bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transition Metals in Personal Samples of PM2.5 and Oxidative Stress in Human Volunteers
Authors: Sørensen Mette , Schins Roel P.F. , Hertel Ole , Loft Steffen 
Published: September 2005

Abstract
Ambient particulate matter (PM) has been associated with increased risk of lung cancer. One proposed mechanism is that PM induces oxidative stress mediated by transition metals contained within this mixture. We examined the relationship between the personal exposure to water-soluble transition metals in PM2.5 and oxidative DNA damage. In 49 students from central Copenhagen, we determined PM2.5 exposure by personal sampling twice in 1 year, and measured in these PM2.5 samples the concentration of the soluble transition metals vanadium, chromium, iron, nickel, copper, and platinum. Collected lymphocytes and 24-hour urine samples were analyzed for DNA damage in terms of 7-hydro-8-oxo-2′-deoxyguanosine (8-oxodG). We found that the 8-oxodG concentration in lymphocytes was significantly associated with the vanadium and chromium concentrations with a 1.9% increase in 8-oxodG per 1 μg/L increase in the vanadium concentration and a 2.2% increase in 8-oxodG per 1 μg/L increase in the chromium concentration. We have previously reported that in this study population the personal exposure to PM2.5 was associated with an increase in 8-oxodG in lymphocytes. However, vanadium and chromium were associated with the 8-oxodG concentration in lymphocytes independently of the PM2.5 mass concentration. The four other transition metals were not associated with 8-oxodG in lymphocytes and none of the transition metals was significantly associated with 8-oxodG in urine. Our results could indicate that vanadium and chromium present in PM2.5 have an effect on oxidative DNA damage that is independent of particle mass and/or other possible toxic compounds contained within this particulate mixture.
A Modified Host Cell Reactivation Assay to Measure DNA Repair Capacity for Removing 4-Aminobiphenyl Adducts: A Pilot Study of Bladder Cancer
Authors: Lin Jie , Kadlubar Fred F. , Spitz Margaret R. , Zhao Hua , Wu Xifeng 
Published: September 2005

Abstract
As DNA repair plays an important role in genetic susceptibility to bladder cancer, assessment of the DNA repair phenotype is critical for the molecular epidemiology of bladder cancer. In this study, we developed and applied an assay using the luciferase (luc) reporter gene in a host-cell reactivation assay to measure DNA repair capacity for DNA damage induced by 4-aminobiphenyl (4-ABP), a well-studied aromatic amine and a known bladder carcinogen. We observed a dose-response relationship for 4-ABP dosage and DNA repair capacity (luc activity). We then applied this assay to measure DNA repair capacity in a pilot study of 89 pairs of bladder cancer patients and healthy controls matched by age, gender, and ethnicity, and we found that DNA repair capacity was significantly lower in cases than in controls (13.0% versus 14.4%; P = 0.006). Poor DNA repair capacity was associated with 3.42-fold increased bladder cancer risk. Further analysis revealed that intermediate and low levels of DNA repair capacity increased bladder cancer risk to 3.43-fold and 4.97-fold, respectively, compared with individuals with the most efficient DNA repair capacity. Moreover, ever smokers with suboptimal DNA repair capacity exhibited a 6.06-fold increased risk compared with never smokers with normal DNA repair capacity. In conclusion, our results support the hypothesis that deficient DNA repair capacity for 4-ABP induced DNA damage and increases bladder cancer risk. Our assay provides a new tool to specifically quantify DNA repair capacity in bladder cancer studies and, therefore, contributes to our goal of further elucidating bladder carcinogenesis.
Sex Differences in Risk of Lung Cancer Associated with Methylene-tetrahydrofolate Reductase Polymorphisms
Authors: Shi Qiuling , Zhang Zhendong , Li Guojun , Pillow Patricia C. , Hernandez Ladia M. , Spitz Margaret R. , Wei Qingyi 
Published: September 2005

