bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluating Organized Breast Cancer Screening Implementation
Authors: Taplin Stephen H. , Ichikawa Laura , Buist Diana S. M. , Seger Deborah , White Emily 
Published: September 2005

AbstractThe objective of our study was to evaluate organized breast cancer screening implementation by measuring the association between screening program enrollment and late-stage disease. Our setting was a health plan using mailed mammography reminders to women ages ≥40. We conducted yearly cross-sectional summaries of mammography experience and late-stage (regional or distant Surveillance Epidemiology and End Results Reporting (SEER) stage) breast cancer occurrence for all of the health-plan women ages ≥40 (1986–1998). We estimated the odds of late-stage breast cancer among health-plan and surrounding community women because it was too early to compare changes in mortality. We also estimated the odds of late-stage disease (1995–1998) associated with program enrollment and mammography screening among health-plan women. We found that mammography-within-two-years increased within the health plan from 25.9% to 51.2% among women ages 40–49 and from 32.9% to 74.7% among women ages ≥50. Health-plan late-stage rates were lower than those in the surrounding community [ages 40–49: odds ratio (OR), 0.87; 95% confidence interval (CI), 0.77–0.99; ages 50–79: OR, 0.86; 95% CI, 0.80–0.92] and declined parallel to the community. Among health-plan cancer cases, women ages ≥43 who were enrolled in the screening program and who had at least one program mammogram were less likely to have late-stage disease compared with the women not enrolled in the program (OR, 0.31; 95% CI, 0.16–0.61) but the odds of late-stage was also reduced among program-enrolled women not receiving program mammograms (OR, 0.45; 95% CI, 0.21–0.95). We concluded that enrollment in organized screening is associated with increased likelihood of mammography and reduced odds of late-stage breast cancer. Addressing the concerns of un-enrolled women and those without mammograms offers an opportunity for further late-stage disease reduction.
HSD17B1
Gene Polymorphisms and Risk of Endometrial and Breast Cancer
Authors: Setiawan Veronica Wendy , Hankinson Susan E. , Colditz Graham A. , Hunter David J. , De Vivo Immaculata 
Published: September 2005

Abstract
Estrogen exposure influences breast and endometrial cancer risk. The HSD17B1 gene produces an enzyme that catalyzes the conversion of estrone to estradiol. We hypothesized that genetic variations in HSD17B1 gene may alter endogenous estrogen levels and, thus, influence endometrial and breast cancer risk. We validated and genotyped polymorphisms in the HSD17B1 gene and assessed whether these single nucleotide polymorphisms (SNPs), or the imputed haplotypes, were associated with endometrial and breast cancer risk. We also assessed whether a priori risk factors modified the associations between HSD17B1 genotype and cancer risk, and whether HSD17B1 genotypes were associated with plasma estrogen levels among postmenopausal women not using hormone replacement therapy. Ten SNPs of HSD17B1 gene were validated in 30 women from the Nurses’ Health Study. Using the expectation maximization algorithm, three common (&gt;5% frequency) haplotypes accounted for 97% of the chromosomes at this locus, and seven SNPs were in complete linkage disequilibrium. We identified and genotyped two haplotype-tagging SNPs (+1004C/T and +1322C/A), and genotyped an additional SNP [+1954A/G (Ser312Gly)] in nested case-control studies of endometrial cancer (cases = 222, controls = 666) and breast cancer (cases = 1007, controls = 1441) in the prospective Nurses’ Health Study. Although no overall association by SNP or haplotype analysis was observed with endometrial or breast cancer risk, the +1954A/A genotype was associated with higher estradiol levels in lean women (P = 0.01) and interaction between the +1954 genotype with body mass index in postmenopausal breast cancer (P = 0.05) was suggested. These findings suggest that the HSD17B1 may be associated with circulating estradiol levels and interact with body mass index in postmenopausal breast cancer.
Increased Rates of Chromosome Breakage in BRCA1 Carriers Are Normalized by Oral Selenium Supplementation
Authors: Kowalska Elzbieta , Narod Steven A. , Huzarski Tomasz , Zajaczek Stanislaw , Huzarska Jowita , Gorski Bohdan , Lubinski Jan 
Published: September 2005

