bluuebunny/crossref_metadata_2025_split huggingface dataset:
Early Life Factors and Incidence of Proliferative Benign Breast Disease
Authors: Baer Heather J. , Schnitt Stuart J. , Connolly James L. , Byrne Celia , Willett Walter C. , Rosner Bernard , Colditz Graham A. 
Published: March 2006

AbstractProliferative benign breast disease is a marker of increased breast cancer risk, yet little is known about its etiology. Most studies of benign breast disease have focused only on risk factors in adulthood, despite growing evidence that factors in early life influence breast cancer risk. We explored the relations of several early life factors with incidence of proliferative benign breast disease among 71,896 premenopausal women in the Nurses' Health Study II who recalled their body fatness at young ages, physical activity in adolescence, birthweight, and history of being breastfed. Between 1991 and 1997, 901 of these women were identified as having proliferative benign breast disease from a centralized pathology review. Relative risks (RR) and 95% confidence intervals (95% CI) were estimated from Cox proportional hazards models. Greater childhood body fatness (ages 5-10) was associated with decreased risk of proliferative benign breast disease; the multivariate RR (95% CI) for the most overweight compared with the most lean was 0.61 (0.44-0.86; Ptrend &lt; 0.0001) and remained significant after adjustment for current body mass index. Body mass index at age 18 was also inversely associated with incidence of proliferative benign breast disease, with a multivariate RR (95% CI) of 0.67 (0.52-0.88) for those who were ≥25 kg/m2 compared with those who were &lt;19 kg/m2 (Ptrend = 0.001). There were no clear associations for physical activity in adolescence, birthweight, or being breastfed. These results indicate that premenopausal women who were heavier at young ages have lower incidence of proliferative benign breast disease, consistent with previous findings for breast cancer. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2889–97)
Unlimited Access to Care: Effect on Racial Disparity and Prognostic Factors in Lung Cancer
Authors: Mulligan Charles R. , Meram Amir D. , Proctor Courtney D. , Wu Hongyu , Zhu Kangmin , Marrogi Aizen J. 
Published: March 2006

Abstract
Study Objective: Evaluate the prognostic factors influencing lung cancer survival under a universal health care system and determine if access to care eliminates clinical outcome disparity.
Design: Retrospective case series review.
Background: Lung cancer survival is worse in men and in African Americans, thought to be related to poor general health in men and limited access to heath care in African Americans. The Military Health Care System, with unlimited access to care, provides an excellent setting for evaluating gender and racial disparities in lung cancer survival.
Methods: Lung cancers diagnosed at Walter Reed Army Medical Center, from 1990 to 2000, were evaluated by chart review for age, gender, race, smoking history, cancer history, histology, stage, and completeness of resection.
Results: Seven hundred thirteen Caucasians and 173 African Americans, 2:1 male predominance, had a 22% 5-year survival. Cox model analysis showed that male gender [hazard ratio (HR, 1.31) 95% confidence interval (95% CI), 1.02-1.68], advanced-stage disease (stage III: HR, 2.58; 95% CI, 1.57-4.26/stage IV: HR, 4.20; 95% CI, 2.51-7.41), and incomplete resection (HR, 4.06; 95% CI, 2.75-5.99) were predictors of poor outcome; whereas bronchoalveolar carcinoma features (HR, 0.35; 95% CI, 0.23-0.52) and smoking cessation &gt;7 years (HR, 0.70; 95% CI, 0.49-0.99) were predictors of favorable outcome. No ethnic differences in survival were observed.
Conclusions: No racial disparities in survival when access to medical care is universal. Male gender, incomplete resection, and advanced stage are significant predictors of poor outcome in lung cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(1):25–31)
Diet, Cancer, and the Lipidome
Authors: Bougnoux Philippe , Giraudeau Bruno , Couet Charles 
Published: March 2006

