bluuebunny/crossref_metadata_2025_split huggingface dataset:
Benzo(a)pyrene Diol Epoxide-Induced Chromosome 9p21 Aberrations Are Associated with Increased Risk of Bladder Cancer
Authors: Gu Jian , Horikawa Yohei , Chen Meng , Dinney Colin P. , Wu Xifeng 
Published: September 2008

Abstract
Purpose: Loss of chromosome 9p21 is one of the most frequent genomic alterations in bladder cancer. Alterations of 9p21 and p16 are also frequently seen in the epithelial cells of chronic smokers. We hypothesize that 9p21 is a molecular target of benzo(a)pyrene diol epoxide (BPDE), the metabolic product of tobacco carcinogen benzo(a)pyrene, and 9p21 BPDE sensitivity is a genetic susceptibility factor for bladder cancer.
Material and Methods: In this case-control study of 203 bladder cancer cases and 198 matched healthy controls, we compared the frequencies of BPDE-induced 9p21 aberrations in cultured peripheral blood lymphocytes using fluorescent in situ hybridization and evaluated the association between 9p21 BPDE sensitivity and bladder cancer risk.
Results: We found that BPDE-induced chromosome 9p21 aberrations were significantly higher in peripheral blood lymphocytes of bladder cancer cases (20.76 ± 6.97 per 1,000) than those of controls (16.58 ± 7.07 per 1,000; P &lt; 0.0001). However, no difference was observed for CEP9, a control centromere locus on chromosome 9. Using the median aberration value in the controls as a cutoff point to dichotomize BPDE sensitivity and after adjustment by age, sex, ethnicity, and smoking status, 9p21 BPDE sensitivity was associated with a significantly increased risk of bladder cancer (odds ratio, 5.29; 95% confidence interval, 3.26-8.59), whereas the odds ratio for the CEP9 locus was 0.99 (95% confidence interval, 0.66-1.50). There was also a dose-response relationship between the 9p21 BPDE sensitivity and increased risk for bladder cancer.
Conclusion: 9p21 may be a molecular target for BPDE damage in bladder cancer cases and 9p21 BPDE sensitivity may be a marker of bladder cancer susceptibility. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2445–50)
Prognostic Value of Signal Transducers and Activators of Transcription 3 in Breast Cancer
Authors: Sheen-Chen Shyr-Ming , Huang Chao-Cheng , Tang Rei-Ping , Chou Fong-Fu , Eng Hock-Liew 
Published: September 2008

Abstract
Introduction: Constitutively activated signal transducers and activators of transcription (STAT) proteins are found in various types of tumors. However, there is still very limited information about the role of STATs in breast cancer. The power of tissue microarray technique is the capability of doing a series of analyses of thousands specimens in a parallel fashion with minimal damage to the origin blocks. This study was designed with the application of tissue microarray to analyze the STAT3 status in breast cancer.
Materials and Methods: Archival tissue specimens from 102 patients with primary invasive breast cancer were selected, and STAT3 expression was analyzed by immunohistochemical staining with tissue microarray. The data of primary tumor staging, age, estrogen receptor status, lymph node status, histologic grading, and tumor-node-metastasis staging were also collected.
Results: By multivariate analysis, the STAT3 expression turned out to be significantly related to the overall 5-year survival rate (P = 0.024).
Conclusion: Immunohistochemical staining with tissue microarray was convenient and feasible for the analysis of STAT3 expression status in breast cancer. Our preliminary results are promising and deserve further evaluation. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2286–90)
Promoter Hypermethylation of the p16 Gene Is Associated with Poor Prognosis in Recurrent Early-Stage Hepatocellular Carcinoma
Authors: Ko Eunkyung , Kim Yujin , Kim Sung-Joo , Joh Jae-Won , Song SangYong , Park Cheol-Keun , Park Joobae , Kim Duk-Hwan 
Published: September 2008