Abstract
Methylenetetrahydrofolate reductase (MTHFR) catalyzes the metabolism of folate and nucleotides needed for DNA synthesis and repair. Variations in MTHFR functions likely play roles in the etiology of lung cancer. The MTHFR gene has three nonsynonymous single nucleotide polymorphisms (i.e., C677T, A1298C, and G1793A) that have a minor allele frequency of &gt;5%. We investigated the associations between the frequencies of MTHFR variant genotypes and risk of lung cancer in a hospital-based case-control study of 1,051 lung cancer patients and 1,141 cancer-free controls in a non-Hispanic White population. We found that compared with the MTHFR 1298AA genotype, the 1298CC genotype was associated with a significantly increased risk of lung cancer in women [(odds ratio (OR), 2.09; 95% confidence interval (95% CI), 1.32-3.29)] but not in men (OR, 0.95; 95% CI, 0.62-1.45). The MTHFR 677TT genotype was associated with a significantly decreased risk of lung cancer in women (OR, 0.60; 95% CI, 0.40-0.92) but not in men. No association was found between the MTHFR G1793A polymorphism and risk of lung cancer. Further analysis suggested evidence of gene-dietary interactions between the MTHFR C677T polymorphism and dietary intake of vitamin B6, vitamin B12, and methionine in women and evidence of gene-environment interactions between the MTHFR C677T and A1298C polymorphisms and tobacco smoking in men. In conclusion, the polymorphisms of MTHFR may contribute to the risk of lung cancer in non-Hispanic Whites and modify the risk associated with the dietary and environmental exposure in a sex-specific manner.
Family History of Cancer, Its Combination with Smoking and Drinking, and Risk of Squamous Cell Carcinoma of the Esophagus
Authors: Garavello Werner , Negri Eva , Talamini Renato , Levi Fabio , Zambon Paola , Dal Maso Luigino , Bosetti Cristina , Franceschi Silvia , La Vecchia Carlo 
Published: September 2005

Abstract
We analyzed the association between history of cancer in first-degree relatives and the risk of squamous cell carcinoma of the esophagus (SCCE) using data from three case-control studies conducted in Italy and Switzerland on 805 incident, histologically confirmed SCCE, and 3,461 hospital controls. The alcohol- and tobacco-adjusted odds ratio (OR) for a family history of esophageal cancer was 3.2 [95% confidence interval (CI), 1.7-6.2], and the OR was higher when the affected relative was a brother or was diagnosed at age &lt;55 years. Compared to subjects without family history of esophageal cancer, noncurrent smokers, drinking &lt;49 drinks per week, the OR was 2.9 (95% CI, 1.1-7.5) for family history alone, 15.5 (95% CI, 11.7-20.5) for current smokers drinking ≥49 drinks per week without family history of esophageal cancer, and 107.0 (95% CI, 13.0-880.2) for current smokers drinking ≥49 drinks per week who also had a family history of esophageal cancer. The risk of SCCE was also increased in subjects with a family history of cancer of the oral cavity/pharynx (OR, 3.7; 95% CI, 1.5-9.0) and stomach (OR, 2.0; 95% CI, 1.1-3.6), but not of other cancers, nor for a family history of any cancer (OR, 1.0; 95% CI, 0.8-1.4). These data show that, as for many other epithelial cancers, the risk of SCCE is increased in subjects with a family history of the disease, and that—in Western countries—avoidance of alcohol and tobacco is also the best way to prevent SCCE in subjects with a family history of the disease.
Associations among Circulating Sex Hormones, Insulin-Like Growth Factor, Lipids, and Mammographic Density in Postmenopausal Women
Authors: Aiello Erin J. , Tworoger Shelley S. , Yasui Yutaka , Stanczyk Frank Z. , Potter John , Ulrich Cornelia M. , Irwin Melinda , McTiernan Anne 
Published: September 2005

Abstract
Objective: Hormone therapy use has been positively associated with mammographic density in several studies. However, few studies have examined the association between endogenous hormone levels and mammographic density. Therefore, we evaluated the relationship of endogenous sex hormones, insulin-like growth factor (IGF), and lipids with mammographic density in 88 overweight, postmenopausal women not taking hormone therapy.
Methods: Percent density and dense area were evaluated as continuous measures using a computer-assisted program. We used multiple linear regression to evaluate the associations of sex hormones, IGF, and cholesterol with mammographic density, adjusting for confounders, including adiposity. We evaluated stratification by history of hormone therapy use (former versus never) and hormone therapy latency (&lt;5 versus ≥5 years).
Results: Among former hormone therapy users, mammographic density was inversely associated with circulating levels of estrone (P = 0.01), estradiol (P = 0.003), free estradiol (P = 0.004), testosterone (P = 0.04), free testosterone (P = 0.02), androstenedione (P &lt; 0.001), dehydroepiandrosterone (P = 0.01), and the ratio of IGF-I to its binding protein (IGF-I/IGFBP-3; P = 0.04). We found similar associations when we limited the analyses to women who had used hormone therapy within the past 5 years. We also noted positive associations of mammographic density with total cholesterol (P = 0.03) and low-density lipoprotein (P = 0.03) among former hormone therapy users. No associations were noted among women who had never used hormone therapy.
Conclusions: These results suggest that there is an inverse relationship between endogenous sex hormones and mammographic density in postmenopausal women among former users of hormone therapy. This is not consistent with the hormone therapy literature and should be confirmed in larger studies.
Absence of TP53 Codon 249 Mutations in Young Guinean Children with High Aflatoxin Exposure
Authors: Turner Paul C. , Sylla Abdoulaye , Kuang Shuang-Yuan , Marchant Clare L. , Diallo Mamadou S. , Hall Andrew J. , Groopman John D. , Wild Christopher P. 
Published: September 2005