Abstract
The potential for dietary fat to interfere with the development of breast cancer by delaying its occurrence makes the identification of defined molecules a mandatory step in cancer prevention. In order to circumvent the limitations and/or bias of dietary exposure assessment tools, biomarkers of past lipid intake such as the fatty acid composition of white adipose tissue have been used. When considered separately, candidate fatty acids identified as favorable on the basis of their association with breast cancer risk have usually led to inconsistent results in animal intervention studies. This inconsistency indicates that any approach based on a single fatty acid should be abandoned for an integrated view over the complex lipid interactions which finally determines the lipidome, the lipid profile that is found in individuals. This article presents a reappraisal of the role of the lipid profile through a comprehensive reanalysis of adipose tissue fatty acid composition obtained in patients with benign or malignant breast tumors as well as in experimental animals during dietary interventions. Rather than a single fatty acid, a composite indicator combining elevated monounsaturates and low ω6/ω3 fatty acid ratio was associated with breast cancer protection. This lipidome may become the template for identifying breast cancer risk related to diet, and for designing proper dietary modifications to delay the occurrence of breast cancer, although the universality of the findings cannot be assessed from a single study. (Cancer Epidemiol Biomarkers Prev 2006;15(3):416–21)
Catechol-O-methyltransferase Gene Polymorphisms in Benign Prostatic Hyperplasia and Sporadic Prostate Cancer
Authors: Tanaka Yuichiro , Sasaki Masahiro , Shiina Hiroaki , Tokizane Takashi , Deguchi Masao , Hirata Hiroshi , Hinoda Yuji , Okayama Naoko , Suehiro Yutaka , Urakami Shinji , Kawakami Toshifumi , Kaneuchi Masanori , Pookot Deepa , Igawa Mikio , Okuyama Akihiko , Ishii Nobuhisa , Dahiya Rajvir 
Published: March 2006

Abstract
Various carcinogenic metabolites, including catechol estrogens, play a role in malignant transformation. An enzyme that is capable of neutralizing the genotoxic effects of these compounds is catechol-O-methyltransferase (COMT). A variant form of this enzyme has been shown to reduce its activity by up to 4-fold; thus, we hypothesize that single nucleotide polymorphisms of the COMT gene can be a risk factor for benign prostatic hyperplasia (BPH) and prostate cancer. To test this hypothesis, the genetic distribution of three different COMT polymorphisms at codon 62 (C→T), codon 72 (G→T), and codon 158 (G→A) were analyzed in 131 normal healthy subjects, 134 BPH, and 178 sporadic prostate cancer samples from a Japanese population. Results of these experiments show that the variant genotype at codon 62 (P = 0.060) and codon 158 (P = 0.047) are risk factors for prostate cancer but not BPH when compared with normal controls. Odds ratio (OR) and 95% confidence interval (95% CI) for cancer were 3.24 and 1.38 to 7.61, respectively, for codon 62 T/T genotype when compared with wild type. At codon 158, the A/A variant for cancer had an OR of 3.00 with a 95% CI of 1.38 to 6.54 compared with wild type. Codons 62 and 158 were in linkage disequilibrium (LD), and when compared with the C-G haplotype, other types (C-A, T-G, T-A) were observed to be associated with prostate cancer (P = 0.040) but not BPH. Codon 72 on the other hand, was not in LD with either codon 62 or 158. The homozygous variant on codon 72 was rare in this Japanese population, and the heterozygous G/T at this codon was not associated with either prostate cancer or BPH. When evaluating the risk of COMT polymorphisms with stage or grade of cancer, no associations were observed for any of the genotypes with the exception of a tendency (P = 0.096) for the variant A allele on codon 158 to be correlated with higher stages (≥T3) of cancer. This is the first report that shows the polymorphisms of COMT to be associated with sporadic prostatic carcinogenesis. These results are important in understanding the role of COMT polymorphisms in the pathogenesis of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(2):238–44)
The Insulin-Like Growth Factor System and Mammographic Features in Premenopausal and Postmenopausal Women
Authors: dos Santos Silva Isabel , Johnson Nichola , De Stavola Bianca , Torres-Mejía Gabriela , Fletcher Olivia , Allen Diane S. , Allen Naomi E. , Key Timothy J. , Fentiman Ian S. , Holly Jeff M.P. , Peto Julian 
Published: March 2006

