bluuebunny/crossref_metadata_2025_split huggingface dataset:
Similar Uptake of Lung Carcinogens by Smokers of Regular, Light, and Ultralight Cigarettes
Authors: Hecht Stephen S. , Murphy Sharon E. , Carmella Steven G. , Li Shelby , Jensen Joni , Le Chap , Joseph Anne M. , Hatsukami Dorothy K. 
Published: September 2005

Abstract
Cigarette design has changed markedly over the past 60 years and sales-weighed levels of tar and nicotine have decreased. Currently, cigarettes are classified as regular (&gt;14.5 mg tar), light (&gt;6.5-14.5 mg tar), and ultralight (≤6.5 mg tar), based on a Federal Trade Commission–specified machine-smoking protocol. Epidemiologic studies suggest that there is no difference in lung cancer risk among people who smoke light or ultralight cigarettes compared with regular cigarettes, but the uptake of lung carcinogens in smokers of these types of cigarettes has never been reported. We recruited 175 smokers, who filled out a tobacco use questionnaire in which their current brand was identified as regular, light, or ultralight. Urine samples were collected and analyzed for 1-hydroxypyrene (1-HOP), total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL plus its glucuronides) and total cotinine (cotinine plus its glucuronides). 1-HOP and total NNAL are biomarkers of uptake of polycyclic aromatic hydrocarbons and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, lung carcinogens in cigarette smoke. Total cotinine is a biomarker of nicotine uptake. There were no statistically significant differences in urinary levels of 1-HOP, total NNAL, and total cotinine in smokers of regular, light, and ultralight cigarettes, whether the results were expressed per mg urinary creatinine, per mL of urine, or per mg creatinine divided by cigarettes per day. Levels of machine measured tar were available for the cigarettes smoked by 149 of the subjects. There was no correlation between levels of tar and any of the biomarkers. These results indicate that lung carcinogen and nicotine uptake, as measured by urinary 1-HOP, total NNAL, and total cotinine is the same in smokers of regular, light, and ultralight cigarettes. The results are consistent with epidemiologic studies that show no difference in lung cancer risk in smokers of these cigarettes.
Fiber Intake and Incidence of Colorectal Cancer among 76,947 Women and 47,279 Men
Authors: Michels Karin B. , Fuchs Charles S. , Giovannucci Edward , Colditz Graham A. , Hunter David J. , Stampfer Meir J. , Willett Walter C. 
Published: September 2005

Abstract
Prospective cohort studies have consistently found no important link between fiber intake and risk of colorectal cancer. The recent large, prospective European Prospective Investigation into Cancer and Nutrition has challenged this paradigm by suggesting significant protection by high fiber intake. We prospectively investigated the association of fiber intake with the incidence of colon and rectal cancers in two large cohorts: the Nurses' Health Study (76,947 women) and the Health Professionals Follow-up Study (47,279 men). Diet was assessed repeatedly in 1984, 1986, 1990, and 1994 among women and in 1986, 1990, and 1994 among men. The incidence of cancer of the colon and rectum was ascertained up to the year 2000. Relative risk estimates were calculated using a Cox proportional hazards model simultaneously controlling for potential confounding variables. During follow-up including 1.8 million person-years and 1,596 cases of colorectal cancer, we found little association with fiber intake after controlling for confounding variables. The hazard ratio for a 5-g/d increase in fiber intake was 0.91 (95% confidence interval, 0.87-0.95) after adjusting for covariates used in the European Prospective Investigation into Cancer and Nutrition study and 0.99 (95% confidence interval, 0.95-1.04) after adjusting for additional confounding variables. Our data from two large prospective cohorts with long follow-up and repeated assessment of fiber intake and of a large number of potential confounding variables do not indicate an important association between fiber intake and colorectal cancer but reveal considerable confounding by other dietary and lifestyle factors.
Human Papillomavirus Types in Head and Neck Squamous Cell Carcinomas Worldwide: A Systematic Review
Authors: Kreimer Aimee R. , Clifford Gary M. , Boyle Peter , Franceschi Silvia 
Published: September 2005

