bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transcriptional Restriction of Human Immunodeficiency Virus Type 1 Gene Expression in Undifferentiated Primary Monocytes
Authors: Dong Chunsheng , Kwas Constance , Wu Li 
Published: February 2009

ABSTRACT
Monocytes are critical precursors of dendritic cells and macrophages, which play an important role in the pathogenesis of human immunodeficiency virus type 1 (HIV-1). HIV-1 postentry infection is blocked in undifferentiated monocytes in vitro, while the underlying mechanisms are not fully understood. HIV-1 Tat-mediated transactivation of the viral long terminal repeat (LTR) promoter is essential for HIV-1 transcription. Two critical cellular cofactors of HIV-1 Tat, cyclin T1 (CycT1) and cyclin-dependent kinase 9 (CDK9), are required for LTR-directed HIV-1 transcription. In addition to the previously identified restrictions in early viral life cycle, we find that HIV-1 gene expression is impaired in undifferentiated primary monocytes. Transfection of monocytes by nucleofection with HIV-1 proviral DNA could not produce infectious HIV-1. The lack of Tat transactivation of the LTR promoter correlated with the impaired HIV-1 gene expression in monocytes. Interestingly, heterokaryons between primary monocytes and a human embryonic kidney cell line restored Tat transactivation of LTR, suggesting that monocytes lack cellular factors required for Tat transactivation. CycT1 protein was undetectable in freshly isolated monocytes and induced in monocyte-differentiated macrophages, while the expression of CDK9 remained constant. Transient expression of CycT1 in undifferentiated monocytes could not rescue Tat transactivation, suggesting that CycT1 is not the only limiting factor of HIV-1 infection in monocytes. Furthermore, monocyte differentiation into macrophages appeared to enhance the phosphorylation of CDK9, which correlated with significantly increased HIV-1 infection in macrophages. Our results provide new insights into HIV-1 infection and regulation in primary monocytes and viral pathogenesis.
High Lifetime Incidence of Adult Acute Lymphoblastic Leukemia among Hispanics in California
Authors: Pullarkat Sheeja T. , Danley Kathleen , Bernstein Leslie , Brynes Russell K. , Cozen Wendy 
Published: February 2009

Abstract
Background: The higher incidence of acute lymphoblastic leukemia (ALL) among Hispanic children relative to that in other racial/ethnic groups is well-known. We evaluated the incidence patterns of ALL in adults.
Methods: We analyzed the incidence patterns of ALL (International Classification of Diseases for Oncology 3 codes 9835-9837) among all patients diagnosed from 1988 to 2004 in California using data from the California Cancer Registry to determine whether adult Hispanics also had higher incidence rates of ALL compared with non–Hispanic Whites (Whites). Age-adjusted incidence rates (AAIR), incidence rate ratios (IRR), and 5-year survival rates were obtained using SEER*Stat. AAIRs of other leukemia subtypes and IRRs relative to non–Hispanic Whites were also examined as references for ALL.
Results: AAIRs of ALL in Hispanic males and females ages 20 to 54 years were higher compared with those in White males and females (IRR, 1.99; 95% confidence interval, 1.74-2.28 and IRR, 1.91; 95% confidence interval, 1.60-2.25, respectively). A higher AAIR of ALL was also observed among older (55+ years) Hispanic females (IRR, 1.84; 95% confidence interval, 1.52-2.21), but not in males (IRR, 1.07; 95% confidence interval, 0.84-1.34). Among Hispanics, low socioeconomic status was associated with a higher AAIR compared with high/middle socioeconomic status (IRR, 1.33; 95% confidence interval, 1.04-1.70). The respective 5-year survival rates among ALL patients were 38% and 30% for Whites and Hispanics ages 20 to 54 years, and 8% and 12% for patients 55 years of age or older. Compared with other racial/ethnic groups, Hispanics did not have an increased IRR of the other major leukemia subtypes.
Conclusion: Hispanics experience a higher incidence of ALL throughout life, but not other subtypes. (Cancer Epidemiol Biomarkers Prev 2009;18(2):611–5)
Serum High-Density Lipoprotein Cholesterol and Breast Cancer Risk by Menopausal Status, Body Mass Index, and Hormonal Receptor in Korea
Authors: Kim Yeonju , Park Sue K. , Han Wonshik , Kim Dong-Hyun , Hong Yun-Chul , Ha Eun Hee , Ahn Sei-Hyun , Noh Dong-Young , Kang Daehee , Yoo Keun-Young 
Published: February 2009

