bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of NAT1 and NAT2 Genetic Polymorphisms on Colorectal Cancer Risk Associated with Exposure to Tobacco Smoke and Meat Consumption
Authors: Lilla Carmen , Verla-Tebit Emaculate , Risch Angela , Jäger Birgit , Hoffmeister Michael , Brenner Hermann , Chang-Claude Jenny 
Published: March 2006

Abstract
N-Acetyltransferases 1 and 2 (NAT1 and NAT2), both being highly polymorphic, are involved in the metabolism of aromatic and heterocyclic aromatic amines present in cigarette smoke and red meat cooked by high-temperature cooking techniques. We investigated the effect of differences in acetylation capacity, determined by NAT1 and NAT2 genotypes, on colorectal cancer risk associated with exposure to tobacco smoke or red meat consumption. In this population-based case-control study in Germany, 505 patients with incident colorectal cancer and 604 age- and sex-matched control individuals with genotyping data and detailed risk factor information were included. Genotyping of NAT1 and NAT2 genetic polymorphisms was done using a fluorescence-based melting curve analysis method. The association between genotypes, environmental exposures, and colorectal cancer risk was estimated using multivariate logistic regression. Colorectal cancer risk associated with active smoking was elevated after accumulation of 30+ pack-years of smoking [odds ratio (OR), 1.4; 95% confidence interval (95% CI), 0.9-2.2] but not significantly modified by either NAT1 or NAT2 genotype. Exposure to environmental tobacco smoke was associated with an increased risk for colorectal cancer only among NAT2 fast acetylators (OR, 2.6; 95% CI, 1.1-5.9 for exposure in childhood and adulthood). Frequent consumption of red meat significantly increased colorectal cancer risk for the group comprising all NAT2 fast acetylators or carriers of the NAT1*10 allele (OR, 2.6; 95% CI, 1.1-6.1) but not among those with “slow” NAT1 and NAT2 genotypes. Our findings indicate that NAT1 and NAT2 genotypes may contribute jointly to individual susceptibility and that heterocyclic aromatic amines may play an important role in colorectal cancer associated with red meat and possibly also exposure to environmental tobacco smoke. (Cancer Epidemiol Biomarkers Prev 2006;15(1):99–107)
Plasma C-Reactive Protein and Risk of Cancer: A Prospective Study from Greece
Authors: Trichopoulos Dimitrios , Psaltopoulou Theodora , Orfanos Philippos , Trichopoulou Antonia , Boffetta Paolo 
Published: March 2006

Abstract
Background: Inflammation is an important component of carcinogenesis but little research has been conducted on whether inflammation markers can be predictive of cancer risk in humans.
Methods: We analyzed C-reactive protein (CRP), a marker of inflammation, in plasma samples of 496 cases of cancer and 996 controls selected among participants in a prospective study from Greece.
Results: Plasma CRP level was higher in cancer cases than controls (odds ratio for increase in CRP level of 3.2 mg/L, 1.20; 95% confidence interval, 1.10-1.32): The corresponding odds ratio after exclusion of the first year of follow-up and of individuals with CRP level above 20 mg/L was 1.32 (95% confidence interval, 1.15-1.52). Although based on small number of cases, the association between elevated plasma CRP level and risk was stronger for cancers of the liver, lung, skin, kidney, and bladder, as well as for lymphoma and leukemia than for other neoplasms.
Conclusions: Our results confirm the important role of inflammation in human cancer and suggest that plasma CRP level is a potential marker of increased cancer risk. (Cancer Epidemiol Biomarkers Prev 2006;15(2):381–4)
Does “Clock” Matter in Prostate Cancer?
Authors: Zhu Yong , Zheng Tongzhang , Stevens Richard G. , Zhang Yawei , Boyle Peter 
Published: March 2006