Abstract
Mucosal human papillomaviruses (HPV) are the cause of cervical cancer and likely a subset of head and neck squamous cell carcinomas (HNSCC), yet the global prevalence and type distribution of HPV in HNSCC remains unclear. We systematically reviewed published studies of HNSCC biopsies that employed PCR-based methods to detect and genotype HPV to describe the prevalence and type distribution of HPV by anatomic cancer site. Geographic location and study size were investigated as possible sources of variability. In the 5,046 HNSCC cancer specimens from 60 studies, the overall HPV prevalence was 25.9% [95% confidence interval (95% CI), 24.7-27.2]. HPV prevalence was significantly higher in oropharyngeal SCCs (35.6% of 969; 95% CI, 32.6-38.7) than oral SCCs (23.5% of 2,642; 95% CI, 21.9-25.1) or laryngeal SCCs (24.0% of 1,435; 95% CI, 21.8-26.3). HPV16 accounted for a larger majority of HPV-positive oropharyngeal SCCs (86.7%; 95% CI, 82.6-90.1) compared with HPV-positive oral SCCs (68.2%; 95% CI, 64.4-71.9) and laryngeal SCCs (69.2%; 95% CI, 64.0-74.0). Conversely, HPV18 was rare in HPV-positive oropharyngeal SCCs (2.8%; 95% CI, 1.3-5.3) compared with other head and neck sites [34.1% (95% CI, 30.4-38.0) of oral SCCs and 17.0% (95% CI, 13.0-21.6) of laryngeal SCCs]. Aside from HPV16 and HPV18, other oncogenic HPVs were rarely detected in HNSCC. Tumor site–specific HPV prevalence was higher among studies from North America compared with Europe and Asia. The high HPV16 prevalence and the lack of HPV18 in oropharyngeal compared with other HNSCCs may point to specific virus-tissue interactions. Small sample size and publication bias complicate the assessment of the prevalence of HPV in head and neck sites beyond the oropharynx.
Contemporary Lung Cancer Trends among U.S. Women
Authors: Jemal Ahmedin , Ward Elizabeth , Thun Michael J. 
Published: September 2005

Abstract
The age-standardized lung cancer incidence rate among women in the United States has decreased for each of the last 3 years for which data are available (1999-2001). We conducted this study to assess the stability and near-term sustainability of this decrease. We examined temporal trends in age-specific lung cancer incidence by calendar year and birth cohort and measured trends in the age-standardized rate in each geographic area within the Surveillance, Epidemiology, and End Results (SEER) Program using joinpoint regression analyses. Age-standardized lung cancer incidence rates have peaked or are decreasing in all geographic areas within SEER, although the decline is statistically significant only in San Francisco-Oakland. Age-specific incidence rates are decreasing in six of the seven 5-year age groups between ages 50 and 84 years in all areas of SEER combined. Rates in these age groups contribute nearly 95% of the total age-standardized incidence rate; consequently, trends in incidence at these ages will determine future trends in the overall age-standardized incidence rate for the next 20 to 25 years. Birth cohort patterns suggest that the decrease in the age-standardized rate will continue for at least 20 years, but will be slowed by aging of women born in the late 1950s and early 1960s. Given calendar year and birth cohort age-specific incidence patterns, the early decline in lung cancer incidence among women is likely to persist through at least 2025. Sustaining the downward trend beyond 2025 will require continued reductions in smoking initiation among children and increases in cessation among addicted smokers.
Circulating Levels of Insulin-like Growth Factors, their Binding Proteins, and Breast Cancer Risk
Authors: Schernhammer Eva S. , Holly Jeff M. , Pollak Michael N. , Hankinson Susan E. 
Published: September 2005

