bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasma Alkylresorcinols and Urinary Alkylresorcinol Metabolites as Biomarkers of Cereal Fiber Intake in Finnish Women
Authors: Aubertin-Leheudre Mylène , Koskela Anja , Marjamaa Annukka , Adlercreutz Herman 
Published: September 2008

Abstract
Alkylresorcinols (AR) could be good biomarkers of consumption of fiber-rich cereal products. The aim of this study was to examine the relationship between plasma ARs or urinary AR metabolites and cereal fiber intake in women consuming their habitual diet. Twenty-five postmenopausal and 31 premenopausal women were recruited. The subjects included also vegetarians (n = 20) to obtain a broad range of cereal intake. Dietary intake, plasma ARs, and urinary AR metabolites [3,5-dihydroxybenzoic acid and 3-(3,5-dihydroxyphenyl)-1-propanoic acid] were measured. Pearson's and Partial correlation tests were done between dietary fiber intake and plasma ARs or urinary AR metabolites. Cereal fiber intake correlated significantly with plasma AR C17:0 (r = 0.387), AR C19:0 (r = 0.350), AR C21:0 (r = 0.428), AR C23:0 (r = 0.409), AR C25:0 (r = 0.283), and total AR (r = 0.406) and with urinary AR metabolites DHBA (r = 0.359) and DHPPA (r = 0.402) even after adjustment for body mass index and age, which could be confounding variables. This is the first study to show a significant correlation between plasma ARs or urinary AR metabolites and cereal fiber intake during consumption of a habitual diet. These results indicate that assay of plasma ARs or urinary AR metabolites may be used as biomarkers in epidemiologic studies in free-living populations to evaluate the role of cereal fiber intake in various diseases. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2244–8)
Myeloperoxidase-Positive Cell Infiltration in Colorectal Carcinogenesis as Indicator of Colorectal Cancer Risk
Authors: Roncucci Luca , Mora Erika , Mariani Francesco , Bursi Serena , Pezzi Annalisa , Rossi Giuseppina , Pedroni Monica , Luppi Davide , Santoro Luisa , Monni Sebastiano , Manenti Antonio , Bertani Angela , Merighi Alberto , Benatti Piero , Di Gregorio Carmela , Ponz de Leon Maurizio 
Published: September 2008

Abstract
Colorectal mucosa is targeted by toxic agents, which can initiate or promote colon cancer. The mechanism of damage might be a focal irritation with loss of normal epithelial cell barrier function. Genetic alterations in tumors may also affect host inflammatory response. The aim of this study was to define the extent of inflammation in colorectal mucosa, along colorectal carcinogenesis, and in microsatellite stable and unstable colorectal carcinomas. We collected 103 samples of normal colorectal mucosa from 65 patients (35 with colorectal cancer or adenoma, 8 with inflammatory bowel diseases, and 22 controls with normal colonoscopy). We also examined 24 aberrant crypt foci, 14 hyperplastic polyps, 16 adenomas, and 67 samples of colorectal carcinoma. Immunohistochemistry was used to count myeloperoxidase (MPO)-positive cells (neutrophils and monocytes) in ×100 optical fields under a light microscope. Patients with colorectal tumors had a higher mean number of MPO-positive cells in normal mucosa than controls (mean ± SD, 2.7 ± 2.0 versus 1.4 ± 1.4; P = 0.017). MPO-positive cell number was tightly linked to dysplasia in aberrant crypt foci and adenomas, and it was higher in carcinomas microsatellite unstable than those microsatellite stable (21.6 ± 15.5 versus 11.9 ± 8.0; P &lt; 0.01). MPO immunohistochemistry is a simple and reliable technique for the quantification of inflammation in colorectal mucosa., and it may be a potential marker of colorectal cancer risk. Microsatellite instability seems to influence host immune responses to colorectal carcinoma. These observations strongly support a key role of inflammation in colorectal carcinogenesis. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2291–7)
Repair of UV Dimers in Skin DNA of Patients with Basal Cell Carcinoma
Authors: Segerbäck Dan , Strozyk Malgorzata , Snellman Erna , Hemminki Kari 
Published: September 2008