Abstract
Women who are born with constitutional heterozygous mutations of the BRCA1 gene face greatly increased risks of breast and ovarian cancer. The product of the BRCA1 gene is involved in the repair of double-stranded DNA breaks and it is believed that increased susceptibility to DNA breakage contributes to the cancer phenotype. It is hoped therefore that preventive strategies designed to reduce chromosome damage will also reduce the rate of cancer in these women. To test for increased mutagenicity of cells from BRCA1 carriers, the frequency of chromosome breaks was measured in cultured blood lymphocytes following in vitro exposure to bleomycin in female BRCA1 carriers and was compared with noncarrier relatives. The frequency of chromosome breaks was also measured in BRCA1 carriers following oral selenium supplementation. Carriers of BRCA1 mutations showed significantly greater mean frequencies of induced chromosome breaks per cell than did healthy noncarrier relatives (0.58 versus 0.39; P &lt; 10−4). The frequency of chromosome breaks was greatly reduced following 1 to 3 months of oral selenium supplementation (mean, 0.63 breaks per cell versus 0.40; P &lt; 10−10). The mean level of chromosome breaks in carriers following supplementation was similar to that of the noncarrier controls (0.40 versus 0.39). Oral selenium is a good candidate for chemoprevention in women who carry a mutation in the BRCA1 gene.
Use of Colonoscopy for Colorectal Cancer Screening: Evidence from the 2000 National Health Interview Survey
Authors: Subramanian Sujha , Amonkar Mayur M. , Hunt Timothy L. 
Published: September 2005

Abstract
Background: The use of colonoscopy as a primary screening tool for colorectal cancer is gaining momentum owing to several studies suggesting superior effectiveness and the recent, favorable decision by Medicare to cover all routine screening colonoscopies. This study documents the use of colonoscopy versus other tests to screen for colorectal cancer.
Materials and Methods: Data from the 2000 National Health Interview Survey were analyzed. Fecal occult blood test (FOBT), sigmoidoscopy, and colonoscopy done for any reason and for routine screening only were analyzed for those ≥50 years without previously diagnosed colorectal cancer (n = 12,505).
Results: The proportion of the total eligible population receiving any of the recommended tests for all possible reasons and for screening purposes only is 34.6% and 25.1%, respectively. For routine screening purposes, the test most commonly utilized was FOBT (55.6%) followed by colonoscopy (29.1%) and sigmoidoscopy (15.3%). When usage was assessed for all reasons, FOBT was still most commonly utilized (45.8%) followed by colonoscopy (38.7%) and sigmoidoscopy (15.5%). The elderly, non-White males and those with private insurance have a higher probability of receiving colonoscopy than FOBT. Several regional differences exist, including higher probability of undergoing sigmoidoscopy versus colonoscopy in the West.
Conclusions: Only one fourth (upper limit one third) of the study population complied with colorectal cancer screening recommendations. Nearly one third of the routine screening tests done in 2000 were colonoscopies. This study provides baseline values that can be used to project future colonoscopy demand and identify potential supply barriers.
Methods and Strategies to Recruit African Americans into Cancer Prevention Surveillance Studies
Authors: Satia Jessie A. , Galanko Joseph A. , Rimer Barbara K. 
Published: September 2005

AbstractObjective: Recruitment of African Americans into health research studies is a major challenge. This report describes a study of different methods and strategies to recruit African Americans into a population-based assessment of cancer behavioral risk factors.Methods: African Americans ages 18 to 70 years in North Carolina (n = 5,000) were randomly selected from the Department of Motor Vehicle rosters and assigned at random to one of five different recruitment strategies based on variations of approach letters (generic versus culturally sensitive) and inclusion, exclusion, or promise of a small incentive. Prospective participants were sent an 11-page questionnaire by mail but could complete it by telephone or Internet as well as by mail.Results: The overall response rate was 17.5% (747 completed surveys of 4,276 delivered): 655, 84, and 8 by mail, Internet, and telephone, respectively. Among eligible respondents, response was significantly higher for incentive-based than nonincentive strategies; 23.9% for the generic letter plus incentive compared with 15.8% for the generic letter only (P &lt; 0.001). The culturally sensitive letter had little effect on participation (15.8% for both the generic and culturally sensitive letters). The mean age of eligible respondents was 43.9 years, 41% were male, 37% were college graduates, and 75% were overweight/obese. There were no differences in respondent characteristics by assigned recruitment strategy.Conclusions: Incentive-based strategies yielded the highest survey responses, whereas a culturally sensitive letter did not appreciably increase participation among African Americans in North Carolina. This study adds to what is known about culturally sensitive recruitment strategies for African Americans and challenges their usefulness in survey-based studies.
Hepatocellular Carcinoma and Polymorphisms in Carcinogen-Metabolizing and DNA Repair Enzymes in a Population with Aflatoxin Exposure and Hepatitis B Virus Endemicity
Authors: Kirk Gregory D. , Turner Paul C. , Gong Yunyun , Lesi Olufunmilayo A. , Mendy Maimuna , Goedert James J. , Hall Andrew J. , Whittle Hilton , Hainaut Pierre , Montesano Ruggero , Wild Christopher P. 
Published: September 2005