AbstractHigh levels of circulating insulin-like growth factor-I (IGF-I) and its major binding protein (IGFBP-3) at premenopausal ages have been associated with an increased breast cancer risk. We conducted a cross-sectional study (215 premenopausal women and 241 after natural menopause) nested within the Guernsey prospective studies to examine the relationship between the IGF system and mammographic features of the breast. The mammographically dense area in the breast increased with increasing serum levels of IGF-I (P for linear trend, Pt = 0.05), IGF-II (Pt = 0.08), and IGFBP-3 (Pt = 0.01) only in premenopausal women. IGF-II and IGFBP-3 serum levels were associated with increases in the mammographically lucent area in both premenopausal (Pt = 0.01 and 0.04, respectively) and postmenopausal women (Pt &lt; 0.001 for both), but these associations were no longer statistically significant after adjustment for body mass index and waist circumference. Neither the IGF-I/IGFBP-3 nor the IGF-II/IGFBP-3 molar ratio was associated with any of these mammographic features. The number of A alleles at a polymorphic locus in the promoter region of the IGFBP-3 gene was associated with increasing mean IGFBP-3 levels in both premenopausal (Pt = 0.01) and postmenopausal (Pt &lt;0.001) women but not with mammographically dense area. These results support the hypothesis that the IGF system may affect the amount of mammographically dense tissue in premenopausal women, possibly by promoting cell proliferation and inhibiting apoptosis in the fibroglandular tissue. The findings also show strong relations between IGF-II and IGFBP-3 levels and the amount of mammographically lucent tissue, reflecting the associations between body adiposity and amount of fat tissue in the breast and between body adiposity and circulating levels of these growth factors. (Cancer Epidemiol Biomarkers Prev 2006;15(3):449–55)
GSTP1 and GSTA1 Polymorphisms Interact with Cruciferous Vegetable Intake in Colorectal Adenoma Risk
Authors: Tijhuis Mariken J. , Wark Petra A. , Aarts Jac M.M.J.G. , Visker Marleen H.P.W. , Nagengast Fokko M. , Kok Frans J. , Kampman Ellen 
Published: March 2006

Abstract
The possible interplay between cruciferous vegetable consumption, functional genetic variations in glutathione S-transferases (GST) M1, T1, P1, and A1, and colorectal adenomas, was investigated in a Dutch case-control study. The GSTM1 and GSTT1 deletion polymorphisms, and the single nucleotide polymorphisms in GSTP1 (A313G) and in GSTA1 (C-69T) were assessed among 746 cases who developed colorectal adenomas and 698 endoscopy-based controls without any type of colorectal polyps. High and low cruciferous vegetable consumption was defined based on a median split in the control group. High consumption was slightly positively associated with colorectal adenomas [odds ratio (OR) 1.15; 95% confidence interval, 0.92-1.44]. For GSTP1, a positive association with higher cruciferous vegetable intake was only apparent in individuals with the low-activity GSTP1 genotype (GG genotype, OR 1.94; 95% confidence interval, 1.02-3.69). This interaction was more pronounced in men, with higher age and with higher meat intake. The GSTA1 polymorphism may have a modifying role as well: the OR for higher intake compared with lower intake was 1.57 (0.93-2.65) for individuals homozygous for the low expression variant (TT genotype). This seemed to be stronger with younger age and higher red meat intake. Cruciferous vegetable consumption and the combined GSTA1 and GSTP1 genotypes showed a statistically significant interaction (P = 0.034). The GSTM1 and GSTT1 genotypes did not seem to modify the association between cruciferous vegetable intake and colorectal adenomas. In conclusion, GSTP1 and GSTA1 genotypes might modulate the association between cruciferous vegetable intake and colorectal adenomas. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2943–51)
Effect of Physical Activity on Women at Increased Risk of Breast Cancer: Results from the E3N Cohort Study
Authors: Tehard Bertrand , Friedenreich Christine M. , Oppert Jean-Michel , Clavel-Chapelon Francoise 
Published: March 2006

Abstract
Purpose: There is a need to investigate the type, duration, frequency, and intensity of physical activity that are critical to reduce the risk of breast cancer, and if this relation differs among subgroups of women.
Methods: We analyzed the relation between physical activity and breast cancer incidence between 1990 and 2002 (n = 3,424 cases), among 90,509 women of the French E3N cohort, ages between 40 and 65 years in 1990. We gave special attention to effect modification by body mass index (BMI), family history of breast cancer, parity, and hormone replacement therapy (HRT).
Results: A linear decrease in risk of breast cancer was observed with increasing amounts of moderate (Ptrend &lt; 0.01) and vigorous (Ptrend &lt; 0.0001) recreational activities. Compared with women who reported no recreational activities, those with more than five weekly hours of vigorous recreational activity had a relative risk of 0.62 (0.49-0.78). This decrease was still observed among women who were overweight, nulliparous, had a family history of breast cancer, or used HRT. Compared with the whole cohort, among nulliparous women, the reduction of risk observed was of a higher magnitude, although the test for heterogeneity did not reach statistical significance.
Conclusion: A risk reduction of breast cancer was particularly observed with vigorous recreational activity. Further investigations are needed to confirm that intensity is an important variable to consider in risk reduction and to identify the precise biological mechanisms involved in such a risk reduction. (Cancer Epidemiol Biomarkers Prev 2006;15(1):57–64)
RNASELMutation Screening and Association Study in Ashkenazi and Non-Ashkenazi Prostate Cancer Patients
Authors: Orr-Urtreger Avi , Bar-Shira Anat , Bercovich Dani , Matarasso Noa , Rozovsky Uri , Rosner Serena , Soloviov Sonya , Rennert Gad , Kadouri Luna , Hubert Ayala , Rennert Hanna , Matzkin Haim 
Published: March 2006