Abstract
Epidemiologic studies suggest that exposure to sunlight is the primary etiologic agent for basal cell carcinoma. Formation of UV-induced DNA damage is believed to be a crucial event in the process leading to skin cancer. In this study, repair of photoproducts in DNA was followed in the skin of patients with basal cell carcinoma and control subjects. The subjects were exposed to 800 J/m2 Commission Internationale de 1'Éclairag of solar-simulating radiation on buttock skin. Biopsies were taken at 0 hour, 24 hours, and 3 weeks after the exposure. Two cyclobutane pyrimidine dimers, TT=C and TT=T, were measured using a sensitive 32P-postlabeling assay. Initial levels of both TT=C and TT=T differed between individuals in both groups. The levels of TT=T in patients with basal cell carcinoma and controls were similar (9.9 ± 4.0 and 9.2 ± 2.9 products per 106 normal nucleotides), whereas the level of TT=C was significantly lower in controls than in patients with basal cell carcinoma (6.2 ± 3.1 versus 10.9 ± 4.5 products per 106 normal nucleotides). The fractions of TT=T remaining after 24 hours and 3 weeks were significantly higher in patients with basal cell carcinoma (72% and 11%) compared with controls (48% and 5%). A slower removal in patients with basal cell carcinoma than in controls was indicated also for TT=C (52% versus 42% remaining at 24 hours); however, the difference between groups was not significant. When including data from our previously reported small-scale study, the fraction of dimers remaining at 24 hours was significantly higher in patients with basal cell carcinoma for both TT=C and TT=T. The data suggest that patients with basal cell carcinoma have a reduced capacity to repair UV-induced DNA lesions. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2388–92)
Age and Severity of Mucosal Lesions Influence the Performance of Serologic Markers in Helicobacter pylori–Associated Gastroduodenal Pathologies
Authors: Camorlinga-Ponce Margarita , Flores-Luna Lourdes , Lazcano-Ponce Eduardo , Herrero Rolando , Bernal-Sahagún Fernando , Abdo-Francis Juan Miguel , Aguirre-García Jesús , Muñoz Nubia , Torres Javier 
Published: September 2008

Abstract
Objective: The course of Helicobacter pylori infection and antibody response to CagA in patients with preneoplastic lesions and gastric cancer has not been thoroughly studied. We aimed to study H. pylori infection and antibody response to CagA in patients with non–atrophic gastritis, preneoplastic lesions, and gastric cancer.
Methods: We studied patients attending one Oncology Hospital and one General Hospital in Mexico City. Diagnosis was based on endoscopy and histopathology in biopsies from six stomach regions. H. pylori infection was assessed by histology and serology, and antibodies against CagA were measured with immunoassay.
Results: We included 618 patients, 368 with non–atrophic gastritis, 126 with precancerous lesions, and 65 with gastric cancer; in addition, 59 patients with duodenal ulcer were studied. Detection of infection and IgG against CagA had a significant increase from non–atrophic gastritis to mild and up to advanced stages of metaplasia (P &lt; 0.05), followed by decreased infection and IgG to CagA in patients with gastric cancer (P &lt; 0.05). However, infection and CagA antibodies were associated with young gastric cancer cases. Duodenal ulcer showed a significant association with infection detected by histology and serology, particularly among women, and a trend to associate with IgG to CagA.
Conclusions: This study shows that H. pylori infection and CagA are risk markers for intestinal metaplasia. The prevalence of these risk markers decreases in gastric cancer, probably reflecting that infection decreases after advanced atrophy and metaplasia in the gastric mucosa. State of the disease, age, and sex influence the association of H. pylori infection and IgG response to CagA with gastroduodenal diseases. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2498–504)
Genetic Polymorphisms of the E-Cadherin Promoter and Risk of Sporadic Gastric Carcinoma in Chinese Populations
Authors: Zhang Baozhen , Pan Kaifeng , Liu Zhaojun , Zhou Jing , Gu Liankun , Ji Jiafu , Ma Junling , You Wei-cheng , Deng Dajun 
Published: September 2008

