bluuebunny/crossref_metadata_2025_split huggingface dataset:
Polymorphisms in Nucleotide Excision Repair Genes, Polycyclic Aromatic Hydrocarbon-DNA Adducts, and Breast Cancer Risk
Authors: Crew Katherine D. , Gammon Marilie D. , Terry Mary Beth , Zhang Fang Fang , Zablotska Lydia B. , Agrawal Meenakshi , Shen Jing , Long Chang-Min , Eng Sybil M. , Sagiv Sharon K. , Teitelbaum Susan L. , Neugut Alfred I. , Santella Regina M. 
Published: October 2007

AbstractGenes involved in the nucleotide excision repair (NER) pathway, which removes bulky DNA adducts, are potential low-penetrance cancer susceptibility genes. We recently reported an association between detectable polycyclic aromatic hydrocarbon (PAH)-DNA adducts and breast cancer risk. Using a population-based breast cancer case-control study on Long Island, New York, we examined whether polymorphisms in NER genes modified the association between PAH-DNA adducts and breast cancer risk. We examined polymorphisms in ERCC1 (3′-untranslated region 8092C/A), XPA (5′-untranslated region −4G/A), XPD (Asp312Asn in exon 10), XPF (Arg415Gln in exon 8), and XPG (Asp1104His in exon 15) in 1,053 breast cancer cases and 1,102 population-based controls. The presence of at least one variant allele in XPD was associated with a 25% increase in the odds ratio [OR, 1.25; 95% confidence interval (95% CI), 1.04-1.50] for breast cancer. The increase associated with homozygosity of the variant alleles for XPD and ERCC1 was stronger among those with detectable PAH-DNA adduct levels (OR, 1.83; 95% CI, 1.22-2.76 and OR, 1.92; 95% CI, 1.14-3.25 for detectable versus nondetectable adducts and homozygous wild-type genotype for XPD and ERCC1, respectively). We found no association between XPA, XPF, and XPG genotypes, PAH-DNA adducts, and breast cancer risk. When we combined genotypes for these NER pathway genes, there was a significant trend for increasing breast cancer risk with increasing number of putative high-risk alleles. Overall, this study suggests that the risk of breast cancer may be elevated among women with polymorphisms in NER pathway genes and detectable PAH-DNA adducts. (Cancer Epidemiol Biomarkers Prev 2007;16(10):2033–41)
Breast Cancer Risk Is Associated with the Genes Encoding the DNA Double-Strand Break Repair Mre11/Rad50/Nbs1 Complex
Authors: Hsu Huan-Ming , Wang Hui-Chun , Chen Sou-Tong , Hsu Giu-Cheng , Shen Chen-Yang , Yu Jyh-Cherng 
Published: October 2007

Abstract
The evolutionarily conserved Mre11-Rad50-Nbs1 (MRN) complex, consisting of proteins encoded by the genes Mre11, Rad50, and Nbs1, was recently shown to play a crucial role in DNA double-strand break (DSB) repair by recruiting the nuclear protein kinase ataxia telangiectasia mutated to DSB sites, leading to activation of this DNA repair network. Given the fact that carriers of defective mutation and polymorphic variants of ataxia telangiectasia mutated are at higher risk of developing breast cancer, we hypothesized a role of the MRN genes in determining breast cancer susceptibility. This hypothesis was examined both in a case control study of 559 breast cancer patients and 1,125 healthy women of single-nucleotide polymorphisms in Mre11, Rad50, and Nbs1 and by the in vivo detection of binding between Mre11 and BRCA1, encoded by the breast cancer susceptibility gene BRCA1. We were also interested in defining whether any association between MRN genes and breast cancer was modified by reproductive risk factors reflecting the level of estrogen exposure or susceptibility to estrogen exposure, as estrogen is known to initiate breast cancer development due to its metabolites causing DSB formation. Support for the hypothesis came from the observations that (a) one single-nucleotide polymorphism in Nbs1 was significantly associated with breast cancer risk, and a trend toward an increased risk of developing breast cancer was found in women harboring a greater number of putative high-risk genotypes of MRN genes (an adjusted odds ratio of 1.25 for each additional putative high-risk genotype; 95% confidence interval, 1.10-1.44); (b) this association between risk and the number of putative high-risk genotypes was stronger and more significant in women thought to be more susceptible to estrogen, i.e., those with no history of full-term pregnancy, those older (≥26 years of age) at first full-term pregnancy, or those having had fewer (&lt;2) full-term pregnancies; the risk effect conferred by harboring a higher number of high-risk genotypes of MRN genes was more significant in women without a history of breast feeding; and (c) Mre11 and BRCA1 were shown to form a complex in vivo, and this interaction was increased by irradiation. This study supports the role of the MRN pathway in breast cancer development, further strengthening the suggestion that mechanisms regulating DSB repair may play a mutator role driving breast cancer pathogenesis. (Cancer Epidemiol Biomarkers Prev 2007;6(10):2024–32)
Data Sources for Measuring Colorectal Endoscopy Use Among Medicare Enrollees
Authors: Schenck Anna P. , Klabunde Carrie N. , Warren Joan L. , Peacock Sharon , Davis William W. , Hawley Sarah T. , Pignone Michael , Ransohoff David F. 
Published: October 2007

