bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gains and Amplifications of c-myc, EGFR, and 20.q13 Loci in the No Dysplasia–Dysplasia–Adenocarcinoma Sequence of Barrett's Esophagus
Authors: Rygiel Agnieszka M. , Milano Francesca , ten Kate Fibo J. , Schaap Annet , Wang Kenneth K. , Peppelenbosch Mackel P. , Bergman Jacques J.G.H.M. , Krishnadath Kausillia K. 
Published: June 2008

Abstract
The progression of Barrett's esophagus to esophageal adenocarcinoma is often characterized by the accumulation of genetic abnormalities. The goal was to evaluate the copy number alterations of several oncogene loci, including 7p12 [epidermal growth factor receptor (EGFR)], 8q24 (c-myc), and 20q13 in the sequence of no dysplasia–dysplasia–adenocarcinoma of Barrett's esophagus. Fluorescence in situ hybridization with DNA probes for the centromeric region of chromosome 7 and the locus-specific regions of 7p12 (EGFR), 8q24 (c-myc), and 20q13 was applied on 99 brush cytology specimens of patients with Barrett's esophagus with different stages of dysplasia or esophageal adenocarcinoma. Gains (3-4 copies) of chromosome 17, 8q24 (c-myc), and 20q.13 loci were found in the low frequencies in nondysplastic Barrett's esophagus. Their frequencies increased with the stage of dysplasia and reached a high incidence in esophageal adenocarcinoma. Amplification (&gt;4 copies) of at least 1 of the loci was observed in 14% of high-grade dysplasia and increased to 50% in esophageal adenocarcinoma (P = 0.015). The most frequently amplified locus was c-myc (18%), followed by 20q13 (13%) and EGFR (11%) in the high-grade dysplasia/esophageal adenocarcinoma cases. High amplification levels (&gt;10 copies) of the loci were more frequent in esophageal adenocarcinoma (72%) compared with high-grade dysplasia (20%; P = 0.049). Amplifications of the c-myc, EGFR, and 20q12 loci may serve as diagnostic markers to identify patients with Barrett's esophagus with high-grade dysplasia or esophageal adenocarcinoma. Gains of the loci might be of value as prognostic markers because they are already present in nondysplasia cases and may precede the later event of the amplification as observed in high-grade dysplasia and esophageal adenocarcinoma. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1380–5)
Polycyclic Aromatic Hydrocarbon Exposure, Urinary Mutagenicity, and DNA Adducts in Rubber Manufacturing Workers
Authors: Peters Susan , Talaska Glenn , Jönsson Bo A.G. , Kromhout Hans , Vermeulen Roel 
Published: June 2008

Abstract
Objectives: Several studies have suggested that genotoxic risks might still be present in the contemporary rubber manufacturing industry. Previously, we observed elevated levels of urinary mutagenicity and bladder DNA adducts in rubber workers. Presently, we investigated whether DNA adducts in peripheral blood mononuclear cells (PBMC) and/or urothelial cells may be caused by polycyclic aromatic hydrocarbons or other genotoxic compounds.
Methods: Spot urine samples from 116 rubber manufacturing workers were collected on Sunday and during the workweek (post-shift) to determine 1-hydroxypyrene and mutagenicity levels. For 52 nonsmokers, urothelial cell DNA adducts and PBMC DNA adducts were measured additionally.
Results: Urinary 1-hydroxypyrene levels were significantly higher in workweek samples compared with Sunday (P = 0.0001). This increase was not uniform across tasks and only reached statistical significance for the curing department (+99%; P = 0.003). Weekday urinary mutagenicity was significantly increased for mixing (+56%) and curing (+21%) workers when compared with that for Sunday. Total urothelial cell DNA adducts were related to urinary 1-hydroxypyrene (P = 0.021) and mutagenicity (P = 0.027). No significant relationship was found between the adduct levels in PBMC and urothelial cells or between the former and urinary 1-hydroxypyrene or mutagenicity.
Conclusions: Workers in the compounding, mixing, and curing departments were at highest genotoxic risk among rubber manufacturing workers. Increased levels of urinary 1-hydroxypyrene, mutagenicity, and urothelial cell DNA adducts were found in these workers. Urothelial cell and PBMC DNA adducts were not related, hinting possibly to the presence of specific bladder carcinogens in the rubber manufacturing industry. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1452–9)
Differential Expression of Genes Related to Androgen and Estrogen Metabolism in Hereditary versus Sporadic Prostate Cancer
Authors: Fromont Gaelle , Yacoub Mokrane , Valeri Antoine , Mangin Philippe , Vallancien Guy , Cancel-Tassin Geraldine , Cussenot Olivier 
Published: June 2008