Abstract
Frequent mutations and loss of expression of E-cadherin have been reported in a number of cancers. E-cadherin germ line mutations lead to a high risk of familial diffused gastric carcinoma. In the present study, to evaluate the effect of genetic polymorphisms in the E-cadherin promoter on the risk of sporadic gastric carcinoma (SGC), a comprehensive study was conducted in two populations with high and low risk of SGC in China, respectively. Five hundred seventy-two SGC cases and 625 controls from low-risk area and 589 individuals enrolled in a long-term follow-up survey in high-risk area were studied. Polymorphisms of E-cadherin around transcription start site (−437 to +314) were analyzed by sequencing. Five variations of −347del&gt;A, −160C&gt;A, −73A&gt;C, +178T&gt;C, and +234 13N ins&gt;del were linked tightly. The −347del/del and its strongly linked +178T/T, +234 13N ins/ins genotypes increased male SGC risk in the high-risk area significantly [odds ratio (OR), 2.22; 95% confidence intervals (95% CI), 1.10-4.46] and correlated with the severity of gastric lesions. A synergetic effect was also observed between −347del/del genotype and Helicobacter pylori infection (OR, 4.93; 95% CI, 1.65-14.71). Compared with −347del-containing haplotypes, the −347A-containing haplotype [A(−347)-C(−160)-A(−73)-C(+178)-13N del(+234)] decreased the risk of SGC among male subjects (OR, 0.61; 95% CI, 0.37-1.01). Such correlation could not be observed among subjects from the low-risk area. The present data suggest that the −347del allele of E-cadherin strongly links with the +178T and +234 13N ins alleles. The −347del/del genotype may increase the susceptibility of SGC among males in the high-risk area of China. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2402–8)
Residential Traffic Density and Childhood Leukemia Risk
Authors: Behren Julie Von , Reynolds Peggy , Gunier Robert B. , Rull Rudolph P. , Hertz Andrew , Urayama Kevin Y. , Kronish Daniel , Buffler Patricia A. 
Published: September 2008

Abstract
Background: Exposures to carcinogenic compounds from vehicle exhaust may increase childhood leukemia risk, and the timing of this exposure may be important.
Methods: We examined the association between traffic density and childhood leukemia risk for three time periods: birth, time of diagnosis, and lifetime average, based on complete residential history in a case-control study. Cases were rapidly ascertained from participating hospitals in northern and central California between 1995 and 2002. Controls were selected from birth records, individually matched on age, sex, race, and Hispanic ethnicity. Traffic density was calculated by estimating total vehicle miles traveled per square mile within a 500-foot (152 meter) radius area around each address. We used conditional logistic regression analyses to account for matching factors and to adjust for household income.
Results: We included 310 cases of acute lymphocytic leukemias (ALL) and 396 controls in our analysis. The odds ratio for ALL and residential traffic density above the 75th percentile, compared with subjects with zero traffic density, was 1.17 [95% confidence interval (95% CI), 0.76-1.81] for residence at diagnosis and 1.11 (95% CI, 0.70-1.78) for the residence at birth. For average lifetime traffic density, the odds ratio was 1.24 (95% CI, 0.74-2.08) for the highest exposure category.
Conclusions: Living in areas of high traffic density during any of the exposure time periods was not associated with increased risk of childhood ALL in this study. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2298–301)
Height and Prostate Cancer Risk: A Large Nested Case-Control Study (ProtecT) and Meta-analysis
Authors: Zuccolo Luisa , Harris Ross , Gunnell David , Oliver Steven , Lane Jane Athene , Davis Michael , Donovan Jenny , Neal David , Hamdy Freddie , Beynon Rebecca , Savovic Jelena , Martin Richard Michael 
Published: September 2008

Abstract
Background: Height, a marker of childhood environmental exposures, is positively associated with prostate cancer risk, perhaps through the insulin-like growth factor system. We investigated the relationship of prostate cancer with height and its components (leg and trunk length) in a nested case-control study and with height in a dose-response meta-analysis.
Methods: We nested a case-control study within a population-based randomized controlled trial evaluating treatments for localized prostate cancer in British men ages 50 to 69 years, including 1,357 cases detected through prostate-specific antigen testing and 7,990 controls (matched on age, general practice, assessment date). Nine bibliographic databases were searched systematically for studies on the height-prostate cancer association that were pooled in a meta-analysis.
Results: Based on the nested case-control, the odds ratio (OR) of prostate-specific antigen–detected prostate cancer per 10 cm increase in height was 1.06 [95% confidence interval (95% CI): 0.97-1.16; ptrend = 0.2]. There was stronger evidence of an association of height with high-grade prostate cancer (OR: 1.23; 95% CI: 1.06-1.43), mainly due to the leg component, but not with low-grade disease (OR: 0.99; 95% CI: 0.90-1.10). In general, associations with leg or trunk length were similar. A meta-analysis of 58 studies found evidence that height is positively associated with prostate cancer (random-effects OR per 10 cm: 1.06; 95% CI: 1.03-1.09), with a stronger effect for prospective studies of more advanced/aggressive cancers (random-effects OR: 1.12; 95% CI: 1.05-1.19).
Conclusion: These data indicate a limited role for childhood environmental exposures—as indexed by adult height—on prostate cancer incidence, while suggesting a greater role for progression, through mechanisms requiring further investigation. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2325–36)
Serum Calcium and Incident and Fatal Prostate Cancer in the National Health and Nutrition Examination Survey
Authors: Skinner Halcyon G. , Schwartz Gary G. 
Published: September 2008