Abstract
Despite significant advances in the detection and treatment of hepatocellular carcinoma, the prognosis of patients with hepatocellular carcinoma remains very poor, in part due to the high incidence of recurrence. This study was aimed at identifying a prognostic indicator of recurrence in patients with hepatocellular carcinoma. We retrospectively analyzed CpG island hypermethylation of the p14, p15, p16, GSTP1, integrin α4, SYK, and CDH1 genes in fresh-frozen tissues from 265 patients with hepatocellular carcinoma using the methylation-specific PCR. The expression levels of p16 and p53 were evaluated by immunohistochemistry. CpG island hypermethylation was detected in 6% for p14, 21% for p15, 67% for p16, 75% for GSTP1, 23% for integrin α4, 12% for SYK, and 57% for CDH1. Recurrence was observed in 102 (38%) of the 265 patients. There was no association between the risk for recurrence and hypermethylation of any gene studied. However, p16 methylation was associated with a poor survival after surgery for recurrent stage I to II hepatocellular carcinomas (hazard ratio, 4.05; 95% confidence interval, 1.15-14.20; P = 0.03). In addition, the hazard of failure after recurrence was about 3.80 (95% confidence interval, 1.03-14.20; P = 0.04) times higher in patients with p16 methylation than in those without. Negative expression of p16 at a protein level was also associated with poor survival in recurrent stage I to II hepatocellular carcinomas, but p53 expression did not have a synergistic effect on the poor prognosis. In conclusion, the present study suggests that p16 methylation may be associated with a poor prognosis in recurrent early-stage hepatocellular carcinomas. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2260–7)
Mortality among HIV-1– and Human Herpesvirus Type 8–Affected Mother-Infant Pairs in Zambia
Authors: Wojcicki Janet , Mwanahamuntu Mulindi , Minhas Veenu , Djokic Boris , Kankasa Chipepo , Klaskala Winslow , Brayfield Brad , Phiri Saul , Wood Charles , Mitchell Charles D. 
Published: September 2008

Abstract
Objective: To determine the respective trends in mortality of Zambian mother-infant pairs based on maternal infection with HIV-1 and human herpesvirus type 8 (HHV-8).
Methods: A prospective cohort study was done on Zambian mother-infant pairs, stratified by maternal serologic status and followed from 6 weeks postdelivery for 48 months. Statistical analysis of the differences in the calculated mortality rates among the four groups was done using Stata 7.0. Kaplan-Meier analysis and Cox proportional hazard models were used to measure subject survival time.
Results: Between September 1998 and March 2002, a total of 1,425 mother-infant pairs were enrolled. The crude mortality rate among children born to dually infected mothers was ∼9 times higher (245.90 deaths per 1,000 live births) when compared with the death ratio of children born to seronegative mothers (24.63 deaths per 1,000 live births). The incidence rate for death was 0.34/1,000 in infants of co-infected mothers in comparison with 0.32/1,000 among HIV-1–infected mothers, 0.0336/1,000 among uninfected mothers, and 0.0403/1,000 among HHV-8–infected mothers (χ2 = 154.56; P &lt; 0.01). Infants of co-infected mothers had a comparable risk of death in comparison with infants infected with HIV-1 alone {hazard ratio, 9.91 [95% confidence interval (95% CI), 5.08-19.37] for co-infected versus 9.26 [95% CI, 4.75-18.07] for HIV-1–infected alone}. Infants of mothers infected only with HHV-8 also had comparable survival in comparison with uninfected infants (hazard ratio, 1.21; 95% CI, 0.56-2.61).
Conclusion: Infants born to mothers dually infected with both HIV-1 and HHV-8 have comparable survival with infants exposed to HIV-1 alone. Infants born to mothers infected only with HHV-8 have comparable survival with uninfected infants. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2238–43)
Genetic Susceptibility to Renal Cell Carcinoma: The Role of DNA Double-Strand Break Repair Pathway
Authors: Margulis Vitaly , Lin Jie , Yang Hushan , Wang Wei , Wood Christopher G. , Wu Xifeng 
Published: September 2008

Abstract
Alterations in DNA repair genes have been shown to cause a reduction in host DNA repair capacity and may influence host susceptibility to carcinogenesis. The double-strand break repair is a major DNA-repair pathway. This study tested the hypothesis that common sequence variants of the double-strand break pathway genes predispose susceptible individuals to an increased risk for renal cell carcinoma. Toward this end, we evaluated the associations of 13 single-nucleotide polymorphisms in 10 candidate genes involved in the double-strand break pathway with renal cell carcinoma risk in a population-based case-control study that included 326 Caucasian renal cell carcinoma patients and 335 controls. Using the homozygous wild type as the reference group, we observed a significantly increased renal cell carcinoma risk associated with the homozygous variant genotype of NBS1 (rs1805794; odds ratio, 2.13; 95% confidence interval (95% CI), 1.17-3.86). Carrying of at least one copy of the variant XRCC4 allele was also associated with a significantly increased risk (rs1805377; odds ratio, 1.56; 95% CI, 1.08-2.26). Importantly, in pathway analysis, compared with the reference group (1 or less adverse alleles), individuals with two (odds ratio, 1.26; 95% CI, 0.83-1.91), three (odds ratio, 1.00; 95% CI, 0.64-1.56), and more than three adverse alleles (odds ratio, 1.75; 95% CI, 1.03-2.98) were at increased risk for renal cell carcinoma with significant association in subjects carrying more than 3 adverse alleles. Results from this study provide evidence that individuals with a higher number of genetic variations in the DBS repair pathway are at an increased risk for renal cell carcinoma. These findings require further validation in independent populations. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2366–73)
Urinary Lead Exposure and Breast Cancer Risk in a Population-Based Case-Control Study
Authors: McElroy Jane A. , Shafer Martin M. , Gangnon Ronald E. , Crouch Luis A. , Newcomb Polly A. 
Published: September 2008