Abstract
The hereditary predisposition to prostate cancer is rare and accounts for &lt;5% of cases. Except for younger age at diagnosis, no phenotypic features have been clearly associated with hereditary prostate cancer. The aim of the study was to analyze the expression of genes related to androgen and estrogen metabolism in both hereditary and sporadic prostate cancers in patients matched for clinicopathologic features. Tissues were obtained from patients included in a national familial prostate cancer registry. From the 120 cases of hereditary forms suggesting autosomal dominant Mendelian inheritance, 21 patients were treated by radical prostatectomy for whom formalin-fixed tissue was available. Twenty-one sporadic cases were then matched according to age, Gleason score, and pathologic stage. Immunohistochemistry was done on tissue microarray using antibodies directed against androgen receptor (AR), estrogen receptor α (ERA), estrogen receptor β, 5α-reductase I and II, aromatase, and the proliferation marker Ki67. The percentage of AR-positive cancer cells was higher in hereditary cancer compared with sporadic cases (P &lt; 0.004). In contrast, the mean number of ERA-positive stromal cells was lower in hereditary versus sporadic cancer (P &lt; 0.03). This differential expression of AR and ERA suggests that a specific pattern of hormone receptors is associated with hereditary predisposition to prostate cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1505–9)
Antibiotic Use and the Risk of Lung Cancer
Authors: Zhang Hui , García Rodríguez Luis A. , Hernández-Díaz Sonia 
Published: June 2008

Abstract
Antibiotic use has been associated with an increased risk of cancer in epidemiologic studies. We evaluated the association between antibiotic use and the risk of primary lung cancer by conducting a prospective case-control study nested in a cohort of subjects who were 40 to 84 years old in 1995 to 2004, with at least 2 years of enrollment in The Health Improvement Network. There were 4,336 cases of primary lung cancer. A random sample of 10,000 controls was frequency matched to the cases for age, sex, and calendar year of diagnosis. Antibiotic exposure was measured by the total number of antibiotic prescriptions and the cumulative number of days on antibiotics since enrollment. We discounted exposure 1 year before the date of cancer diagnosis. Relative risks (RR) and 95% confidence intervals (95% CI) were estimated using conditional logistic regression. Variables such as smoking, chronic obstructive pulmonary disease, respiratory infections, body mass index, and health care utilization were introduced in the model. Compared with subjects with no prescription of antibiotics before the index date, the crude RR of lung cancer was 2.52 (95% CI, 2.25-2.83) among those who received 10 or more prescriptions. The corresponding RR was 1.31 (95% CI, 1.10-1.57) upon adjustment for confounders. We used directed acyclic graphs to illustrate that the observed higher risk of lung cancer among antibiotic users may be due to the increased frequency of infections in patients with subclinical cancer and to shared causes between cancer and infections. Current evidence is insufficient to support or refute a carcinogenic effect of antibiotics. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1308–15)
Pathway Analysis of Single-Nucleotide Polymorphisms Potentially Associated with Glioblastoma Multiforme Susceptibility Using Random Forests
Authors: Chang Jeffrey S. , Yeh Ru-Fang , Wiencke John K. , Wiemels Joseph L. , Smirnov Ivan , Pico Alexander R. , Tihan Tarik , Patoka Joe , Miike Rei , Sison Jennette D. , Rice Terri , Wrensch Margaret R. 
Published: June 2008

AbstractGlioma is a complex disease that is unlikely to result from the effect of a single gene. Genetic analysis at the pathway level involving multiple genes may be more likely to capture gene-disease associations than analyzing genes one at a time. The current pilot study included 112 Caucasians with glioblastoma multiforme and 112 Caucasian healthy controls frequency matched to cases by age and gender. Subjects were genotyped using a commercially available (ParAllele/Affymetrix) assay panel of 10,177 nonsynonymous coding single-nucleotide polymorphisms (SNP) spanning the genome known at the time the panel was constructed. For this analysis, we selected 10 pathways potentially involved in gliomagenesis that had SNPs represented on the panel. We performed random forests (RF) analyses of SNPs within each pathway group and logistic regression to assess interaction among genes in the one pathway for which the RF prediction error was better than chance and the permutation P &lt; 0.10. Only the DNA repair pathway had a better than chance classification of case-control status with a prediction error of 45.5% and P = 0.09. Three SNPs (rs1047840 of EXO1, rs12450550 of EME1, and rs799917 of BRCA1) of the DNA repair pathway were identified as promising candidates for further replication. In addition, statistically significant interactions (P &lt; 0.05) between rs1047840 of EXO1 and rs799917 or rs1799966 of BRCA1 were observed. Despite less than complete inclusion of genes and SNPs relevant to glioma and a small sample size, RF analysis identified one important biological pathway and several SNPs potentially associated with the development of glioblastoma. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1368–73)
Urinary Total Isothiocyanates and Colorectal Cancer: A Prospective Study of Men in Shanghai, China
Authors: Moy Kristin A. , Yuan Jian-Min , Chung Fung-Lung , Van Den Berg David , Wang Renwei , Gao Yu-Tang , Yu Mimi C. 
Published: June 2008