Abstract
We examined the association between serum calcium levels and the risk for prostate cancer using a prospective cohort, the National Health and Nutrition Examination Survey (NHANES) and the NHANES Epidemiologic Follow-up Study. Eighty-five incident cases of prostate cancer and 25 prostate cancer deaths occurred over 46,188 person-years of follow-up. Serum calcium was determined an average of 9.9 years before the diagnosis of prostate cancer. Comparing men in the top with men in the bottom tertile of serum calcium, the multivariable-adjusted relative hazard for fatal prostate cancer was 2.68 (95% confidence interval, 1.02-6.99; Ptrend = 0.04). For incident prostate cancer, the relative risk for the same comparison was 1.31 (95% confidence interval, 0.77-2.20; Ptrend = 0.34). These results support the hypothesis that high serum calcium or a factor strongly associated with it (e.g., high serum parathyroid hormone) increases the risk for fatal prostate cancer. Our finding of a &gt;2.5-fold increased risk for men in the highest tertile of serum calcium is comparable in magnitude with the risk associated with family history and could add significantly to our ability to identify men at increased risk for fatal prostate cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2302–5)
Domestic and Farm-Animal Exposures and Risk of Non-Hodgkin's Lymphoma in a Population-Based Study in the San Francisco Bay Area
Authors: Tranah Gregory J. , Bracci Paige M. , Holly Elizabeth A. 
Published: September 2008

Abstract
Objective: To assess the association between animal exposures and non-Hodgkin's lymphoma (NHL).
Methods: Exposure data were collected from 1,591 cases and 2,515 controls during in-person interviews in a population-based case-control study of NHL in the San Francisco Bay Area. Odds ratios (OR) and 95% confidence intervals (95% CI) were adjusted for potential confounders.
Results: Pet owners had a reduced risk of NHL (OR, 0.71; 95% CI, 0.52-0.97) and diffuse large-cell lymphoma large cell (DLCL; OR, 0.58; 95% CI, 0.39-0.87) compared with those who never had owned a pet. Ever having owned dogs and/or cats was associated with reduced risk of all NHL (OR, 0.71; 95% CI, 0.54-0.94) and of DLCL (OR, 0.60; 95% CI, 0.42-0.86). Longer duration of cat ownership (Ptrend = 0.008), dog ownership (Ptrend = 0.04), and dog and/or cat ownership (Ptrend = 0.004) was inversely associated with risk of NHL. Ownership of pets other than cats and dogs was associated with a reduced risk of NHL (OR, 0.64; 95% CI, 0.55-0.74) and DLCL (OR, 0.58; 95% CI, 0.47-0.71). Exposure to cattle for ≥5 years was associated with an increased risk of NHL (OR, 1.6; 95% CI, 1.0-2.5) as was exposure to pigs for all NHL (OR, 1.8; 95% CI, 1.2-2.6) and for DLCL (OR, 2.0; 95% CI, 1.2-3.4).
Conclusions: The association between animal exposure and NHL warrants further investigation in pooled analyses. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2382–7)
Association of Prostate-Specific Antigen Promoter Genotype with Clinical and Histopathologic Features of Prostate Cancer
Authors: Cramer Scott D. , Sun Jielin , Zheng S. Lilly , Xu Jianfeng , Peehl Donna M. 
Published: September 2008