Abstract
Background: Lead is a toxic nonessential metal with widespread exposure starting in utero. Lead has been reclassified in 2004 by the International Agency for Research on Cancer Working Group from a “possible” to a “probable” human carcinogen. Lead may be a facilitative or permissive carcinogen, which means that lead may permit or augment the genotoxic effects of other exposures.
Methods: This population-based study in Wisconsin gathered survey data and home-collected urine specimens from 246 women, ages 20 to 69 years, with incident invasive breast cancer identified from the Wisconsin state registry and 254 age-matched control subjects from population lists from September 2004 to February 2005. We measured urinary lead concentrations by inductively coupled plasma mass spectrometry, adjusted the values by specific gravity, and conducted interviews by telephone to obtain information on known and suspected breast cancer risk factors.
Results: Women in the highest quartile of specific gravity–adjusted lead level (≥1.10 μg/L) had twice the breast cancer risk of those in the lowest quartile (&lt;0.42 μg/L; odds ratio, 1.99; 95% confidence interval, 1.1-3.6) after adjustment for established risk factors. Excluding women who were currently taking nonsteroidal aromatase inhibitors (n = 52), we did not observe any increased breast cancer risk after adjustment for established risk factors.
Conclusion: Our population-based case-control study suggests that lead exposure, as determined by specific gravity–adjusted urinary lead concentrations, is not associated with a significant increased risk for breast cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2311–7)
Genomic DNA Methylation among Women in a Multiethnic New York City Birth Cohort
Authors: Terry Mary Beth , Ferris Jennifer S. , Pilsner Richard , Flom Julie D. , Tehranifar Parisa , Santella Regina M. , Gamble Mary V. , Susser Ezra 
Published: September 2008

Abstract
One plausible mechanism for the environment to alter cancer susceptibility is through DNA methylation. Alterations in DNA methylation can lead to genomic instability and altered gene transcription. Genomic DNA methylation levels have been inversely associated with age, suggesting that factors throughout life may be associated with declines in DNA methylation. Using information from a multiethnic New York City birth cohort (born between 1959 and 1963), we examined whether genomic DNA methylation, measured in peripheral blood mononuclear cells, was associated with smoking exposure and other epidemiologic risk factors across the life course. Information on prenatal and childhood exposures was collected prospectively through 1971, and information on adult exposures and blood specimens were collected in adulthood from 2001 to 2007. Methylation levels of leukocyte DNA were determined using a [3H]-methyl acceptance assay where higher values of disintegrations per minute per microgram DNA indicate less DNA methylation. Genomic methylation of leukocyte DNA differed by ethnicity (66% of Blacks, 48% of Whites, and 29% of Hispanics were above the median level of disintegrations per minute per microgram DNA; P = 0.03). In multivariable modeling, DNA methylation was statistically significantly associated with maternal smoking during pregnancy, longer birth length, later age at menarche, nulliparity, and later age at first birth. These data, if replicated in larger samples, suggest that risk factors across the life course may be associated with DNA methylation in adulthood. Larger studies and studies that measure within-individual changes in DNA methylation over time are a necessary next step. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2306–10)
Genetic Variation in Genes for the Xenobiotic-Metabolizing EnzymesCYP1A1, EPHX1, GSTM1, GSTT1, andGSTP1and Susceptibility to Colorectal Cancer in Lynch Syndrome
Authors: Pande Mala , Amos Christopher I. , Osterwisch Daniel R. , Chen Jinyun , Lynch Patrick M. , Broaddus Russell , Frazier Marsha L. 
Published: September 2008