Abstract
The ancient adaptation of a 24-hour circadian clock has profound effect on our daily biochemical, physiologic, and behavioral processes, including the monitoring of sex hormone levels. Although the disruption of the circadian cycle has been implicated in the etiology of hormone-related female breast cancer, few studies have been undertaken to determine if a link exists in the development of the most common cancer type among men whose etiology remains largely unknown: hormone-related prostate cancer. Here, we hypothesize that both altered-lighted environments and genetic variations in genes responsible for maintaining circadian rhythms may result in deregulation of clock-associated biological processes, such as androgen expression, and consequently influence an individual's risk of prostate cancer. There is also a potential for the interaction of genetic variants and exposures, such as evening shift work. Confirmation of this hypothesis will add to our understanding of the role of the circadian clock in prostate tumorigenesis and further facilitate the development of novel risk and prognostic biomarkers for prostate cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(1):3–5)
Changes of Gene Expression in Gastric Preneoplasia following Helicobacter pylori Eradication Therapy
Authors: Tsai Chiaojung Jillian , Herrera-Goepfert Roberto , Tibshirani Robert John , Yang Shufang , Mohar Alejandro , Guarner Jeannette , Parsonnet Julie 
Published: March 2006

Abstract
Helicobacter pylori causes gastric preneoplasia and neoplasia. Eradicating H. pylori can result in partial regression of preneoplastic lesions; however, the molecular underpinning of this change is unknown. To identify molecular changes in the gastric mucosa following H. pylori eradication, we used cDNA microarrays (with each array containing ∼30,300 genes) to analyze 54 gastric biopsies from a randomized, placebo-controlled trial of H. pylori therapy. The 54 biopsies were obtained from 27 subjects (13 from the treatment and 14 from the placebo group) with chronic gastritis, atrophy, and/or intestinal metaplasia. Each subject contributed one biopsy before and another biopsy 1 year after the intervention. Significant analysis of microarrays (SAM) was used to compare the gene expression profiles of pre-intervention and post-intervention biopsies. In the treatment group, SAM identified 30 genes whose expression changed significantly from baseline to 1 year after treatment (0 up-regulated and 30 down-regulated). In the placebo group, the expression of 55 genes differed significantly over the 1-year period (32 up-regulated and 23 down-regulated). Five genes involved in cell-cell adhesion and lining (TACSTD1 and MUC13), cell cycle differentiation (S100A10), and lipid metabolism and transport (FABP1 and MTP) were down-regulated over time in the treatment group but up-regulated in the placebo group. Immunohistochemistry for one of these differentially expressed genes (FABP1) confirmed the changes in gene expression observed by microarray. In conclusion, H. pylori eradication may stop or reverse ongoing molecular processes in the stomach. Further studies are needed to evaluate the use of these genes as markers for gastric cancer risk. (Cancer Epidemiol Biomarkers Prev 2006;15(2):272–80)
Clinical Stage of Breast Cancer by Parity, Age at Birth, and Time Since Birth: A Progressive Effect of Pregnancy Hormones?
Authors: Albrektsen Grethe , Heuch Ivar , Thoresen Steinar , Kvåle Gunnar 
Published: March 2006