AbstractBackground: Estimates of colorectal cancer test use vary widely by data source. Medicare claims offer one source for monitoring test use, but their utility has not been validated. We compared ascertainment of sigmoidoscopy and colonoscopy between three data sources: self reports, Medicare claims, and medical records.Materials and Methods: The study population included Medicare enrollees residing in North Carolina (n = 561) who had participated in a telephone survey on colorectal cancer tests. Medicare claims were obtained for the 5 years preceding the survey (January 1, 1998 to December 31, 2002). Information about sigmoidoscopy and colonoscopy procedures conducted in physician offices were abstracted from medical records. Sensitivity, specificity, positive predictive value, negative predictive value, agreement, and κ statistics were calculated using the medical record as the gold standard. Agreement on specific procedure type and purpose was also assessed.Results: Agreement between claim and medical record regarding whether an endoscopic procedure had been done was high (over 90%). Agreement between self report and medical record and between self report and claim was good (79% and 74%, respectively). All three data sources adequately distinguished the type of procedure done. None of the data sources showed reliable levels of agreement regarding procedure purpose (screening or diagnostic).Conclusion: Medicare claims can provide accurate information on whether a patient has undergone colorectal endoscopy and may be more complete than physician medical records. Medicare claims cannot be used to distinguish screening from diagnostic tests. Recognizing this limitation, researchers who use Medicare claims to assess rates of colorectal testing should include both screening and diagnostic endoscopy procedures in their analyses. (Cancer Epidemiol Biomarkers Prev 2007;16(10):2118–27)
Low-Fat, Low-Glycemic Load Diet and Gene Expression in Human Prostate Epithelium: A Feasibility Study of Using cDNA Microarrays to Assess the Response to Dietary Intervention in Target Tissues
Authors: Lin Daniel W. , Neuhouser Marian L. , Schenk Jeannette M. , Coleman Ilsa M. , Hawley Sarah , Gifford David , Hung Hau , Knudsen Beatrice S. , Nelson Peter S. , Kristal Alan R. 
Published: October 2007

Abstract
Purpose: We examined the feasibility of using gene expression changes in human prostate epithelium as a measure of response to a dietary intervention.
Materials and Methods: Eight men with newly diagnosed prostate cancer were randomized to a low-fat/low-glycemic load intervention arm (&lt;20% energy from fat and total daily glycemic load &lt;100) or a “standard American” control arm (≈35% energy from fat and total daily glycemic load &gt;200). Prostate tissue was collected before randomization and ∼6 weeks later, at the time of radical prostatectomy. Epithelium was acquired by laser capture microdissection, and transcript abundance levels were measured by cDNA microarray hybridization and confirmed by quantitative reverse transcription-PCR.
Results: Men in the intervention arm consumed 39% less total energy (P = 0.004) and the difference in weight change between intervention and control arms was −6.1 kg (P = 0.02). In the intervention arm, 23 (0.46%) of 5,711 cDNAs with measurable expression were significantly altered (P &lt; 0.05; false discovery rate, ≤10%). In the control arm, there were no significant changes in transcript expression, even when using a false discovery rate as high as 50%.
Conclusions: A 6-week, low-fat/low-glycemic load diet was associated with significant gene expression changes in human prostate epithelium. These results show the feasibility of using prostate tissues collected at diagnosis and at surgery to study the effects of dietary manipulation on prostate tissue, which may give insight into the molecular mechanisms underlying the associations of diet and obesity with the development or progression of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(10):2150–4)
Prediagnostic Plasma C-Peptide and Pancreatic Cancer Risk in Men and Women
Authors: Michaud Dominique S. , Wolpin Brian , Giovannucci Ed , Liu Simin , Cochrane Barbara , Manson JoAnn E. , Pollak Michael N. , Ma Jing , Fuchs Charles S. 
Published: October 2007