AbstractIndividuals with Lynch syndrome are predisposed to cancer due to an inherited DNA mismatch repair gene mutation. However, there is significant variability observed in disease expression likely due to the influence of other environmental, lifestyle, or genetic factors. Polymorphisms in genes encoding xenobiotic-metabolizing enzymes may modify cancer risk by influencing the metabolism and clearance of potential carcinogens from the body. In this retrospective analysis, we examined key candidate gene polymorphisms in CYP1A1, EPHX1, GSTT1, GSTM1, and GSTP1 as modifiers of age at onset of colorectal cancer among 257 individuals with Lynch syndrome. We found that subjects heterozygous for CYP1A1 I462V (c.1384A&gt;G) developed colorectal cancer 4 years earlier than those with the homozygous wild-type genotype (median ages, 39 and 43 years, respectively; log-rank test P = 0.018). Furthermore, being heterozygous for the CYP1A1 polymorphisms, I462V and Msp1 (g.6235T&gt;C), was associated with an increased risk for developing colorectal cancer [adjusted hazard ratio for AG relative to AA, 1.78; 95% confidence interval, 1.16-2.74; P = 0.008; hazard ratio for TC relative to TT, 1.53; 95% confidence interval, 1.06-2.22; P = 0.02]. Because homozygous variants for both CYP1A1 polymorphisms were rare, risk estimates were imprecise. None of the other gene polymorphisms examined were associated with an earlier onset age for colorectal cancer. Our results suggest that the I462V and Msp1 polymorphisms in CYP1A1 may be an additional susceptibility factor for disease expression in Lynch syndrome because they modify the age of colorectal cancer onset by up to 4 years. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2393–401)
Talc Use, Variants of theGSTM1, GSTT1, andNAT2Genes, and Risk of Epithelial Ovarian Cancer
Authors: Gates Margaret A. , Tworoger Shelley S. , Terry Kathryn L. , Titus-Ernstoff Linda , Rosner Bernard , De Vivo Immaculata , Cramer Daniel W. , Hankinson Susan E. 
Published: September 2008

AbstractEpidemiologic evidence suggests a possible association between genital use of talcum powder and risk of epithelial ovarian cancer; however, the biological basis for this association is not clear. We analyzed interactions between talc use and genes in detoxification pathways [glutathione S-transferase M1 (GSTM1), glutathione S-transferase T1 (GSTT1), and N-acetyltransferase 2 (NAT2)] to assess whether the talc/ovarian cancer association is modified by variants of genes potentially involved in the response to talc. Our analysis included 1,175 cases and 1,202 controls from a New England-based case-control study and 210 cases and 600 controls from the prospective Nurses' Health Study. We genotyped participants for the GSTM1 and GSTT1 gene deletions and three NAT2 polymorphisms. We used logistic regression to analyze the main effect of talc use, genotype, and gene-talc interactions in each population and pooled the estimates using a random-effects model. Regular talc use was associated with increased ovarian cancer risk in the combined study population (RR, 1.36; 95% CI, 1.14-1.63; Ptrend &lt; 0.001). Independent of talc, the genes examined were not clearly associated with risk. However, the talc/ovarian cancer association varied by GSTT1 genotype and combined GSTM1/GSTT1 genotype. In the pooled analysis, the association with talc was stronger among women with the GSTT1-null genotype (Pinteraction = 0.03), particularly in combination with the GSTM1-present genotype (Pinteraction = 0.03). There was no clear evidence of an interaction with GSTM1 alone or NAT2. These results suggest that women with certain genetic variants may have a higher risk of ovarian cancer associated with genital talc use. Additional research is needed on these interactions and the underlying biological mechanisms. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2436–44)
Fruit and Vegetable Consumption and Risk of Bladder Cancer: A Prospective Cohort Study
Authors: Larsson Susanna C. , Andersson Swen-Olof , Johansson Jan-Erik , Wolk Alicja 
Published: September 2008

