the putative high-risk alleles. When CYP1A1, CYP1A2, and CYP1B1 genotypes were combined and ranked by the number of putative low-risk genotypes carried, women with four or five low-risk genotypes had a reduced risk of endometrial cancer (OR, 0.29; 95% CI, 0.15-0.56) compared with women with one or none. No appreciable alteration in risk was observed among women carrying two or three low-risk genotypes. Some of our findings are consistent with the hypothesis that increased estrogen 2-hydroxylation is associated with decreased endometrial cancer risk, but replication of these results is required before any firm conclusions can be reached.
Increased Retinoic Acid Receptor-β4 Correlates In vivo with Reduced Retinoic Acid Receptor-β2 in Esophageal Squamous Cell Carcinoma
Authors: Xu Xiao-chun , Lee J. Jack , Wu Tsung-Teh , Hoque Ashraful , Ajani Jeffer A. , Lippman Scott M. 
Published: September 2005

Abstract
Different retinoic acid receptor-β (RAR-β) isoforms seem to have contrasting biological effects in human carcinogenesis. Both in vitro and in vivo data indicate that RAR-β2 expression is frequently lost or reduced (and transfecting RAR-β2 suppresses growth and promotes apoptosis) in various cancer cells and tissues, whereas RAR-β4 expression is increased in several cancer cell lines. To clarify the effects of different RAR-β isoforms in esophageal carcinogenesis, we used real-time quantitative reverse transcription-PCR to assess in vivo RAR-β mRNA levels in specimens of normal and malignant human esophageal tissue, comparing these levels with each other and the expressions of other genes. RAR-β2 mRNA expression was significantly reduced (i.e., lower in cancer than normal tissue) in 67% (18 of 27, P = 0.001) and RAR-β4 mRNA was increased in 52% (14 of 27, P = 0.054) of our esophageal cancer cases. The expressions of RAR-β1, chicken ovalbumin upstream promoter-transcription factor-I (COUP-TFI), COUP-TFII, and peroxisome proliferator-activated receptor-γ (PPAR-γ) mRNA were reduced, whereas epidermal growth factor receptor and cyclin D1 expressions were increased in tumor compared with in normal tissues. Reduced RAR-β2 expression correlated with increased RAR-β4 expression (P = 0.002) and with the suppression of COUP-TFI and COUP-TFII (P = 0.050 and 0.023, respectively) in tumor samples. These are the first in vivo expression patterns of RAR-β2 and RAR-β4 reported in humans or animals and support the in vitro data on these isoforms and their contrasting biological effects in human carcinogenesis.
A DNA Pooling Strategy for Family-Based Association Studies
Authors: Lee Wen-Chung 
Published: September 2005

Abstract
Genome-wide association scans for disease susceptibility genes of complex diseases require genotyping on a massive scale. A DNA pooling strategy for family-based association studies is described, which is robust to population stratification biases and to errors in pooling. It can achieve a statistical efficiency of 0.95 with ∼1 of 8 or fewer genotyping efforts, and an efficiency of 0.90 with ∼1 of 16 or fewer efforts compared with individual genotyping. The pooling method described in this article provides a tradeoff between genotyping efforts and subject recruitment efforts.
Dietary Intake of Heterocyclic Amines and Benzo(a)Pyrene: Associations with Pancreatic Cancer
Authors: Anderson Kristin E. , Kadlubar Fred F. , Kulldorff Martin , Harnack Lisa , Gross Myron , Lang Nicholas P. , Barber Cheryl , Rothman Nat , Sinha Rashmi 
Published: September 2005