AbstractLaboratory and epidemiologic evidence suggests that dietary isothiocyanates (ITCs) may have a chemopreventive effect on cancer. Humans are exposed to ITCs primarily through ingestion of cruciferous vegetables that contain glucosinolates, the precursors to ITCs. The association between urinary total ITC level and colorectal cancer risk was examined in a cohort of 18,244 men in Shanghai, China, with 16 years of follow-up. Urinary total ITCs were quantified on 225 incident cases of colorectal cancer and 1,119 matched controls. Odds ratios (ORs) and their 95% confidence intervals (95% CIs) were calculated using logistic regression models. High levels of urinary total ITCs were associated with a reduced risk of colorectal cancer 5 years after baseline measurements of ITCs, whereas a statistically nonsignificant increase in the risk of colorectal cancer was observed for cases within 5 years of post-enrollment (OR, 1.93; 95% CI, 0.85-4.39 for the upper three quartiles of urinary ITCs versus the lowest quartile). The inverse ITC-colorectal cancer association became stronger with a longer duration of follow-up. Compared with the first quartile, ORs (95% CIs) for the second, third, and fourth quartiles of total ITCs in urine collected 10 or more years before cancer diagnosis were 0.61 (0.35-1.05), 0.51 (0.29-0.92), and 0.46 (0.25-0.83), respectively, for risk of colorectal cancer (P for trend = 0.006). The present study suggests that dietary ITCs may exert tumor inhibitory effects, especially during earlier stages of the multistage process of carcinogenesis. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1354–9)
Risk of Second Primary Cancer among Esophageal Cancer Patients: a Pooled Analysis of 13 Cancer Registries
Authors: Chuang Shu-Chun , Hashibe Mia , Scelo Ghislaine , Brewster David H. , Pukkala Eero , Friis Soren , Tracey Elizabeth , Weiderpass Elisabete , Hemminki Kari , Tamaro Sharon , Chia Kee-Seng , Pompe-Kirn Vera , Kliewer Erich V. , Tonita Jon M. , Martos Carmen , Jonasson Jon G. , Dresler Carolyn M. , Boffetta Paolo , Brennan Paul 
Published: June 2008

Abstract
Background: The objective of this study is to assess the risk of second primary cancers following a first primary esophageal cancer as well as the risk of esophageal cancer as a second primary, following first primary cancers of other sites.
Methods: The present investigation is a multicenter study of 13 population-based cancer registries in Europe, Australia, Canada, and Singapore. To assess excess occurrence of second cancers after esophageal cancers, we calculated standardized incidence ratios (SIR) by dividing the observed numbers of second cancers by the expected number of cancers calculated from the accumulated person-years and the age-, sex-, calendar period-, and registry-specific first primary cancer incidence rates.
Results: During the study period, 959 cases of second primary cancers occurred after an initial esophageal cancer, resulting in a SIR of 1.15 (95% confidence interval, 1.08-1.22). Second primary stomach cancers were associated with first primary esophageal adenocarcinomas (SIR, 2.13; 95% confidence interval, 1.26-3.37) and second primary cancers of the oral cavity and pharynx (6.68; 5.33-8.26), stomach (1.53; 1.14-2.01), larynx (3.24; 1.88-5.18), lung (1.55; 1.28-1.87), kidney (1.88; 1.18-2.85), and thyroid (2.92; 1.18-6.02) were associated with first primary squamous cell carcinomas of the esophagus. An excess of esophageal cancer as a second primary were observed following first primary cancers of the aerodigestive tract, female breast, cervix, testis, bladder, Hodgkin's lymphoma, and non–Hodgkin lymphoma.
Conclusion: We observed associations of esophageal cancer with second primary head and neck cancers and lung cancer regardless of years of follow-up, which may suggest that common risk factors play a role in multiple tumor development. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1543–9)
Does Folic Acid Supplementation Prevent or Promote Colorectal Cancer? Results from Model-Based Predictions
Authors: Luebeck E. Georg , Moolgavkar Suresh H. , Liu Amy Y. , Boynton Alanna , Ulrich Cornelia M. 
Published: June 2008