Abstract
Background: Hyperinsulinemia and insulin resistance have been proposed as underlying mechanisms for the increase in pancreatic cancer among long-standing diabetics and obese individuals. An association between serum insulin levels and pancreatic cancer risk was reported in a recent study, but the population was composed of heavy smokers and their findings may not be generalizable to nonsmokers.
Methods: Pancreatic cancer cases and matched controls were obtained from four large-scale prospective cohorts to examine the association between prediagnostic plasma levels of C-peptide and insulin and pancreatic cancer. One hundred ninety-seven pancreatic cancer cases were diagnosed during a maximum of 20 years of follow-up, after excluding cases diagnosed within 2 years of blood collection or with baseline diabetes. We estimated OR and confidence intervals (CI) using conditional logistic regression with adjustment for pancreatic cancer risk factors.
Results: Prediagnostic plasma C-peptide was positively associated with pancreatic cancer risk (OR, 1.52; 95% CI, 0.87-2.64, highest compared with the lowest quartile, Ptrend = 0.005). The association was not modified by body mass index or physical activity but seemed to be slightly stronger among never smokers than ever smokers. Fasting C-peptide and insulin were not related to pancreatic cancer; however, we observed a strong linear association for nonfasting C-peptide and pancreatic cancer (OR, 4.24; 95% CI, 1.30-13.8, highest versus lowest quartile, Ptrend &lt; 0.001).
Conclusions: Based on our finding of a strong positive association with nonfasting C-peptide levels, we propose that insulin levels in the postprandial state may be the relevant exposure for pancreatic carcinogenesis; however, other studies will need to examine this possibility. (Cancer Epidemiol Biomarkers Prev 2007;16(10):2101–9)
Bulky DNA Adduct Formation and Risk of Bladder Cancer
Authors: Castaño-Vinyals Gemma , Talaska Glenn , Rothman Nathaniel , Alguacil Juan , Garcia-Closas Montserrat , Dosemeci Mustafa , Cantor Kenneth P. , Malats Núria , Real Francisco X. , Silverman Debra , Serra Consol , Carrato Alfredo , Tardon Adonina , Garcia-Closas Reina , Kogevinas Manolis , Vermeulen Roel 
Published: October 2007

Abstract
Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with risk of bladder cancer and with increased bulky DNA adduct levels in several studies, mainly in smokers. We investigated the relation between bulky PAH-DNA adducts in peripheral blood mononuclear cells and bladder cancer in nonsmoking subjects from a large hospital-based case-control study in Spain. Additionally, we examined the association between DNA adduct formation and several air pollution proxies. The study comprised 76 nonsmoking cases and 76 individually matched controls by sex, region of residence, age, and smoking status (never, former). To maximize the relevance of the DNA adduct measurement as a proxy of PAH exposure, subjects selected had not changed residence, occupation, and major lifestyle factors during the last 10 years. Bulky DNA adducts were measured using the 32P-postlabeling technique, nuclease P1 treatment. The percentage of detectable adducts was higher in controls (41%) than in cases (32%) with an odds ratio of 0.75 (95% confidence interval, 0.36-1.58). In an analysis limited to controls, a higher percentage of DNA adducts was found among those whose last residence was in a big city (50%) compared with those living in villages (19%; P = 0.04). No consistent associations were found for other markers of air pollution. In this study, among nonsmokers with stable environmental and lifestyle factors, bulky DNA adducts were not associated with bladder cancer risk. Results do not support an association of bladder cancer risk with low-level exposure to PAHs as measured through the formation of bulky DNA adducts in peripheral mononuclear cells. (Cancer Epidemiol Biomarkers Prev 2007;16(10):2155–9)
Responses of Biomarkers of Folate and Riboflavin Status to Folate and Riboflavin Supplementation in Healthy and Colorectal Polyp Patients (The FAB2 Study)
Authors: Powers Hilary J. , Hill Marilyn H. , Welfare Mark , Spiers Alison , Bal Wendy , Russell Jean , Duckworth Yvonne , Gibney Eileen , Williams Elizabeth A. , Mathers John C. 
Published: October 2007