Abstract
Objective: Heterocyclic amines (HCA) and polycyclic aromatic hydrocarbons, formed in temperature- and time-dependent manners during the cooking of meat, are mutagens and carcinogens. We sought to assess the association between dietary intake of HCA and benzo(a)pyrene [B(a)P] and exocrine pancreatic cancer in a population-based case-control study.
Methods: Subjects (193 cases and 674 controls) provided information on their usual meat intake and preparation method, e.g., stewed, fried, or grilled/barbecued, etc. Meat doneness preferences were measured using photographs that showed internal doneness and external brownness. We used a meat-derived HCA, B(a)P, and mutagen database with a questionnaire to estimate intake of PhIP, DiMeIQx, MeIQx, B(a)P, and mutagenic activity (revertants/g of daily meat intake). Data were analyzed with unconditional logistic regression.
Results: In analyses adjusted for age, sex, smoking, education, race, and diabetes, the odds ratio and 95% confidence interval for the highest compared with the lowest quintile were as follows: PhIP, 1.8 (1.0-3.1); DiMeIQx, 2.0 (1.2-3.5); MeIQx, 1.5 (0.9-2.7); B(a)P, 2.2 (1.2-4.0); and mutagenic activity, 2.4 (1.3-4.3).
Conclusions: HCAs and B(a)P from well-done barbecued and pan-fried meats may be associated with increased risk for pancreatic cancer.
Body Mass Index in Relation to Ovarian Cancer Survival
Authors: Zhang Min , Xie Xing , Lee Andy H. , Binns Colin W. , Holman C. D'Arcy J. 
Published: September 2005

Abstract
Evidence for an association between indicators of adiposity and survival after ovarian cancer has been inconsistent. A prospective cohort study was conducted in China to examine the relationship between ovarian cancer survival and body mass index (BMI). From the 214 patients recruited in 1999 to 2000 with histopathologically confirmed invasive epithelial ovarian cancer, 207 patients or their close relatives (96.7% of cases) were traced and followed to 2003. Deaths were recorded and Cox proportional hazards regression was used to obtain hazard ratios (HR) and 95% confidence intervals (95% CI) from multivariate models. Reduced survival was observed among patients with BMI ≥ 25 kg/m2 at 5 years before diagnosis (P = 0.001). There were 98 (59.8%) of 164 patients with BMI &lt;25 kg/m2 survived to the time of interview compared with only 15 women (34.9%) among the 43 patients whose BMI was ≥25 kg/m2. The HRs significantly increased with higher BMI at 5 years before diagnosis but not at diagnosis nor at age 21 years. The adjusted HR was 2.33 (95% CI, 1.12-4.87) for BMI of ≥25 versus &lt;20 kg/m2, with a significant dose-response relationship. The HR was 3.31 (95% CI, 1.26-8.73) among patients who had been overweight or obese at age 21 years, but a linear dose-response was not found. We conclude that premorbid BMI may have independent prognostic significance in ovarian cancer.
The Effect of a School-Based Sun Protection Intervention on the Development of Melanocytic Nevi in Children: 6-Year Follow-up
Authors: English Dallas R. , Milne Elizabeth , Jacoby Peter , Giles-Corti Billie , Cross Donna , Johnston Robyn 
Published: September 2005

Abstract
Because nevi share risk factors with melanoma and are strong risk factors for melanoma, they are suitable biomarkers for evaluating sun protection programs. Kidskin was a trial of a school-based sun protection program in Western Australia that included high and moderate intervention groups and a control group. Schools were assigned nonrandomly to groups. The primary outcome was number of nevi on the back. Nevi were counted at baseline, after 4 years intervention and again 2 years later. Linear growth models, allowing for correlated data within schools and children were fitted to the data. The primary analysis included 639 control children, 414 in the moderate and 355 in the high intervention group. Compared with the control group, the relative increase in number of nevi on the back was 0.89 (95% confidence interval, 0.81-0.99) for the high intervention group and 0.94 (95% confidence interval, 0.86-1.04) for the moderate group (P = 0.09). In subgroup analyses of nevi on the back, the association was stronger in boys (P &lt; 0.001) than in girls (P = 0.7), although the test for interaction was not significant (P = 0.11). For the chest, examined in boys, the associations were similar to that for nevi on the back in boys. Associations were weak for nevi on the face and arms (P = 0.2); for this site, there was weak evidence of heterogeneity by sex. Overall, there was weak evidence that the Kidskin intervention reduced the number of new nevi over a 6-year period, but there was stronger evidence of an effect on the trunk in boys.
CYP3A43 Pro340Ala Polymorphism and Prostate Cancer Risk in African Americans and Caucasians
Authors: Stone Angie , Ratnasinghe Luke D. , Emerson Ginny L. , Modali Rama , Lehman Terri , Runnells Gail , Carroll Alindria , Carter Weleetka , Barnhart Samuel , Rasheed Al A. , Greene Graham , Johnson Don E. , Ambrosone Christine B. , Kadlubar Fred F. , Lang Nicholas P. 
Published: September 2005