Abstract
Folate is essential for nucleotide synthesis, DNA replication, and methyl group supply. Low-folate status has been associated with increased risks of several cancer types, suggesting a chemopreventive role of folate. However, recent findings on giving folic acid to patients with a history of colorectal polyps raise concerns about the efficacy and safety of folate supplementation and the long-term health effects of folate fortification. Results suggest that undetected precursor lesions may progress under folic acid supplementation, consistent with the role of folate role in nucleotide synthesis and cell proliferation. To better understand the possible trade-offs between the protective effects due to decreased mutation rates and possibly concomitant detrimental effects due to increased cell proliferation of folic acid, we used a biologically based mathematical model of colorectal carcinogenesis. We predict changes in cancer risk based on timing of treatment start and the potential effect of folic acid on cell proliferation and mutation rates. Changes in colorectal cancer risk in response to folic acid supplementation are likely a complex function of treatment start, duration, and effect on cell proliferation and mutations rates. Predicted colorectal cancer incidence rates under supplementation are mostly higher than rates without folic acid supplementation unless supplementation is initiated early in life (before age 20 years). To the extent to which this model predicts reality, it indicates that the effect on cancer risk when starting folic acid supplementation late in life is small, yet mostly detrimental. Experimental studies are needed to provide direct evidence for this dual role of folate in colorectal cancer and to validate and improve the model predictions. (Cancer Epidemiol Biomarkers Prev 2008;17(6):OF1360–8)
Long-term Stability of Human Aflatoxin B1 Albumin Adducts Assessed by Isotope Dilution Mass Spectrometry and High-Performance Liquid Chromatography–Fluorescence
Authors: Scholl Peter F. , Groopman John D. 
Published: June 2008

Abstract
The measurement of the aflatoxin B1-lysine serum albumin adduct in human blood samples is the most facile biomarker for the assessment of chronic exposure to aflatoxin B1. Many technologies have been developed for the measurement of this protein adduct including immunoassays, high-performance liquid chromatography (HPLC) with fluorescence detection, and a newly developed isotope-dilution mass spectrometry method. Irrespective of the technology used to determine this adduct level, an important question remains about the long-term stability of this damage product in stored samples. To address this issue, 19 human serum samples that had been previously analyzed for the aflatoxin B1-lysine adduct by high-performance liquid chromatography–fluorescence in 1989 were re-analyzed by isotope dilution mass spectrometry after storage at −80°C. The adduct concentrations measured by these two techniques were identical within 4% over the range 5 to 100 pg of aflatoxin B1-lysine/mg albumin. In addition, the specific chemical structure of the aflatoxin B1-lysine adduct in human samples was confirmed for the first time by collision-induced dissociation full scan mass spectrometry analysis of the protonated adduct molecular ion. These results illustrate that the aflatoxin B1-lysine serum albumin adduct can be stable in human serum stored at −80°C since 1989, and this provides confidence for the measurement of this biomarker in repository samples from epidemiologic investigations. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1436–9)
CDKN2A/p16 Genetic Test Reporting Improves Early Detection Intentions and Practices in High-Risk Melanoma Families
Authors: Aspinwall Lisa G. , Leaf Samantha L. , Dola Erin R. , Kohlmann Wendy , Leachman Sancy A. 
Published: June 2008