AbstractEpidemiologic and genetic studies support the considerable effect of heritable factors on prostate tumorigenesis, although to date, no unequivocal susceptibility gene has been identified. The extensive study of RNASEL in prostate cancer patients worldwide has yielded conflicting results. We reevaluated the role of the RNASEL 471delAAAG Ashkenazi founder mutation in 1,642 Ashkenazi patients with prostate, bladder, breast/ovarian, and colon cancers; Ashkenazi controls; and in non-Ashkenazi prostate cancer patients and controls. The entire RNASEL coding sequence was also screened using denaturing high-performance liquid chromatography and multiplex ligation–dependent probe amplification for possible sequence variations or copy number changes in a population of prostate cancer patients. The 471delAAAG mutation was detected in 2.4% of the Ashkenazi prostate cancer patients; in 1.9% of patients with bladder, breast/ovarian, and colon cancers; and in 2.0% of the Ashkenazi controls. Seven additional variants were detected in RNASEL, including a novel potentially pathogenic splice site mutation, IVS5+1delG, although none were associated with increased prostate cancer risk. Multiplex ligation–dependent probe amplification analysis showed two RNASEL gene copies in all 300 prostate cancer patients tested. We estimated that the RNASEL 471delAAAG founder mutation, which was detected in 2% of the Ashkenazi Jews, originated between the 2nd and 5th centuries A.D., compared with the less frequent (1%) BRCA1 185delAG founder mutation, which originated hundreds of years earlier. Taken together, our analysis does not support a role for the RNASEL 471delAAAG Ashkenazi mutation nor for the other alterations detected in RNASEL in prostate cancer risk in Jewish men. (Cancer Epidemiol Biomarkers Prev 2006;15(3):474–9)
Meat Consumption among Black and White Men and Risk of Prostate Cancer in the Cancer Prevention Study II Nutrition Cohort
Authors: Rodriguez Carmen , McCullough Marjorie L. , Mondul Alison M. , Jacobs Eric J. , Chao Ann , Patel Alpa V. , Thun Michael J. , Calle Eugenia E. 
Published: March 2006

Abstract
Previous epidemiologic studies have suggested that intake of red meat may be associated with increased risk of prostate cancer. Few studies, however, have examined these associations by race. We examined intake of red meat, processed meat, and poultry in relation to incident prostate cancer among Black and White men in the Cancer Prevention Study II Nutrition Cohort. Participants in the study completed a detailed questionnaire on diet, medical history, and lifestyle in 1992 to 1993. After excluding men with a history of cancer and incomplete dietary information, 692 Black and 64,856 White men were included in the cohort. During follow-up through August 31, 2001, we documented 85 and 5,028 cases of incident prostate cancer among Black and White men, respectively. Cox proportional hazards models were used to estimate rate ratios (RR) and 95% confidence intervals (95% CI). No measure of meat consumption was associated with risk of prostate cancer among White men. Among Black men, total red meat intake (processed plus unprocessed red meat) was associated with higher risk of prostate cancer (RR, 2.0; 95% CI, 1.0-4.2 for highest versus lowest quartile; Ptrend = 0.05); this increase in risk was mainly due to risk associated with consumption of cooked processed meats (sausages, bacon, and hot dogs; RR, 2.7; 95% CI, 1.3-5.3 for highest versus lowest quartile; Ptrend = 0.008). This study suggests that high consumption of cooked processed meats may contribute to prostate cancer risk among Black men in the United States.(Cancer Epidemiol Biomarkers Prev 2006;15(2):211–6)
How Well Do HapMap Haplotypes Identify Common Haplotypes of Genes? A Comparison with Haplotypes of 334 Genes Resequenced in the Environmental Genome Project
Authors: Taylor Jack A. , Xu Zong-Li , Kaplan Norman L. , Morris Richard W. 
Published: March 2006