Abstract
High rates of hepatocellular carcinoma (HCC) in The Gambia, West Africa, are primarily due to a high prevalence of chronic hepatitis B virus infection and heavy aflatoxin exposure via groundnut consumption. We investigated genetic polymorphisms in carcinogen-metabolizing (GSTM1, GSTT1, HYL1*2) and DNA repair (XRCC1) enzymes in a hospital-based case-control study. Incident HCC cases (n = 216) were compared with frequency-matched controls (n = 408) with no clinically apparent liver disease. Although the prevalence of variant genotypes was generally low, in multivariable analysis (adjusting for demographic factors, hepatitis B virus, hepatitis C virus, and TP53 status), the GSTM1-null genotype [odds ratio (OR), 2.45; 95% confidence interval (95% CI), 1.21-4.95] and the heterozygote XRCC1-399 AG genotype (OR, 3.18; 95% CI, 1.35-7.51) were significantly associated with HCC. A weak association of the HYL1*2 polymorphism with HCC was observed but did not reach statistical significance. GSTT1 was not associated with HCC. The risk for HCC with null GSTM1 was most prominent among those with the highest groundnut consumption (OR, 4.67; 95% CI, 1.45-15.1) and was not evident among those with less than the mean groundnut intake (OR, 0.64; 95% CI, 0.20-2.02). Among participants who had all three suspected aflatoxin-related high-risk genotypes [GSTM1 null, HLY1*2 (HY/HH), and XRCC1 (AG/GG)], a significant 15-fold increased risk of HCC was observed albeit with imprecise estimates (OR, 14.7; 95% CI, 1.27-169). Our findings suggest that genetic modulation of carcinogen metabolism and DNA repair can alter susceptibility to HCC and that these effects may be modified by environmental factors.
Loss of FHIT Expression in Breast Cancer Is Correlated with Poor Prognostic Markers
Authors: Arun Banu , Kilic Gokhan , Yen Charles , Foster Barbara , Yardley Denise A. , Gaynor Richard , Ashfaq Raheela 
Published: September 2005

Abstract
Objective: The fragile histidine triad (FHIT) gene is a putative tumor suppressor gene that is thought to be involved in the carcinogenesis of breast cancer. Loss of FHIT expression has been observed in up to 72% of breast cancers and has been associated with increased p53, a high proliferation index, and increased tumor size and grade. However, loss of FHIT expression has not been investigated in association with apoptosis and cyclooxygenase-2 (COX-2) expression in breast cancer. Furthermore, expression of FHIT in primary breast tumors and their metastatic axillary lymph nodes has also not been previously described. The purpose of this study was to evaluate the expression of FHIT, COX-2, bcl-2, and p53 in primary breast tumor tissue; correlate their expression with known clinical and pathologic markers; and in cases when tissue was available, evaluate the expression of FHIT and COX-2 in the corresponding metastatic axillary lymph node in the same patient.
Methods: Primary breast tumor specimens from 80 patients were examined for the presence of FHIT, COX-2, bcl-2, and p53 expression by immunohistochemistry using standard methods. When tissue was available, the expression of FHIT and COX-2 was also evaluated in the corresponding metastatic axillary lymph node specimen.
Results: FHIT expression in primary breast tumors was 56%. There was a significant correlation between FHIT expression in primary breast tumor and bcl-2 expression (P = 0.017). We also observed a significant inverse correlation between FHIT expression in primary breast tumor tissue and p53 expression (P = 0.023) in lymph node–negative cases. A significant inverse correlation between FHIT expression in the primary tumor and Ki-67 (P = 0.009) was also observed in lymph node–negative cases. FHIT expression in primary tumors correlated with FHIT expression in the metastatic lymph node (52.5%; P = 0.001). FHIT expression in primary tumors did not correlate with COX-2 expression.
Conclusion: Our results suggest that loss of FHIT expression in breast cancer is associated with poor prognostic features. Furthermore, loss of FHIT expression is also seen in metastatic axillary lymph node. The prognostic and predictive value of these findings needs to be further evaluated in larger trials with longer follow-up.
Nipple Aspirate Fluid Cytology and the Gail Model for Breast Cancer Risk Assessment in a Screening Population
Authors: Tice Jeffrey A. , Miike Rei , Adduci Kelly , Petrakis Nicholas L. , King Eileen , Wrensch Margaret R. 
Published: September 2005