Abstract
Genetic testing for melanoma has yet to enter routine clinical use because of the scarcity of available data on the effect of test reporting. A prospective study of 59 members of Utah CDKN2A/p16 mutation–positive pedigrees was conducted to establish the effect of CDKN2A/p16 genetic test reporting on melanoma early detection intentions and behaviors (total body skin examination and skin self-examination) in a high-risk population. Behavioral assessments were made at baseline, immediately after CDKN2A/p16 test reporting and counseling, and at 1-month follow-up (42 participants). Baseline screening practices were poor relative to current recommendations, especially among participants without a personal history of melanoma. Changes from baseline practice were evaluated in three groups of participants (CDKN2A/p16+ with history of melanoma, CDKN2A/p16+ without melanoma history, and CDKN2A/p16−). Across multiple measures, test reporting caused CDKN2A/p16 mutation carriers without a melanoma history to improve to the level of adherence reported by participants with a melanoma history, without decreasing compliance of the CDKN2A/p16− group. Compared with baseline, CDKN2A/p16+ participants without a melanoma history reported greater intention to obtain total body skin examinations (P &lt; 0.0001), increased intentions and adherence to skin self-examination recommendations (P &lt; 0.01 and P &lt; 0.001, respectively), and increased number of body sites examined at 1 month (P &lt; 0.002); further, 55% reported adopting a new screening behavior at follow-up. Test reporting also improved skin self-examination adherence among CDKN2A/p16− participants (P &lt; 0.03). The finding that CDKN2A/p16 test reporting enhances compliance with early detection measures among CDKN2A/p16+ participants without diminishing the compliance of CDKN2A/p16− participants suggests a favorable risk-benefit ratio for melanoma genetic testing in high-risk patients. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1510–9)
Familial and Perceived Risk of Breast Cancer in Relation to Use of Complementary Medicine
Authors: Myers Cynthia D. , Jacobsen Paul B. , Huang Yifan , Frost Marlene H. , Patten Christi A. , Cerhan James R. , Sellers Thomas A. 
Published: June 2008

Abstract
Aim: To examine the use of complementary and alternative medicine (CAM) by women with varying levels of familial and perceived risk of breast cancer with the goal of preventing breast cancer.
Methods: Cross-sectional data on CAM use were collected on 2,198 women (mean age, 63 years) personally unaffected by breast cancer in the Minnesota Breast Cancer Family Study. CAM use was compared across women at high, moderate, or average risk based on family history, as well as across categories of perceived risk of breast cancer. CAM use was also examined in relation to screening and general health behaviors, worry about breast cancer, and optimism.
Results: Half (49.5%) of the women reported using at least one CAM modality with the intent of preventing breast cancer. Univariate analyses indicated that greater overall CAM use was related to greater perceived risk (P = 0.018), more general health behaviors (P &lt; 0.0001), more breast cancer screening behaviors (P = 0.0002), greater optimism (P = 0.0002), and higher educational attainment (P &lt; 0.0001). Multivariate analysis revealed that general health behaviors (P &lt; 0.0001), education (P = 0.0027), and optimism (P = 0.037) were significant predictors of CAM use when in the same model with perceived risk and breast cancer screening behaviors.
Conclusions: Many women use CAM with the goal of preventing breast cancer. General health-promoting behaviors, education, and optimism predict CAM use. Evidence-based guidance is needed for the public and health care providers on the potential and limitations of specific CAM approaches to affect cancer risk. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1527–34)
Anti-Mesothelin Antibodies and Circulating Mesothelin Relate to the Clinical State in Ovarian Cancer Patients
Authors: Hellstrom Ingegerd , Friedman Eitan , Verch Thorsten , Yang Yi , Korach Jacob , Jaffar Jade , Swisher Elizabeth , Zhang Boxin , Ben-Baruch Gilad , Tan Marcus C.B. , Goedegebuure Peter , Hellstrom Karl Erik 
Published: June 2008

AbstractMost human ovarian carcinomas express mesothelin, which is shed as a diagnostically useful biomarker. We applied an ELISA to measure antibodies to native mesothelin in serum from a series of patients with divergent clinical outcomes. The level of anti-mesothelin antibodies determined as OD450 nm and referred to as absorption units (AU) for 1:20 diluted serum was higher in patients who remained disease-free after therapy [no evidence of disease (NED); n = 14] than in patients whose disease recurred [clinical evidence of disease (CED); n = 21; P &lt; 0.01]. Applying AU ≥ 0.5 at a serum dilution of 1:20 as cutoff, 10 of 14 (71%) ovarian carcinoma patients with NED and 9 of 21 (43%) patients with CED had antibodies to mesothelin compared with 6 of 23 (26%) healthy women (P &lt; 0.008) and 5 of 24 (21%) women with other benign gynecologic diseases (P &lt; 0.003), whereas 7 of 9 (78%) of women with pelvic inflammatory disease were positive. Three of the 14 (21%) NED patients had circulating mesothelin detected as an AU ≥ 0.2 at a serum dilution of 1:40 (P &lt; 0.005) compared with 15 of 21 (71%) CED patients, and 9 of 14 (64%) NED patients (P &lt; 0.0002) were positive for antibodies and negative for antigen compared with 1 of 21 (5%) CED patients. Although our data indicate that an antibody response to mesothelin is an important correlate of ovarian carcinoma, prospective studies are needed to show whether the measurement of such antibodies (alone or together with antigen) aids the diagnosis and monitoring of patients. (Cancer Epidemiol Biomarkers Prev 2008;17(6):1520–6)