Abstract
Infection with hepatitis viruses and chronic exposure to high levels of dietary aflatoxins are the major etiologic agents for hepatocellular carcinoma in west Africa. A challenge for the prevention of hepatocellular carcinoma in this region is that both hepatitis B virus and aflatoxin exposures start early in life; indeed, aflatoxin exposures can start in utero and continue unabated throughout childhood. A mutation in the TP53 tumor suppressor gene at codon 249 (TP53 Ser249 mutation) has been reported previously for hepatocellular carcinoma tumors and matched plasma DNA samples in individuals from areas with high aflatoxin exposure. We examined whether the TP53 Ser249 mutation could be observed in DNA found in plasma of young children (ages 2-5 years) from Guinea, west Africa, a region of high aflatoxin exposure. Plasma aflatoxin-albumin adducts were present in 119 of 124 (96%) of the children, geometric mean of positives 9.9 pg/mg albumin (95% confidence interval, 8.8-11.0 pg/mg). This is the level and prevalence of exposure observed previously in adults. Following PCR amplification of plasma-derived DNA and detection using mass spectrometry, none of the samples were found to contain the TP53 Ser249 mutation. Because ∼50% of the hepatocellular carcinomas in adults in west Africa have this specific TP53 Ser249 mutation, a lack of detection in samples from children ages &lt;5 years may indicate that a window of opportunity for intervention exists that could be exploited to lower hepatocellular carcinoma risk.
Determinants of Prevalence, Acquisition, and Persistence of Human Papillomavirus in Healthy Mexican Military Men
Authors: Lajous Martín , Mueller Nancy , Cruz-Valdéz Aurelio , Aguilar Luis Victor , Franceschi Silvia , Hernández-Ávila Mauricio , Lazcano-Ponce Eduardo 
Published: September 2005

Abstract
Background: Human papillomavirus (HPV) infection is sexually transmitted, but the nature of the infection in males is poorly understood. We sought to identify determinants of HPV infection, acquisition, and persistence in 1,030 healthy military men in Mexico.
Methods: From July 2000 to July 2003, trained interviewers administered a questionnaire, conducted a genital examination, and collected samples. The presence of multiple HPV types in genital cells from the urethra, urethral meatus, scrotum, penile shaft, and coronal sulcus was evaluated. At baseline 1,030 participants and after 1-year follow-up 336 individuals were sampled using a highly sensitive DNA reverse blot strip assay.
Results: HPV prevalence was 44.6%; infection with high-risk types was observed in 34.8% participants and 51.1% were multiply infected. After 1-year follow-up, 165 men remained free of HPV, 68 cleared their infection, 45 acquired one, and 37 remained infected with the same HPV type. The period prevalence was 50.9%, the incidence rate was 17.9/1,000 men-months [95% confidence interval (95% CI), 13.0-23.9], clearance was 54%, and persistence was 29.4%. At baseline, the number of partners before age 20 years, a history of a sexually transmitted disease, and the presence of condilomas significantly increased the association with HPV infection. Having anal intercourse with males was associated with the risk of acquiring a HPV infection (odds ratio, 5.2; 95% CI, 1.2-23). The odds ratio for persistent infection was 0.10 (95% CI, 0-0.87) in men who reported being circumcised compared with those who did not.
Conclusions: High-risk sexual behavior increases the risk of HPV infection in males, whereas circumcision may lower the risk of persistence.
Significant Difference in the Trends of Female Breast Cancer Incidence Between Taiwanese and Caucasian Americans: Implications from Age-Period-Cohort Analysis
Authors: Shen Ying-Chun , Chang Chee-Jen , Hsu Chiun , Cheng Chia-Chi , Chiu Chang-Fang , Cheng Ann-Lii 
Published: September 2005