Abstract
Background: Recent guidelines suggest that chemoprevention with tamoxifen may be appropriate for women who have a 5-year risk of breast cancer greater than 1.66% calculated using the Gail model.
Objectives: To determine whether nipple aspirate fluid (NAF) cytology combined with the Gail model provides breast cancer risk assessment that is superior to either method alone.
Methods: Prospective observational cohort of 6,904 asymptomatic women. Breast cancer cases were identified through follow-up with the women and linkage to cancer registries. We used proportional hazards modeling to recalculate the coefficients for the predictor variables used in the Gail model. NAF cytology was added to create a second model. The two models were compared using the concordance statistic (c-statistic).
Results: During 14.6 years of follow-up, 400 women were diagnosed with breast cancer. There were 940 (14%) women with hyperplasia and 109 (1.6%) women with atypical hyperplasia found in NAF. Adding NAF cytology results to the Gail model significantly improved the model fit (P &lt; 0.0001). The c-statistic for the Gail model was 0.62, indicating only modest discriminatory accuracy. Adding NAF cytology to the model increased the c-statistic to 0.64. NAF cytology results had the largest effect on discriminatory accuracy among women in the upper third of Gail model risk. The relative incidence for the highest quintile of risk score compared with the lowest quintile was 7.2 for the Gail model and 8.0 for the model including NAF cytology.
Conclusion: NAF cytology has the potential to improve prediction models of breast cancer incidence, particularly for high-risk women.
Genetic Polymorphisms of CYP2E1, GSTT1, GSTP1, GSTM1, ALDH2, and ODC and the Risk of Advanced Precancerous Gastric Lesions in a Chinese Population
Authors: You Wei-cheng , Hong Jun-Yan , Zhang Lian , Pan Kai-feng , Pee David , Li Ji-you , Ma Jun-ling , Rothman Nathaniel , Caporaso Neil , Fraumeni Joseph F. , Xu Guang-wei , Gail Mitchell H. 
Published: September 2005

Abstract
There have been few studies of the associations of genetic polymorphisms with precancerous gastric lesions. We conducted a cross-sectional study to compare the prevalences of several genetic polymorphisms in 302 subjects with mild chronic atrophic gastritis with prevalences in 606 subjects with deep intestinal metaplasia or dysplasia. This stratified random sample of 908 subjects was selected and analyzed for genetic polymorphisms from 2,628 individuals who had gastric biopsies with histopathology in 1989 in Linqu County, Shandong Province, China. In subjects with mild chronic atrophic gastritis, the frequencies of the variant (less common) alleles of CYP2E1 RsaI, CYP2E1 DraI, GSTP1, ALDH2, and ODC were, respectively, 0.156, 0.201, 0.189, 0.190, and 0.428. The frequencies of the null genotypes of GSTM1 and GSTT1 in the mild chronic atrophic gastritis group were 0.509 and 0.565, respectively. Comparing mild chronic atrophic gastritis with deep intestinal metaplasia or any degree of dysplasia, we found no statistically significant associations with any genotype from these loci for dominant, additive, or recessive inheritance models. There was no statistically significant evidence of multiplicative interactions between any pair of genotypes based on CYP2E1 RsaI, CYP2E1 DraI, GSTP1, GSTM1, or GSTT1; nor between Helicobacter pylori status and any of these five loci; nor between smoking status and GSTP1, GSTM1, or GSTT1; nor between alcohol consumption and ALDH2. Statistically significant interactions were noted between salt consumption and GSTP1 and between sour pancake consumption and CYP2E1 RsaI. There was, moreover, a statistically significant interaction (odds ratio, 1.78; 95% confidence interval, 1.03-3.08) between CYP2E1 DraI and smoking at least one cigarette per day. A positive but not statistically significant interaction was also seen between CYP2E1 RsaI and smoking status. These polymorphisms do not seem to govern progression from mild chronic atrophic gastritis to advanced precancerous gastric lesions, but the effects of smoking may be accentuated in individuals carrying variants of CYP2E1.
Risk of Prostate Cancer in a Randomized Clinical Trial of Calcium Supplementation
Authors: Baron John A. , Beach Michael , Wallace Kristin , Grau Maria V. , Sandler Robert S. , Mandel Jack S. , Heber David , Greenberg E. Robert 
Published: September 2005