Abstract
Fruit and vegetable consumption has been inconsistently associated with risk of bladder cancer. We used data from a prospective population-based cohort study of 82,002 Swedish women and men to examine the association between fruit and vegetable consumption and bladder cancer incidence. Diet was assessed with a validated food frequency questionnaire. During a mean follow-up of 9.4 years, 485 incident cases of bladder cancer were identified in the Swedish cancer registries. We found no statistically significant association between intakes of total fruits and vegetables, total fruits, or total vegetables and bladder cancer risk after adjustment for age, sex, education, and cigarette smoking. The multivariate rate ratios (95% confidence intervals) comparing the highest with the lowest quartile of intake were 0.80 (0.60-1.05) for total fruits and vegetables, 0.93 (0.69-1.25) for fruits, and 0.89 (0.67-1.19) for vegetables. Likewise, no associations were observed for citrus fruits, cruciferous vegetables, or green leafy vegetables. The associations did not differ by sex or smoking status. In conclusion, findings from this prospective study suggest that fruit and vegetable intakes are not likely to be appreciably associated with the risk of bladder cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2519–22)
No Association of MMP-7, MMP-8, and MMP-21 Polymorphisms with the Risk of Hepatocellular Carcinoma in a Chinese Population
Authors: Qiu Wei , Zhou Gangqiao , Zhai Yun , Zhang Xiumei , Xie Weimin , Zhang Hongxing , Yang Hao , Zhi Lianteng , Yuan Xiaoyan , Zhang Xiaoai , He Fuchu 
Published: September 2008

Abstract
Previous studies have suggested that the functional polymorphisms in the promoters of matrix metalloproteinases (MMP) genes were associated with the risk of cancers, but no study has ever explored these polymorphisms as risk factors for hepatocellular carcinoma. Recently, we firstly examined whether seven functional polymorphisms in the promoters of MMP-1, MMP-2, MMP-3, MMP-9, MMP-12, and MMP-13 have any bearing on the risk of hepatocellular carcinoma, but we found none. In this study, we focused on an additional six MMP polymorphisms, including four functional polymorphisms in the promoters of MMP-7 (A-181G and C-153T) and MMP-8 (C-799T and A-381G), and two nonsynonymous polymorphisms in MMP-10 (A180G) and MMP-21 (C572T). With the polymorphism validation, we found that only MMP-7 A-181G, MMP-8 C-799T, and MMP-21 C572T were polymorphic. These three polymorphisms were then genotyped in 434 patients with hepatocellular carcinoma and 480 controls by PRC-RFLP analysis. The associations between the polymorphisms and hepatocellular carcinoma risk were evaluated while controlling for confounding factors. No significant association with the risk of hepatocellular carcinoma was observed with the three polymorphisms in the overall sample, hepatitis B virus carriers, and non–hepatitis B virus carriers after correction for multiple comparisons. Furthermore, when the analyses were stratified by age, sex, status of smoking and drinking, pack-years of smoking, and family history of hepatocellular carcinoma, there was also no significant association between these polymorphisms and hepatocellular carcinoma risk. Our findings suggest that the polymorphisms MMP-7 A-181G, MMP-8 C-799T, and MMP-21 C572T may not play a major role in mediating susceptibility to hepatocellular carcinoma. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2514–8)
Linking Tobacco Control Policies and Practices to Early Cancer Endpoints: Surveillance as an Agent for Change
Authors: Hartman Anne M. , Thun Michael J. , Ballard-Barbash Rachel ,   for the Organizing Committee
Published: September 2008

AbstractState tobacco control programs provide an important laboratory for the development, implementation, and evaluation of comprehensive tobacco control interventions. Studies have shown that states and municipalities with aggressive tobacco control programs have experienced more rapid decreases in per capita cigarette sales, smoking prevalence, lung cancer, and heart disease than entities without such programs. Despite strong evidence that population-level interventions are critical in achieving large and sustained reductions in tobacco use, states do not fund tobacco control efforts at levels recommended by the Centers for Disease Control and Prevention. Research on the effectiveness and cost effectiveness of these activities is essential to inform and strengthen tobacco control at the state level. A workshop, co-organized by the American Cancer Society, the National Cancer Institute, the American Association for Cancer Research, and the Centers for Disease Control and Prevention, was held in Philadelphia in December, 2007, to discuss the topic “Linking tobacco control policies and practices to early cancer endpoints: surveillance as an agent for change.” Participants represented three different disciplines. Tobacco surveillance researchers described the data currently collected on state-level tobacco control policies, protobacco countermeasures by the industry, public attitudes toward tobacco use, and measures of smoking prevalence and consumption. Cancer registry experts described the geographic coverage of high quality, population-based cancer registries. Mathematical modeling experts discussed various modeling approaches that can be used to relate upstream tobacco promotion and control activities to downstream measures such as public attitudes, changes in tobacco use, and trends in tobacco-related diseases. The most important recommendation of the Workshop was a call for national leadership to enhance the collection and integration of data from multiple sources as a resource to further study and strengthen the scientific basis for tobacco control. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2215–9)