Abstract
One of the goals of the International HapMap Project is the identification of common haplotypes in genes. However, HapMap uses an incomplete catalogue of single nucleotide polymorphisms (SNPs) and might miss some common haplotypes. We examined this issue using data from the Environmental Genome Project (EGP) which resequenced 335 genes in 90 people, and thus, has a nearly complete catalogue of gene SNPs. The EGP identified a total of 45,243 SNPs, of which 10,780 were common SNPs (minor allele frequency ≥0.1). Using EGP common SNP genotype data, we identified 1,459 haplotypes with frequency ≥0.05 and we use these as “benchmark” haplotypes. HapMap release 16 had genotype information for 1,573 of 10,780 (15%) EGP common SNPs. Using these SNPs, we identified common HapMap haplotypes (frequency ≥0.05) in each of the four HapMap ethnic groups. To compare common HapMap haplotypes to EGP benchmark haplotypes, we collapsed benchmark haplotypes to the set of 1,573 SNPs. Ninety-eight percent of the collapsed benchmark haplotypes could be found as common HapMap haplotypes in one or more of the four HapMap ethnic groups. However, collapsing benchmark haplotypes to the set of SNPs available in HapMap resulted in a loss of haplotype information: 545 of 1,459 (37%) benchmark haplotypes were uniquely identified, and only 25% of genes had all their benchmark haplotypes uniquely identified. We resampled the EGP data to examine the effect of increasing the number of HapMap SNPs to 5 million, and estimate that ∼40% of common SNPs in genes will be sampled and that half of the genes will have sufficient SNPs to identify all common haplotypes. This inability to distinguish common haplotypes of genes may result in loss of power when examining haplotype-disease association. (Cancer Epidemiol Biomarkers Prev 2006;15(1):133–7)
Interactions of Sequence Variants inInterleukin-1 Receptor–Associated Kinase4and theToll-Like Receptor 6-1-10Gene Cluster Increase Prostate Cancer Risk
Authors: Sun Jielin , Wiklund Fredrik , Hsu Fang-Chi , Bälter Katarina , Zheng S. Lilly , Johansson Jan-Erik , Chang Baoli , Liu Wennuan , Li Tao , Turner Aubrey R. , Li Liwu , Li Ge , Adami Hans-Olov , Isaacs William B. , Xu Jianfeng , Grönberg Henrik 
Published: March 2006

AbstractChronic or recurrent inflammation has been suggested as a causal factor in several human malignancies, including prostate cancer. Genetic predisposition is also a strong risk factor in the development of prostate cancer. In particular, Toll-like receptors (TLR), especially the TLR6-1-10 gene cluster, are involved in prostate cancer development. Interleukin-1 receptor-associated kinases (IRAK) 1 and 4 are critical components in the TLR signaling pathway. In this large case-control study, we tested two hypotheses: (a) sequence variants in IRAK1 and IRAK4 are associated with prostate cancer risk and (b) sequence variants in IRAK1/4 and TLR1-6-10 interacts and confers a stronger risk to prostate cancer. We analyzed 11 single nucleotide polymorphisms (four in IRAK1 and seven in IRAK4) among 1,383 newly diagnosed prostate cancer patients and 780 population controls in Sweden. Although the single-nucleotide polymorphisms in IRAK1 and IRAK4 alone were not significantly associated with prostate cancer risk, one single-nucleotide polymorphism in IRAK4, when combined with the high-risk genotype at TLR6-1-10, conferred a significant excess risk of prostate cancer. In particular, men with the risk genotype at TLR6-1-10 and IRAK4-7987 CG/CC had an odds ratio of 9.68 (P = 0.03) when compared with men who had wild-type genotypes. Our findings suggest synergistic effects between sequence variants in IRAK4 and the TLR 6-1-10 gene cluster. Although this study was based on a priori hypothesis and was designed to address many common issues facing this type of study, our results need confirmation in even larger studies. (Cancer Epidemiol Biomarkers Prev 2006;15(3):480–5)