Abstract
Epidemiologic data suggest that increasing folate intake may protect against colorectal cancer. Riboflavin may interact with folate to modulate the effect. A double-blind randomized placebo-controlled intervention study (the FAB2 Study) was carried out in healthy controls and patients with colorectal polyps (adenomatous and hyperplastic) to examine effects of folic acid and riboflavin supplements on biomarkers of nutrient status and on putative biomarkers of colorectal cancer risk (DNA methylation and DNA damage; to be reported elsewhere). Ninety-eight healthy controls and 106 patients with colorectal polyps were stratified for the thermolabile variant of methylene tetrahydrofolate reductase, MTHFR C677T, and were randomized to receive 400 μg of folic acid, 1,200 μg of folic acid, or 400 μg of folic acid plus 5 mg of riboflavin or placebo for 6 to 8 weeks. Blood samples and colon biopsy samples were collected for the measurement of biomarkers of folate and riboflavin status. Supplementation with folic acid elicited a significant increase in mucosal 5-methyl tetrahydrofolate, and a marked increase in RBC and plasma, with a dose-response. Measures of riboflavin status improved in response to riboflavin supplementation. Riboflavin supplement enhanced the response to low-dose folate in people carrying at least one T allele and having polyps. The magnitude of the response in mucosal folate was positively related to the increase in plasma 5-methyl tetrahydrofolate but was not different between the healthy group and polyp patients. Colorectal mucosal folate concentration responds to folic acid supplementation to an extent comparable to that seen in plasma, but with a suggestion of an upper limit. (Cancer Epidemiol Biomarkers Prev 2007;16(10):2128–35)
Relationship between Age Maximum Height Is Attained, Age at Menarche, and Age at First Full-Term Birth and Breast Cancer Risk
Authors: Li Christopher I. , Littman Alyson J. , White Emily 
Published: October 2007

Abstract
Several pubertal and reproductive events are well established risk factors for breast cancer. Age maximum height attained is an understudied potential breast cancer risk factor that may affect risk through mechanisms different from those of other pubertal and reproductive events. We assessed the relationships between different pubertal/reproductive events and risk of different types of breast cancer in a prospective cohort of 27,536 women. Women were recruited between 2000 and 2002 and completed a mailed questionnaire. As of 2005, 585 women were diagnosed with breast cancer. Using a Cox proportional hazards model, women who reached their maximum height at ≤12 years of age had a 1.4-fold [95% confidence interval (95% CI), 1.0-1.8] increased risk of breast cancer compared with women who reached their maximum height at ≥17 years of age (Ptrend = 0.04). This association was primarily limited to more aggressive tumors, specifically those that were estrogen receptor–negative (hazard ratio, 1.9; 95% CI, 1.0-3.9) and diagnosed at a regional or distant stage (hazard ratio, 1.8; 95% CI, 1.0-3.1). There was no difference in the relation of age at menarche with breast cancer by tumor stage, whereas late age at first full-term pregnancy primarily increased risks of less-aggressive disease, including lobular, estrogen receptor–positive, and localized stage tumors. Age at maximum height seems to be an independent risk factor for breast cancer that is more strongly associated with relatively aggressive tumors that have a poorer prognosis compared with the types of tumors that are associated with ages at menarche and first full-term birth. (Cancer Epidemiol Biomarkers Prev 2007;16(10):2144–9)
Polymorphisms in Apoptosis- and Proliferation-Related Genes, Ionizing Radiation Exposure, and Risk of Breast Cancer among U.S. Radiologic Technologists
Authors: Sigurdson Alice J. , Bhatti Parveen , Doody Michele M. , Hauptmann Michael , Bowen Laura , Simon Steven L. , Weinstock Robert M. , Linet Martha S. , Rosenstein Marvin , Stovall Marilyn , Alexander Bruce H. , Preston Dale L. , Struewing Jeffrey P. , Rajaraman Preetha 
Published: October 2007