Abstract
Background: Earlier data support the hypothesis that the relation between circulating insulin-like growth factor-I (IGF-I) levels and breast cancer risk differs by menopausal status. The strong association of IGF-I with height in childhood and weak or no association between adult levels and adult height also suggest that IGF levels in young women may better reflect an exposure time period of importance to breast cancer. Few studies have assessed IGF binding protein-1 (IGFBP-1) or free IGF and breast cancer risk.
Materials and Methods: We conducted a large case-control study nested within the prospective Nurses' Health Study. Plasma concentrations of IGF-I, free IGF, IGFBP-3, and IGFBP-1 were measured in blood samples collected in 1989 to 1990. Eight hundred women were identified who had a diagnosis of invasive or in situ breast cancer after blood collection, up to 1998, 27% of whom were premenopausal at blood collection. To those 800 women, one to two controls were age-matched for a total of 1,129 controls. We used logistic regression models to estimate the relative risk (RR) of breast cancer associated with IGF levels.
Findings: Among postmenopausal women, neither IGF-I, IGFBP-3, IGFBP-1, nor free IGF was associated with breast cancer risk [RRs, top versus bottom quintile: IGF-I, 1.0; 95% confidence interval (95% CI), 0.7-1.4; IGFBP-3, 0.8; 95% CI, 0.6-1.1; IGFBP-1, 0.9; 95% CI, 0.6-1.5; and free IGF, 1.0; 95% CI, 0.6-1.4]. Among premenopausal women, IGFBP-3, IGFBP-1, and free IGF similarly were not associated with breast cancer risk (RRs, top versus bottom quintile: IGFBP-3, 1.2; 95% CI, 0.8-2.3; IGFBP-1, 1.5; 95% CI, 0.8-3.0; and free IGF, 1.1; 95% CI, 0.7-2.1). Higher IGF-I plasma levels, however, were associated with a modestly elevated breast cancer risk (RR, 1.6; 95% CI, 1.0-2.6) among the premenopausal women, with a stronger association among premenopausal women ages ≤50 (RR, 2.5; 95% CI, 1.4-4.3); further adjustment for IGFBP-3 did not greatly change these estimates.
Interpretation: Circulating IGF-I levels seem to be modestly associated with breast cancer risk among premenopausal women, but not among postmenopausal women. IGFBP-3, IGFBP-1, and free IGF are not associated with breast cancer risk in either premenopausal or postmenopausal women in this cohort.
Neighborhood Socioeconomic Status and Hodgkin's Lymphoma Incidence in California
Authors: Clarke Christina A. , Glaser Sally L. , Keegan Theresa H.M. , Stroup Antoinette 
Published: September 2005

Abstract
Hodgkin's lymphoma occurrence has long been noted to associate with higher socioeconomic status (SES). However, the Hodgkin's lymphoma-SES association has not been examined recently or across important, possibly etiologically distinct, patient subgroups. In ∼150 million person-years of observation in the multiethnic population of California, we examined the association of Hodgkin's lymphoma incidence with a composite measure of neighborhood-level SES in patient subgroups defined by age, sex, race/ethnicity, and Hodgkin's lymphoma histologic subtype. Using population-based cancer registry data on 3,794 Hodgkin's lymphoma patients diagnosed 1988 to 1992 and 1990 census data, we assigned a previously validated, multidimensional SES index to census block groups of patient residence. We then calculated neighborhood SES-specific incidence rates and estimated rate ratios using Poisson regression. Positive neighborhood SES gradients in Hodgkin's lymphoma incidence were observed only in young adults (ages 15-44 years at diagnosis) with nodular sclerosis Hodgkin's lymphoma and older adult (ages ≥45 years) White and Hispanic males with mixed cellularity Hodgkin's lymphoma. For young adults, associations were marked in Hispanic and Asian women, weaker in Hispanic and White men and White women, and subtle to nonexistent in Blacks and Asian men. Neighborhood SES gradients in Hodgkin's lymphoma incidence varied by age, sex, race/ethnicity, and histologic subtype, underscoring etiologic complexity in Hodgkin's lymphoma. Racial/ethnic gradients were not entirely explained by neighborhood SES. In California, etiologically relevant exposures for young adult Hodgkin's lymphoma, the most common form, could associate more with race/ethnicity or foreign birthplace than neighborhood SES and may be modified by reproductive or other sex-specific factors.
No Evidence for BRAF as a Melanoma/Nevus Susceptibility Gene
Authors: Jackson Sharon , Harland Mark , Turner Faye , Taylor Claire , Chambers Philip A. , Randerson-Moor Juliette , Swerdlow Anthony J. , dos Santos Silva Isabel , Beswick Samantha , Bishop D. Timothy , Newton Bishop Julia A. 
Published: September 2005