Abstract
The human cytochrome P450 3A subfamily of enzymes is involved in the metabolism of steroid hormones, carcinogens, and many drugs. A cytosine-to-guanine polymorphism in CYP3A43 results in a proline-to-alanine substitution at codon 340. Although the functional significance of this polymorphism is unknown, we postulate that the substitution of proline, an α-imino acid, with alanine, an amino acid, could be of biochemical significance. In a case-control study with 490 incident prostate cancer cases (124 African Americans and 358 Caucasians) and 494 controls (167 African Americans and 319 Caucasians), we examined the association between CYP3A43 Pro340Ala polymorphism and prostate cancer risk. When all subjects were considered, there was a 3-fold increase in risk of prostate cancer among individuals with the CYP3A43-Ala/Ala genotype (odds ratio, 3.0; 95% confidence interval, 1.2-7.2) compared with those with the CYP3A43-Pro/Pro genotype after adjusting for age, race, and smoking. The prevalence of the polymorphism was significantly higher in African Americans than Caucasians (45% versus 13%). In African Americans, there was a 2.6-fold increase in prostate cancer risk among individuals with the CYP3A43-Ala/Ala genotype (odds ratio, 2.6; 95% confidence interval, 1.0-7.0) compared with those with the CYP3A43-Pro/Pro genotype. Among Caucasians, the small number of homozygotes precluded computing risk estimates; there were only three individuals with the CYP3A43-Ala/Ala genotype. Our results suggest that the CYP3A43-Pro340Ala polymorphism contributes to prostate cancer risk.
Trends in Cervical Squamous Cell Carcinoma Incidence in 13 European Countries: Changing Risk and the Effects of Screening
Authors: Bray Freddie , Loos Anja H. , McCarron Peter , Weiderpass Elizabete , Arbyn Mark , Møller Henrik , Hakama Matti , Parkin D. Max 
Published: September 2005

Abstract
Despite there being sufficient evidence for the effectiveness of screening by cytology in preventing cancer of the cervix uteri, screening policies vary widely among European countries, and incidence is increasing in younger women. This study analyzes trends in squamous cell carcinoma (SCC) of the cervix uteri in 13 European countries to evaluate effectiveness of screening against a background of changing risk. Age-period-cohort models were fitted and period and cohort effects were estimated; these were considered as primarily indicative of screening interventions and changing etiology, respectively. A unique set of estimates was derived by fixing age slopes to one of several plausible age curves under the assumption that the relation between age and cervical cancer incidence is biologically determined. There were period-specific declines in cervical SCC in several countries, with the largest decreases seen in northern Europe. A pattern emerged across Europe of escalating risk in successive generations born after 1930. In the western European countries, a decrease followed by a stabilization of risk by cohort was accompanied by period-specific declines. In southern Europe, stable period, but increasing cohort trends, were observed. Substantial changes have occurred in cervical SCC incidence in Europe and well-organized screening programs have been highly effective in reducing the incidence of cervical SCC. Screening and changing sexual mores largely explain the changing period- and cohort-specific patterns, respectively. The increasing risk in recent cohorts is of obvious concern particularly in countries where no screening programs are in place. Further investigation of the effectiveness of opportunistic screening is warranted as is the observation of differing risk patterns in young cohorts in countries with relatively similar societal structures.