Abstract
Background: Although genes involved in apoptosis pathways and DNA repair pathways are both essential for maintaining genomic integrity, genetic variants in DNA repair have been thought to increase susceptibility to radiation carcinogenesis, but similar hypotheses have not generally been raised about apoptosis genes. For this reason, potential modification of the relationship between ionizing radiation exposure and breast cancer risk by polymorphic apoptosis gene variants have not been investigated among radiation-exposed women.
Methods: In a case-control study of 859 cases and 1,083 controls within the U.S. Radiologic Technologists cohort, we assessed breast cancer risk with respect to 16 candidate variants in eight genes involved in apoptosis, inflammation, and proliferation. Using carefully reconstructed cumulative breast dose estimates from occupational and personal diagnostic ionizing radiation, we also investigated the joint effects of these polymorphisms on the risk of breast cancer.
Results: In multivariate analyses, we observed a significantly decreased risk of breast cancer associated with the homozygous minor allele of CASP8 D302H [rs1045485, odds ratio (OR), 0.3; 95% confidence interval (95% CI), 0.1-0.8]. We found a significantly increased breast cancer risk with increasing minor alleles for IL1A A114S (rs17561); heterozygote OR 1.2 (95% CI, 1.0-1.4) and homozygote OR 1.5 (95% CI, 1.1-2.0), Ptrend = 0.008. Assuming a dominant genetic model, IL1A A114S significantly modified the dose-response relationship between cumulative personal diagnostic radiation and breast cancer risk, adjusted for occupational dose (Pinteraction = 0.004).
Conclusion: The U.S. Radiologic Technologists breast cancer study provided a unique opportunity to examine the joint effects of common genetic variation and ionizing radiation exposure to the breast using detailed occupational and personal diagnostic dose data. We found evidence of effect modification of the radiation and breast cancer dose-response relationship that should be confirmed in studies with more cases and controls and quantified radiation breast doses in the low-to-moderate range. (Cancer Epidemiol Biomarkers Prev 2007;16(10):2000–7)
Assessment of 54 Biomarkers for Biopsy-Detectable Prostate Cancer
Authors: Parekh Dipen J. , Ankerst Donna Pauler , Baillargeon Jacques , Higgins Betsy , Platz Elizabeth A. , Troyer Dean , Hernandez Javier , Leach Robin J. , Lokshin Anna , Thompson Ian M. 
Published: October 2007

Abstract
Objective: We analyzed the association of 54 biomarkers from seven classes including adipokines, immune response metalloproteinases, adhesion molecules, and growth factors with prostate cancer risk adjusting for the Prostate Cancer Prevention Trial (PCPT) risk score.
Methods: A total of 123 incident prostate cancer cases and 127 age-matched controls were selected from subjects in the San Antonio Center for Biomarkers of Risk of Prostate Cancer cohort study. Prediagnostic serum concentrations were measured in the sample collected at baseline using LabMAP technology. The odds ratios (OR) of prostate cancer risk associated with serum concentrations of 54 markers were estimated using univariate conditional logistic regression before and after adjustment for the PCPT risk score. Two-way hierarchical unsupervised clustering techniques were used to evaluate whether the 54-marker panel distinguished cases from controls.
Results: Vascular endothelial growth factor, resistin, interleukin 1Ra (IL-1Ra), granulocyte colony-stimulating factor, matrix metalloproteinase-3, plasminogen activator inhibitor, and kallikrein-8 were statistically significantly (P &lt; 0.05) underexpressed in prostate cancer cases, and α-fetoprotein was statistically significantly overexpressed in prostate cancer cases, but all had area underneath the receiver-operating characteristic curve &lt;60%; none were statistically significant adjusting for multiple comparisons (P &lt; 0.0008) or after adjustment for the PCPT risk score. Statistical clustering of patients by the marker panel did not distinguish a separate group of cases from controls.
Conclusions: This age-matched case-control study did not support findings of increased diagnostic potential from a 54-marker panel when compared with the conventional risk factors incorporated in the PCPT risk calculator. Future discovery of new biomarkers should always be tested and compared against conventional risk factors before applying them in clinical practice. (Cancer Epidemiol Biomarkers Prev 2007;16(10):1966–72)