Abstract
Somatic mutations of BRAF have been identified in both melanoma tumors and benign nevi. Germ line mutations in BRAF have not been identified as causal in families predisposed to melanoma. However, a recent study suggested that a BRAF haplotype was associated with risk of sporadic melanoma in men. Polymorphisms or other variants in the BRAF gene may therefore act as candidate low-penetrance genes for nevus/melanoma susceptibility. We hypothesized that promoter variants would be the most likely candidates for determinants of risk. Using denaturing high-pressure liquid chromatography and sequencing, we screened peripheral blood DNA from 184 familial melanoma cases for BRAF promoter variants. We identified a promoter insertion/deletion in linkage disequilibrium with the previously described BRAF polymorphism in intron 11 (rs1639679) reported to be associated with melanoma susceptibility in males. We therefore investigated the contribution of this BRAF polymorphism to melanoma susceptibility in 581 consecutively recruited incident cases, 258 incident cases in a study of late relapse, 673 female general practitioner controls, and the 184 familial cases. We found no statistically significant difference in either genotype or allele frequencies between cases and controls overall or between male and female cases for the BRAF polymorphism in the two incident case series. Our results therefore suggest that the BRAF polymorphism is not significantly associated with melanoma and the promoter insertion/deletion linked with the polymorphism is not a causal variant. In addition, we found that there was no association between the BRAF genotype and mean total number of banal or atypical nevi in either the cases or controls.
A Prospective Study of Dietary Folate Intake and Risk of Colorectal Cancer: Modification by Caffeine Intake and Cigarette Smoking
Authors: Larsson Susanna C. , Giovannucci Edward , Wolk Alicja 
Published: September 2005

AbstractEpidemiologic evidence indicates an inverse association of folate intake with risk of colorectal cancer, but whether this association is modified by intake of caffeine (in coffee and tea) or cigarette smoking—factors that possibly interfere with folate—has not been studied. Thus, we examined whether the association between dietary folate intake and incidence of colorectal cancer is modified by caffeine intake and smoking. Cox proportional hazards modeling was used to estimate rate ratios relating dietary folate intake to colorectal cancer incidence among 61,433 women ages 40 to 75 years at recruitment into the Swedish Mammography Cohort in 1987 to 1990. From March 1987 through June 2004, a total of 805 incident cases of colorectal cancer were diagnosed. After controlling for age and other potential confounders, we observed an inverse association between dietary folate intake and risk of colon cancer (rate ratio for the highest versus the lowest quintile, 0.61; 95% confidence interval, 0.41-0.91; Ptrend = 0.02), but not of rectal cancer (rate ratio, 0.93; 95% confidence interval, 0.55-1.56; Ptrend = 0.97). The inverse association between dietary folate intake and colon cancer risk was most pronounced among smokers (Pinteraction = 0.03). We found no apparent modification of risk by caffeine intake. Findings from this population-based cohort study support an inverse association between dietary folate intake and risk of colon cancer and suggest that smokers might benefit most from a high dietary folate intake.
Chlamydia pneumoniae and Lung Cancer: Epidemiologic Evidence
Authors: Littman Alyson J. , Jackson Lisa A. , Vaughan Thomas L. 
Published: September 2005

Abstract
Chlamydia pneumoniae is a common cause of acute respiratory infection and has been hypothesized to cause several chronic diseases, including lung cancer. The purpose of this article is to identify, describe, and critically examine the published studies on the association between C. pneumoniae infection and risk of lung cancer. In the six studies identified, previous C. pneumoniae infection was defined on the basis of serologic criteria, which varied between studies. All studies reported elevated relative risk estimates for the association of serologic evidence of infection and risk of lung cancer. The three studies in which past infection was defined based on testing of prediagnostic blood specimens tended to have weaker results (odds ratio range, 1.2-2.1) than those based on postdiagnostic blood specimens (odds ratio range, 1.4-9.9). Selection bias, measurement error, and inadequate control for confounding are concerns in some of these studies. Nevertheless, results were relatively consistent, supporting a causal association. Inflammation caused by chronic infection with C. pneumoniae may be involved in the carcinogenic process but this relationship will be difficult to further define through serologic data. To better understand the nature of this association, both experimental study designs, such as those based on animal models or randomized controlled antibiotic treatment trials in humans, and observational study designs (e.g., studies that involve detection of C. pneumoniae in pulmonary specimens obtained before cancer onset) could be explored and may shed additional light on this important association.
Gene-Smoking Interaction Associations for the ERCC1 Polymorphisms in the Risk of Lung Cancer
Authors: Zhou Wei , Liu Geoffrey , Park Sohee , Wang Zhaoxi , Wain John C. , Lynch Thomas J. , Su Li , Christiani David C. 
Published: September 2005