AbstractBreast cancer diagnosed during pregnancy or 1 to 2 years after birth often occurs at a late stage. Little is known about tumor characteristics in the high-risk period shortly after a childbirth. We here explore whether stage of disease differs according to timing of births. Results are based on 22,351 Norwegian breast cancer patients of parity 0 to 5, ages 20 to 74 years. The proportion of stage II to IV tumors was considerably higher among parous than nulliparous women at age &lt;30 years (52.7% versus 36.8%, P = 0.009), but similar or lower in other age groups (Pinteraction = 0.029). In general, the largest proportion of stage II to IV tumors was found among women diagnosed during pregnancy or &lt;2 years after birth. However, among women with late-age births (first or second birth ≥30 years, third birth ≥35 years), as well as women with an early second birth (&lt;25 years), the proportion with advanced disease was rather similar or even higher among those diagnosed 2 to 6 years after birth (49.3-56.0%). The association between clinical stage and time since birth reached statistical significance among women with a late first or second birth and among all triparous women (P ≤ 0.032). The subgroups with a high proportion of advanced disease 2 to 6 years after birth corresponded quite well to those previously found to have the most pronounced transient increase in risk after birth. Thus, pregnancy hormones may have a progressive effect on breast cancer tumors in addition to a possible promoting effect. A potential effect of prolactin is discussed. (Cancer Epidemiol Biomarkers Prev 2006;(15)1:65–9)
Leanness, Smoking, and Enhanced Oxidative DNA Damage
Authors: Mizoue Tetsuya , Kasai Hiroshi , Kubo Tatsuhiko , Tokunaga Shoji 
Published: March 2006

Abstract
An increased risk of some forms of cancer, including lung cancer, among lean individuals has been consistent; however, there is a paucity of biological evidence supporting this relation. Subjects analyzed were 177 healthy Japanese workers who participated in a lifestyle intervention study. The levels of urinary 8-hydroxydeoxyguanosine (8-OHdG), a marker of oxidative DNA damage, were measured using an automated high-pressure liquid chromatography and urinary creatinine levels were adjusted for before statistical analysis. A clear inverse association was found between body mass index (BMI) and 8-OHdG levels among smokers [Pearson correlation coefficient (r) = −0.48], and the association did not materially change after adjustment for potential confounding factors. In contrast, no apparent relation was observed between BMI and 8-OHdG levels among nonsmokers (r = −0.12), although lean nonsmokers had a slightly higher mean of 8-OHdG levels compared with nonlean nonsmokers. The interaction of smoking and BMI reached statistical significance (P = 0.04). Leanness may enhance oxidative DNA damage induced by smoking and thus serve as a marker of host susceptibility to smoking-related cancers. (Cancer Epidemiol Biomarkers Prev 2006;15(3):582–5)
Patterns of Colorectal Cancer Screening Uptake among Men and Women in the United States
Authors: Meissner Helen I. , Breen Nancy , Klabunde Carrie N. , Vernon Sally W. 
Published: March 2006

Abstract
Objective: The purpose of this report is to examine (a) gender-specific correlates of colorectal cancer test use using recent national data from 2003 and (b) patterns of colorectal cancer screening by gender and test modality over time.
Methods: We analyze data from the 1987, 1992, 1998, 2000, and 2003 National Health Interview Surveys. Our sample consists of men and women ≥50 years never diagnosed with colorectal cancer and who reported a recent fecal occult blood test and/or endoscopy.
Results: In 2003, both men and women reported higher rates of colonoscopy (32.2% and 29.8%, respectively) than use of FOBT (16.1% and 15.3%, respectively) or sigmoidoscopy (7.6% and 5.9%, respectively). Men reported higher use of endoscopy than women if they had a usual source of health care, had talked to a general doctor, and had two to five visits to the doctor in the past year. Men and women 65 years and older had higher rates of any recommended colorectal cancer test (55.8% and 48.5%, respectively) than persons 50 to 64 years (males, 41.0%; females, 31.4%). Use of colorectal cancer tests also was higher among both genders if they were not Hispanic, had higher educational attainment, were former smokers, had health insurance or a usual source of care, or if they talked to a general doctor. Recent use of colorectal cancer tests has increased since 2000 for both women and men largely due to increased use of colonoscopy.
Conclusions: Colorectal cancer testing is increasing for both men and women, although the prevalence of testing remains higher in men. Our data support previous findings documenting socioeconomic disparities in colorectal cancer test use. Access barriers to screening could be particularly difficult to overcome if colonoscopy becomes the preferred colorectal cancer screening modality. (Cancer Epidemiol Biomarkers Prev 2006;15(2):389–94)
Dietary Selenium Intake and Genetic Polymorphisms of the GSTP1 and p53 Genes on the Risk of Esophageal Squamous Cell Carcinoma
Authors: Cai Lin , Mu Li-Na , Lu Hua , Lu Qing-Yi , You Nai-Chieh Yuko , Yu Shun-Zhang , Le Anh D. , Zhao Jinkou , Zhou Xue-Fu , Marshall James , Heber David , Zhang Zuo-Feng 
Published: March 2006