Abstract
The serum test for the secreted protease prostate-specific antigen (PSA) is the most widely used screening tool for prostate cancer. The PSA gene contains multiple functional and nonfunctional single nucleotide polymorphisms (SNP) in its promoter. We showed previously that the rs925013 G/A SNP, but not the rs266882 G/A SNP, was significantly associated with serum PSA in healthy men. In this study, we evaluated the association of the PSA promoter genotype with clinical data in a cohort of 1,224 men with prostate cancer. Previous work with a subset of this cohort has shown that percent high-grade (Gleason grades 4 and 5) cancer was the strongest predictor of biochemical recurrence (PSA relapse). We found a statistically significant association (P &lt; 0.05) of the rs925013 SNP with several clinical and histomorphologic variables. The G allele was associated with higher serum PSA at diagnosis, higher percent Gleason grade 3 cancer, and lower percent high-grade and Gleason grade 4 cancer. The rs266882 SNP was modestly associated with PSA at diagnosis in a dominant model but was not associated with cancer grade. Neither SNP was associated with biochemical recurrence. The statistically significant predictors of biochemical recurrence were tumor location in the peripheral zone [odds ratio (OR), 10.71; 95% confidence interval (95% CI), 3.15-36.49], presence of any Gleason grade 4/5 cancer (OR, 4.26; 95% CI, 1.30-14.00), presence of any intraductal cancer (OR, 1.03; 95% CI, 1.00-1.04), and serum PSA at diagnosis (OR, 2.04; 95% CI, 1.50-2.77). (Cancer Epidemiol Biomarkers Prev 2008;17(9):2451–7)
Estrogen plus Progestin and Risk of Benign Proliferative Breast Disease
Authors: Rohan Thomas E. , Negassa Abdissa , Chlebowski Rowan T. , Lasser Norman L. , McTiernan Anne , Schenken Robert S. , Ginsberg Mindy , Wassertheil-Smoller Sylvia , Page David L. 
Published: September 2008

Abstract
Women with benign proliferative breast disease are at increased risk of subsequent breast cancer. Estrogens and progesterone exert proliferative effects on mammary epithelium, and combined hormone replacement therapy has been associated with increased breast cancer risk. We tested the effect of conjugated equine estrogen plus progestin on the risk of benign proliferative breast disease in the Women's Health Initiative (WHI) randomized controlled trial. In the WHI trial of estrogen plus progestin, 16,608 postmenopausal women were randomly assigned either to 0.625 mg/day of conjugated equine estrogen plus 2.5 mg/day of medroxyprogesterone acetate or to placebo. Baseline and annual breast exams and mammograms were required. The trial was terminated early (average follow-up, 5.5 years). We identified women who had had a biopsy for benign breast disease, and subjected histologic sections from the biopsies to standardized review. Overall, 178 incident cases of benign proliferative breast disease were ascertained in the estrogen plus progestin group and 99 in the placebo group. The use of estrogen plus progestin was associated with a 74% increase in the risk of benign proliferative breast disease [hazard ratio, 1.74; 95% confidence interval (CI), 1.35-2.25]. For benign proliferative breast disease without atypia the hazard ratio was 2.00 (95% CI, 1.50-2.66), while for atypical hyperplasia it was 0.76 (95% CI, 0.38-1.52). The risk varied little by levels of baseline characteristics. The results of this study suggest that the use of estrogen plus progestin may increase the risk of benign proliferative breast disease. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2337–43)
Placental Weight and Risk of Invasive Epithelial Ovarian Cancer with an Early Age of Onset
Authors: Cnattingius Sven , Eloranta Sandra , Adami Hans-Olov , Axelsson Ove , Dickman Paul W. , Hsieh Chung-cheng , Mucci Lorelei A. , Trichopoulos Dimitrios , Lambe Mats , Johansson Anna L.V. 
Published: September 2008

Abstract
Background: Epithelial ovarian cancer is associated with reproductive factors, but we lack knowledge if hormonal factors during pregnancy influence the mother's risk. Because pregnancy hormones are primarily produced by the placenta, placental weight may be an indirect marker of hormone exposure during pregnancy.
Methods: In a nationwide Swedish cohort study, we included women with singleton births from 1982 to 1989. Women were followed for occurrence of invasive epithelial ovarian cancer, death, or emigration through 2004. Hazard ratios (HR) with 95% confidence intervals (95% CI) from Cox models were used to estimate associations between pregnancy exposures and epithelial ovarian cancer.
Results: Among 395,171 women with information on placental weight in their first recorded birth, 316 women developed invasive epithelial ovarian cancer. Mean age at diagnosis was 44 years. Compared with women with a placental weight of 500 to 699 g, women with a high (≥700 g) placental weight had an increased risk of developing epithelial ovarian cancer (HR, 1.47; 95% CI, 1.14-1.90). Compared with women with term pregnancies (40-41 weeks), women with post-term (≥42 weeks) pregnancies had an increased risk of developing epithelial ovarian cancer (HR, 1.48; 95% CI, 1.00-2.19). These associations were slightly stronger when we included information about women's overall first birth, and slightly weaker when we included information about last recorded birth or ever last birth from 1982 to 1989.
Conclusions: Because pregnancy hormone levels increase with placental weight, our study supports the hypothesis that hormone exposures during pregnancy influence the risk of invasive epithelial ovarian cancer among young women. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2344–9)