Abstract
Cigarette smoking may induce DNA damage. Lower DNA repair capacities have been associated with higher risk of lung cancer. Excision repair cross-complementing group 1 (ERCC1) is the lead enzyme in the nucleotide excision repair process, and low expression of ERCC1 mRNA levels has been associated with higher risk of cancers. We examined the association between two polymorphisms of ERCC1, 8092C &gt; A (rs3212986) and 19007T &gt; C (codon 118, rs11615), which are associated with altered ERCC1 mRNA stability and mRNA levels, in 1,752 Caucasian lung cancer patients and 1,358 controls. The results were analyzed using logistic regression models, adjusting for relevant covariates. The two polymorphisms were in Hardy-Weinberg disequilibrium and in linkage disequilibrium. There was no overall association between ERCC1 polymorphisms and lung cancer risk, with the adjusted odds ratios (AOR) of 1.26 [95% confidence interval (95% CI), 0.81-1.96] for the 8092C &gt; A polymorphism (A/A versus C/C) and 0.93 (95% CI, 0.67-1.30) for the 19007T &gt; C polymorphism (C/C versus T/T). Stratified analyses revealed that the AORs for the 8092C &gt; A polymorphism (A/A versus C/C) decreased significantly as pack-years increased, with the AOR of 2.11 (95% CI, 1.03-4.31) in never smokers and 0.50 (95% CI, 0.25-1.01) in heavy smokers (≥56 pack-years), respectively. Consistent results were found when gene-smoking interaction was incorporated by joint effects and interactions models that considered both discrete and continuous variables for cumulative smoking exposure. The same direction for the gene-smoking interaction was found for the 19007T &gt; C polymorphism, although the interaction was not statistically significant. In conclusion, ERCC1 8092C &gt; A polymorphism may modify the associations between cumulative cigarette smoking and lung cancer risk.
Levels of Physical Activity for Colon Cancer Prevention Compared with Generic Public Health Recommendations: Population Prevalence and Sociodemographic Correlates
Authors: Cerin Ester , Leslie Eva , Bauman Adrian , Owen Neville 
Published: September 2005

AbstractBackground: The proportion of Australian adults achieving physical activity levels believed to be sufficient for colon cancer prevention was estimated, and sociodemographic correlates (age, gender, educational attainment, occupation, marital status, and children in household) of meeting these levels of activity were analyzed.Methods: Data from the 2000 National Physical Activity Survey were used to estimate the prevalence of participation in physical activity in relation to three criteria: generic public health recommendations, weekly amount of at least moderate-intensity physical activity currently believed to reduce risk of colon cancer, and weekly amount of vigorous-intensity physical activity believed to reduce risk of colon cancer.Results: Overall, 46% of adults met the generic public health criterion, 26% met the colon cancer criterion based on participation in at least moderate-intensity physical activity, and 10% met the colon cancer criterion based on vigorous-intensity physical activity. Women were less likely than men to meet the colon cancer criteria. Younger and more educated persons were more likely to meet all three criteria. The most pronounced differences between gender, age, and educational attainment groups were found for meeting the amount of vigorous-intensity physical activity believed to reduce risk of colon cancer.Conclusions: The population prevalence for meeting proposed physical activity criteria for colon cancer prevention is low and much lower than that related to the more generic public health recommendations. If further epidemiologic studies confirm that high volumes and intensities of activity are required, the public health challenges for colon cancer will be significant.
A Noninvasive Objective Measure of Sunscreen Use and Reapplication
Authors: O'Riordan David L. , Lunde Kevin B. , Urschitz Johann , Glanz Karen 
Published: September 2005

Abstract
Objectives: To study whether a noninvasive swabbing technique can detect sunscreen use for up to 6 hours, and whether the technique can detect reapplication of sunscreen.
Methods: Thirty volunteer office workers were randomly assigned to have one of a variety of sunscreens applied using recommended application techniques, and half were randomly assigned to have sunscreen reapplied after 3 hours. Alcohol-based swabs were used to obtain a sample from participants' arm at 20 minutes, and hourly from 1 to 6 hours post-application. Absorption readings were analyzed using an UV-visible spectrophotometer.
Results: The swabbing technique was consistently able to distinguish the sunscreen from control swabs for up to 6 hours. The absorption readings between 20 minutes and 6 hours were significantly higher than control swabs. There were no differences between the group that had sunscreen reapplied and the group that did not.
Conclusion: The sunscreen swabbing technique is an effective noninvasive method for detecting a variety of sunscreen products in adults over a 6-hour period. No differences in absorption readings were found with sunscreen reapplication. This procedure will be a useful adjunct to other objective measures of sun protection and UV radiation exposure, resulting in a more accurate picture of the sun protection habits of individuals.