Abstract
Few studies have assessed potential effect modifications by polymorphisms of susceptibility genes on the association between selenium intake and esophageal squamous cell carcinoma (ESCC). We studied the joint effects of dietary selenium and the GSTP1 and p53 polymorphisms on ESCC risk in a population-based case-control study with 218 ESCC cases and 415 controls in Taixing City, China. Dietary selenium intake was estimated from a food frequency questionnaire with 97 food items. GSTP1 and p53 polymorphisms were detected by RFLP-PCR assays. Logistic regression analyses were done to estimate odds ratios (OR) and 95% confidence intervals (95% CI). Reduced ESCC risk was observed among individuals in the highest quartile of dietary selenium intake (adjusted OR, 0.31; 95% CI, 0.13-0.70) with a dose-dependent gradient (Ptrend = 0.01). The p53 Pro/Pro genotype was associated with increased risk of ESCC compared with the Arg/Arg genotype (adjusted OR, 2.02; 95% CI, 1.19-3.42). When combined with selenium consumption, an obvious increased risk was observed among individuals with the p53 Pro/Pro or GSTP1 Ile/Ile genotype with adjusted ORs of 3.19 (95% CI, 1.74-5.84) and 1.90 (95% CI, 1.03-3.51), respectively. Among smokers and alcohol drinkers, elevation of ESCC risk was more prominent among p53 Pro/Pro individuals who consumed a low level of dietary selenium (adjusted OR, 3.59; 95% CI, 1.49-8.66 for smokers and 6.19; 95% CI, 1.83-20.9 for drinkers). Our study suggests that the effect of dietary selenium on the risk of ESCC may be modulated by tobacco smoking, alcohol drinking, and p53 Pro/Pro and GSTP1 Ile/Ile genotypes. (Cancer Epidemiol Biomarkers Prev 2006;15(2):294–300)
Variation in Incidence and Fatality of Melanoma by Season of Diagnosis in New South Wales, Australia
Authors: Boniol Mathieu , Armstrong Bruce K. , Doré Jean-François 
Published: March 2006

Abstract
Seasonal variation in cutaneous melanoma incidence with a summer peak is poorly understood. It has been hypothesized to be due to increased diagnosis in summer or a late-promoting effect of sun exposure. We analyzed the characteristics of incident cases of cutaneous melanoma and their outcome by season of diagnosis in the population of New South Wales, Australia. Cases of melanoma (25,845 cases; 10,869 females and 14,976 males) were registered by the New South Wales Central Cancer Registry in 1989 to 1998. There was significant seasonal variation in incidence (P &lt; 0.0001, Nam test). The summer to winter ratio was greater for women, younger people, lesions on the limbs, and superficial spreading melanoma. Melanomas were thicker in winter than in summer (medians 0.75 and 0.70 mm, respectively; P &lt; 0.0001, Kruskal-Wallis test). Cases were followed for a median of 63 months and 2,710 (10.5%) died from their melanoma. Fatality from melanoma was lower for melanomas diagnosed in summer than winter (relative fatality = 0.72; 95% confidence interval, 0.65-0.81); the 5-year survival rate was 92.1% for diagnosis in summer and 89.0% for diagnosis in winter. This result remained significant after adjustment for year of diagnosis, age, sex, Breslow thickness, anatomic location, and histologic type (relative fatality = 0.82; 95% confidence interval, 0.72-0.94). Seasonality in melanoma incidence is probably caused mainly by increased and earlier diagnosis in summer, although a late-stage promotional effect of sun exposure cannot be excluded completely. Earlier diagnosis may also reduce fatality when melanoma is diagnosed in summer. Independence of variation in fatality with season from seasonal variation in thickness, however, suggests that sun exposure around the time of diagnosis decreases fatality of melanoma. (Cancer Epidemiol Biomarkers Prev 2006;15(3):524–8)
Breast and Ovarian Cancer in Relatives of Cancer Patients, with and without BRCA Mutations
Authors: Lee Jennifer S. , John Esther M. , McGuire Valerie , Felberg Anna , Ostrow Kimberly L. , DiCioccio Richard A. , Li Frederick P. , Miron Alexander , West Dee W. , Whittemore Alice S. 
Published: March 2006