Abstract
Female invasive breast cancer (FIBC) in Taiwan is characterized by a striking recent increase of incidence and a relatively young median age (45-49 years) at diagnosis. The Westernization of lifestyle that is increasingly affecting younger generations of Taiwanese may have an important impact on this change. We compared epidemiologic data on FIBC in Taiwanese obtained from the Taiwan Cancer Registry with data for Caucasian Americans obtained from the database of the Surveillance, Epidemiology, and End Results Program for the period from 1980 to 1999. Age-specific incidence rates of FIBC were plotted by calendar year at diagnosis and by birth cohort for both populations. The individual effects of time period and birth cohort on the incidence trends of FIBC in both populations were evaluated using the age-period-cohort analysis. The incidence rate of FIBC was continuously increased in Taiwanese throughout the past 2 decades, whereas the increase of incidence was slowing down in Caucasian Americans. The incidence rates in Taiwanese women born after the 1960s were approaching that of Caucasian Americans. The age-period-cohort analysis showed a much stronger birth cohort effect on the incidence trend of FIBC in Taiwanese than in Caucasian Americans. This strong birth cohort effect corresponded to the Westernization of lifestyle in Taiwan since 1960. These findings indicate that a continued shift in the incidence and age distribution pattern of FIBC in Taiwanese toward that of Caucasian Americans should be anticipated.
Season, Sun, Sex, and Cervical Cancer
Authors: Hrushesky William J.M. , Sothern Robert B. , Rietveld Wop J. , Du Quiton Jovelyn , Boon Mathilde E. 
Published: September 2005

Abstract
Introduction: Sunlight's UV B component, a known cellular immunosupressant, carcinogen, and activator of viral infections, is generally seasonally available. Venereal human papillomavirus (HPV) transmission, at least in part, causes cervical cancer. We have previously inspected the monthly rates of venereal HPV infection and sunlight fluency in Southern Holland over 16 consecutive years. Both peak in August with at least 2-fold seasonality. The amount of available sunlight and the rate of Papanicolaou (Pap) smear screen–detected HPV are positively correlated. We now investigate whether premalignant and malignant cervical epithelial changes are also seasonal and related to seasonal sunlight fluency.
Methods: We have studied &gt;900,000 consecutive, serially independent, interpretable screening Pap smears obtained by a single cervical cancer screening laboratory in Leiden, Holland, during a continuous 16-year span from 1983 through 1998. The average monthly rates of premalignant and malignant epithelial change were inspected and the annual patterns contrasted to the annual pattern of sunlight fluency at this global location and to monthly average HPV infection rate. Because HPV is venereally transmitted, Dutch seasonal sexual behavior was evaluated by assessment of the annual pattern of Dutch conception frequency as a competing cause for cervical cancer seasonality.
Results: (a) Twice as many premalignant and malignant epithelial changes were found among Pap smears obtained in the summer months, with an August peak concurrent with histopathologic evidence of HPV infection and sunlight fluency in Southern Holland. (b) Monthly sunlight fluency is correlated positively with both the monthly rates of Pap smear–detected cervical epithelial dysplasia and carcinomatous histopathology, as well as HPV. (c) Conception frequency, in this location, peaks in Spring not summer, and has a 4.8% annual amplitude.
Conclusions: (a) Cervical epithelial HPV infection and HPV-induced cervical epithelial dysplasia and carcinomatous change may each be novel sun exposure risks and thereby behaviorably avoidable. (b) Because screening Pap smears uncover many abnormalities that resolve spontaneously (false positives), these data may argue for screening and follow-up Pap smear examinations in seasons other than summer in the Northern Hemisphere, to diminish the false-positive smear rate. Global data are available to confirm and further test each of these conclusions.
Racial Differences in Premenopausal Endogenous Hormones
Authors: Pinheiro Simone P. , Holmes Michelle D. , Pollak Michael N. , Barbieri Robert L. , Hankinson Susan E. 
Published: September 2005