Abstract
Background: In some studies, high calcium intake has been associated with an increased risk of prostate cancer, but no randomized studies have investigated this issue.
Methods: We randomly assigned 672 men to receive either 3 g of calcium carbonate (1,200 mg of calcium), or placebo, daily for 4 years in a colorectal adenoma chemoprevention trial. Participants were followed for up to 12 years and asked periodically to report new cancer diagnoses. Subject reports were verified by medical record review. Serum samples, collected at randomization and after 4 years, were analyzed for 1,25-(OH)2 vitamin D, 25-(OH) vitamin D, and prostate-specific antigen (PSA). We used life table and Cox proportional hazard models to compute rate ratios for prostate cancer incidence and generalized linear models to assess the relative risk of increases in PSA levels.
Results: After a mean follow-up of 10.3 years, there were 33 prostate cancer cases in the calcium-treated group and 37 in the placebo-treated group [unadjusted rate ratio, 0.83; 95% confidence interval (95% CI), 0.52-1.32]. Most cases were not advanced; the mean Gleason's score was 6.2. During the first 6 years (until 2 years post-treatment), there were significantly fewer cases in the calcium group (unadjusted rate ratio, 0.52; 95% CI, 0.28-0.98). The calcium risk ratio for conversion to PSA &gt;4.0 ng/mL was 0.63 (95% CI, 0.33-1.21). Baseline dietary calcium intake, plasma 1,25-(OH)2 vitamin D and 25-(OH) vitamin D levels were not materially associated with risk.
Conclusion: In this randomized controlled clinical trial, there was no increase in prostate cancer risk associated with calcium supplementation and some suggestion of a protective effect.
Genetic Polymorphisms of Ataxia Telangiectasia Mutated and Breast Cancer Risk
Authors: Lee Kyoung-Mu , Choi Ji-Yeob , Park Sue Kyung , Chung Hye-Won , Ahn Byungchan , Yoo Keun-Young , Han Wonshik , Noh Dong-Young , Ahn Sei-Hyun , Kim Ho , Wei Qingyi , Kang Daehee 
Published: September 2005

AbstractTo evaluate the role of genetic polymorphisms of ataxia telangiectasia mutated (ATM) in the etiology of breast cancer, a hospital-based case-control study was conducted in Korea. Nine-hundred ninety-six histologically confirmed incident breast cancer cases and 1,181 cancer-free controls were recruited in Seoul between 1995 and 2003. Genotypes of the ATM polymorphisms-5144A&gt;T, IVS21+1049T&gt;C, IVS33−55T&gt;C, IVS34+60G&gt;A, and 3393T&gt;G were determined by the 5′-nuclease assay. Individual haplotypes were estimated from genotype data by a Bayesian method. Five ATM alleles were found to be in strong linkage disequilibrium (D′ &gt; 0.82; P &lt; 0.001). Haplotype frequencies were significantly different between cases and controls (χ2 test, P &lt; 0.001). The ATM IVS21+1049 TC or CC, IVS34+60 GA or AA, and 3393 TG or GG genotypes were associated with increased breast cancer risk, particularly in premenopausal women [odds ratios (OR), 1.51; 95% confidence interval (CI), 1.11-2.05; OR, 1.42; 95% CI, 1.08-1.88; and OR, 1.37; 95% CI, 1.04-1.80, respectively]. Compared with diploid of TCCAG:TCCAG, the most common haplotype, the ATTGT:ATTGT was associated with decreased risk of breast cancer with borderline significance (OR, 0.77; 95% CI, 0.58-1.04) and TCCAG:ATCGT and ATTGT:ACCAG were associated with increased breast cancer risk (OR, 2.30; 95% CI, 1.18-4.48 and OR, 2.43; 95% CI, 1.1.07-5.52, respectively) after adjusting for age, education, age at first full-term pregnancy, parity, family history of breast cancer, alcohol consumption, and smoking. As the number of ATTGT haplotype decreased, the risk of breast cancer increased (P for trend &lt;0.01). Our results thus suggest that genetic polymorphisms of ATM play an important role in the development of breast cancer in Korean women.