AbstractBackground: First-degree relatives of patients with breast or ovarian cancer have increased risks for these cancers. Little is known about how their risks vary with the patient's cancer site, carrier status for predisposing genetic mutations, or age at cancer diagnosis.Methods: We evaluated breast and ovarian cancer incidence in 2,935 female first-degree relatives of non-Hispanic White female patients with incident invasive cancers of the breast (n = 669) or ovary (n = 339) who were recruited from a population-based cancer registry in northern California. Breast cancer patients were tested for BRCA1 and BRCA2 mutations. Ovarian cancer patients were tested for BRCA1 mutations. We estimated standardized incidence ratios (SIR) and 95% confidence intervals (95% CI) for breast and ovarian cancer among the relatives according to the patient's mutation status, cancer site, and age at cancer diagnosis.Results: In families of patients who were negative or untested for BRCA1 or BRCA2 mutations, risks were elevated only for the patient's cancer site. The breast cancer SIR was 1.5 (95% CI, 1.2-1.8) for relatives of breast cancer patients, compared with 1.1 (95% CI, 0.8-1.6) for relatives of ovarian cancer patients (P = 0.12 for difference by patient's cancer site). The ovarian cancer SIR was 0.9 (95% CI, 0.5-1.4) for relatives of breast cancer patients, compared with 1.9 (95% CI, 1.0-4.0) for relatives of ovarian cancer patients (P = 0.04 for difference by site). In families of BRCA1-positive patients, relatives' risks also correlated with the patient's cancer site. The breast cancer SIR was 10.6 (95% CI, 5.2-21.6) for relatives of breast cancer patients, compared with 3.3 (95% CI, 1.4-7.3) for relatives of ovarian cancer patients (two-sided P = 0.02 for difference by site). The ovarian cancer SIR was 7.9 (95% CI, 1.2-53.0) for relatives of breast cancer patients, compared with 11.3 (3.6-35.9) for relatives of ovarian cancer patients (two-sided P = 0.37 for difference by site). Relatives' risks were independent of patients' ages at diagnosis, with one exception: In families ascertained through a breast cancer patient without BRCA mutations, breast cancer risks were higher if the patient had been diagnosed before age 40 years.Conclusion: In families of patients with and without BRCA1 mutations, breast and ovarian cancer risks correlate with the patient's cancer site. Moreover, in families of breast cancer patients without BRCA mutations, breast cancer risk depends on the patient's age at diagnosis. These patterns support the presence of genes that modify risk specific to cancer site, in both carriers and noncarriers of BRCA1 and BRCA2 mutations. (Cancer Epidemiol Biomarkers Prev 2006;15(2):359–63)
TheAIB1Polyglutamine Repeat Does Not Modify Breast Cancer Risk inBRCA1andBRCA2Mutation Carriers
Authors: Spurdle Amanda B. , Antoniou Antonis C. , Kelemen Livia , Holland Helene , Peock Susan , Cook Margaret R. , Smith Paula L. , Greene Mark H. , Simard Jacques , Plourde Marie , Southey Melissa C. , Godwin Andrew K. , Beck Jeanne , Miron Alexander , Daly Mary B. , Santella Regina M. , Hopper John L. , John Esther M. , Andrulis Irene L. , Durocher Francine , Struewing Jeffery P. , Easton Douglas F. , Chenevix-Trench Georgia ,   Australian Breast Cancer Family Study,   Australian Jewish Breast Cancer Study,   Breast Cancer Family Registry,   Interdisciplinary Health Research International Team on Breast Cancer Susceptibility,   The Kathleen Cunningham Foundation Consortium for Research into Familial Breast Cancer,   Epidemiological Study of Familial Breast Cancer Study Collaborators
Published: March 2006