Abstract
Differences in breast cancer incidence across racial groups are well documented. African Americans have the highest rates of premenopausal breast cancer and Asians have lower breast cancer rates across all age groups. We hypothesized that levels of premenopausal endogenous hormones and growth factors, risk factors that have been predictive of breast cancer, would differ by race. Using a cross-sectional study design, we tested this hypothesis in the Nurses' Health Study II. We assayed estradiol, progesterone, prolactin, sex hormone binding globulin (SHBG), insulin-like growth factor-I (IGF-I), and IGFBP-3 in 111 African American and 111 Asian American women, matched to 111 Caucasian women on age, day of luteal phase, and day, time, and fasting status at blood collection. We analyzed the association between race and hormone levels using robust linear regression methods. In multivariate models, compared with Caucasians, African Americans had 18% higher levels of estradiol (P &lt; 0.01), 17% higher free estradiol (P &lt; 0.01), 11% lower SHBG (P = 0.05), 11% higher IGF-I (P &lt; 0.01), 25% higher free IGF-I (P &lt; 0.01), and 9% lower IGFBP-3 (P &lt; 0.01) levels. In multivariate models, compared with Caucasian women, Asian Americans had 22% higher calculated free estradiol (P &lt; 0.01), 31% lower SHBG (P &lt; 0.01), and 25% higher free IGF-I (P &lt; 0.01) levels. No racial differences were found in progesterone and prolactin levels. Our study showed hormone differences consistent with breast cancer risk between Caucasians and African Americans but inconsistent with breast cancer risk between Asian Americans and Caucasians. Further research is needed to explore differences across racial groups and the link between endogenous hormones and breast cancer risk.
Investigation of Genetic Variants of Genes of the Hemochromatosis Pathway and Their Role in Breast Cancer
Authors: Abraham Benny K. , Justenhoven Christina , Pesch Beate , Harth Volker , Weirich Gregor , Baisch Christian , Rabstein Sylvia , Ko Yon-Dschun , Brüning Thomas , Fischer Hans-Peter , Haas Susanne , Brod Sandra , Oberkanins Christian , Hamann Ute , Brauch Hiltrud ,   for the GENICA Network
Published: September 2005

AbstractIron overload has been noticed as a feature of human breast cancer. Cellular iron uptake is regulated by the hemochromatosis and transferrin receptor system, mutations of which cause the iron storage disease hereditary hemochromatosis. To understand the role of hemochromatosis and transferrin receptor system mutations in breast cancer, we analyzed 19 sequence variations at HFE, TFR1, TFR2, and FPN1 and compared genotype frequencies between cases and controls in a German population. There were 688 breast cancer patients and 724 population-based and age-matched controls. For genotyping, we applied the Hemochromatosis Strip Assay and TaqMan allelic discrimination analyses. In addition to genotype frequencies, we established frequencies of compound genotypes. The frequencies of HFE at His63Asp, Ser65Cys, and Cys282Tyr, and of TFR1 at Ser142Gly minor alleles in this German population were 15.9%, 1.8%, 5.6%, and 46.0%, respectively. No rare variants at 15 more loci at HFE, TFR2, and FPN1 were observed in breast cancer patients. There were no significant differences of allele and genotype frequencies between cases and controls. Triple and quadruple compound genotypes at HFE_His63_Cys282-TFR1_Ser142Gly and HFE_His63_Ser65_Cys282-TFR1_Ser142Gly showed a nonsignificant increase in cases. Although limited by low numbers, an increased prevalence of the HFE Tyr282 minor allele was observed in breast cancer cases with a high number of affected lymph nodes (P = 0.032). Our data suggest that variants of the hemochromatosis-transferrin receptor system have no direct effect on the incidence of breast cancer in Germany. Possible effects on tumor progression and prognosis remain elusive.
Cyclooxygenase-2 Expression in FAP Patients Carrying Germ Line MYH Mutations
Authors: Frattini Milo , Carnevali Ileana , Signoroni Stefano , Balestra Debora , Moiraghi Maria Luisa , Radice Paolo , Varesco Liliana , Gismondi Viviana , Ballardini Giovanni , Sala Paola , Pierotti Marco A. , Pilotti Silvana , Bertario Lucio 
Published: September 2005

Abstract
Familial adenomatous polyposis (FAP) is an autosomal condition caused by inherited mutations in the adenomatous polyposis coli (APC) or in the MYH genes. Clinical trials have established that nonsteroidal anti-inflammatory drugs (NSAID) are effective in preventing the development as well as reducing the size and decreasing the number of adenomas in FAP patients. Our aim was to evaluate the cyclooxygenase-2 (COX-2) expression in surgical specimens from patients with no evidence of germ line APC mutations but carrying germ line MYH mutations. COX-2 expression was evaluated through immunohistochemical and mRNA analysis in carcinomas, adenomas, and healthy mucosa from six patients carrying germ line biallelic MYH mutations. A modulation of COX-2 expression from adenoma (lower level) to carcinoma (higher level) was observed in all patients by both immunohistochemical and mRNA analysis. Moreover, patients with MYH mutations showed a weak COX-2 expression in the whole colorectal mucosa, as for classic FAP patients carrying germ line APC mutations. All together, our data suggest that biallelic MYH patients might benefit from NSAID treatment, because in these patients COX-2 is overexpressed in the whole colorectal mucosa, a finding possibly related to the interplay between COX-2 and APC protein being the APC gene a common target of mutations in MYH patients.