AbstractThis is by far the largest study of its kind to date, and further suggests that AIB1 does not play a substantial role in modifying the phenotype of BRCA1 and BRCA2 carriers. The AIB1 gene encodes the AIB1/SRC-3 steroid hormone receptor coactivator, and amplification of the gene and/or protein occurs in breast and ovarian tumors. A CAG/CAA repeat length polymorphism encodes a stretch of 17 to 29 glutamines in the HR-interacting carboxyl-terminal region of the protein which is somatically unstable in tumor tissues and cell lines. There is conflicting evidence regarding the role of this polymorphism as a modifier of breast cancer risk in BRCA1 and BRCA2 carriers. To further evaluate the evidence for an association between AIB1 glutamine repeat length and breast cancer risk in BRCA1 and BRCA2 mutation carriers, we have genotyped this polymorphism in 1,090 BRCA1 and 661 BRCA2 mutation carriers from Australia, Europe, and North America. There was no evidence for an increased risk associated with AIB1 glutamine repeat length. Given the large sample size, with more than adequate power to detect previously reported effects, we conclude that the AIB1 glutamine repeat does not substantially modify risk of breast cancer in BRCA1 and BRCA2 mutation carriers. (Cancer Epidemiol Biomarkers Prev 2006;15(1):76–9)
Prediagnostic Circulating Antibodies to JC and BK Human Polyomaviruses and Risk of Non-Hodgkin Lymphoma
Authors: Rollison Dana E. , Engels Eric A. , Halsey Neal A. , Shah Keerti V. , Viscidi Raphael P. , Helzlsouer Kathy J. 
Published: March 2006

Abstract
Viral infections have been associated with increased risk of non–Hodgkin's lymphoma (NHL). We conducted a nested case-control study to investigate the association between prediagnostic serum antibodies to the human polyomaviruses, JC (JCV) and BK (BKV), and subsequent risk of NHL. Two research serum banks were established in Washington County, Maryland, in 1974 and 1989, with the collection of blood samples from &gt;45,000 volunteers. Incident NHL cases diagnosed through 2002 (n = 170) were identified among participants by linkage to population-based cancer registries. Two controls were matched to each case (n = 340) on age, sex, and blood draw date. Prediagnostic IgG antibodies to JCV and BKV were measured using virus-like particle ELISA. Associations between JCV and BKV antibody seropositivity and NHL were estimated using conditional logistic regression. Overall, neither antibodies to JCV [odds ratio (OR), 0.83; 95% confidence interval (95% CI), 0.56-1.23] nor BKV (OR, 0.98; 95% CI, 0.64-1.48) were associated with an increased risk of NHL. Results were similar after stratification by NHL subtype or induction period and adjustment for EBV seropositivity. Among those who donated blood in both 1974 and 1989, an increase in JCV antibody levels over time was associated with a 4-fold increased risk of NHL compared with a steep decline in antibody levels (OR, 4.59; 95% CI, 1.30-16.25; Ptrend = 0.02). Whereas JCV seropositivity was not associated with NHL overall, the finding of an increased risk of NHL associated with increasing antibody levels among those who were seropositive at baseline warrants further research into factors influencing reactivation of JCV infection. (Cancer Epidemiol Biomarkers Prev 2006;15(3):543–50)