AbstractHigh-density lipoprotein cholesterol (HDL-C) has been suggested to be associated with breast cancer. However, the roles of HDL-C and hypertriglyceridemia on breast cancer still have been controversial. The goal of this study was to investigate the association between HDL-C with breast cancer risk, stratifying by menopausal status, and body mass index. The hormonal receptor status of breast has been proposed to modify the effect of HDL-C on breast cancer. Multicenter hospital-based case-control study was conducted from November 2004 to December 2005 in Korea. After one to two individual matchings by age (±5 years) and menopausal status, 690 cases and 1,380 controls were included in the analysis. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by conditional, unconditional, and multinomial logistic regressions. Protective effect of HDL-C on breast cancer was only observed among premenopausal women with an OR (95% CI) of 0.49 (0.33-0.72) for HDL-C ≥60 versus &lt;50 mg/dL (Ptrend &lt; 0.01). Only nonobese premenopausal women had a significant decreased risk (OR, 0.34; 95% CI, 0.22-0.53). OR (95% CI) of low HDL-C (&lt;50 mg/dL) and high triglyceride (TG; ≥150 mg/dL) category was 2.20 (1.32-3.67) on estrogen receptor-negative and progesterone receptor-negative breast cancer compared with high HDL-C (≥50 mg/dL) and low TG (&lt;150 mg/dL) category. This study suggests that higher level of HDL-C may reduce breast cancer risk among premenopausal women. Estrogen receptor-negative and progesterone receptor-negative breast cancer was associated with dyslipidemia, which implicates that association among HDL-C, TG, and breast cancer may be modified by receptor status. (Cancer Epidemiol Biomarkers Prev 2009;18(2):508–15)
The Impact of Human Papillomavirus Information on Perceived Risk of Cervical Cancer
Authors: Marlow Laura A.V. , Waller Jo , Wardle Jane 
Published: February 2009

Abstract
There is a need to develop public education about the link between human papillomavirus (HPV) and cervical cancer. Explaining that a sexually transmitted virus causes cervical cancer may affect perceived risk of cervical cancer. We hypothesized that presenting HPV information would have differential effects depending on age and screening attendance. Data were collected during face-to-face interviews with a sample of British women age 16 to 75 years who had not heard of HPV before (n = 965). A repeated measures design was used, assessing perceived risk of cervical cancer before and after providing information about HPV. Perceived risk was assessed using a comparative risk measure with a five-point response scale. Preinformation, the mean perceived risk score was 2.64 (SE, 0.03). Overall, presentation of HPV information did not have an effect on perceived risk of cervical cancer [χ2(1) = .72; P = 0.396], but as expected, there was a significant time by age interaction for the change in perceived risk [χ2(5) = 33.56; P &lt; 0.001], which increased in the youngest age group (16-25 years) and decreased in the oldest age group (65-75 years). In a separate analysis with women in the screening age range (25-64 years; n = 709), there was a significant time by screening attendance interaction [χ2(1) = 5.25; P = 0.022], with an increase in perceived risk among women who did not regularly attend screening. This is the first study to examine the effect of HPV information on perceived risk across different population groups. Interventions to increase awareness of HPV could benefit from tailoring information to prescreening age, screening age, and postscreening age women. (Cancer Epidemiol Biomarkers Prev 2009;18(2):373–6)
Serum Levels of Soluble Mesothelin-Related Peptides in Malignant and Nonmalignant Asbestos-Related Pleural Disease: Relation with Past Asbestos Exposure
Authors: Rodríguez Portal José A. , Rodríguez Becerra Eulogio , Rodríguez Rodríguez David , Alfageme Michavila Inmaculada , Quero Martínez Aida , Diego Roza Carmen , León Jiménez Antonio , Isidro Montes Isabel , Cebollero Rivas Pilar 
Published: February 2009

Abstract
Background: Malignant pleural mesothelioma (MPM) results from malignant transformation of mesothelial cells. Past asbestos exposure represents a major risk factor for MPM and other benign pleural disease. Soluble mesothelin-related peptides (SMRP) have been regarded as a promising serum biomarker for MPM. The aim of this study was to investigate serum levels of SMRP in malignant and nonmalignant asbestos-related pleural disease.
Patients: Four groups of patients were investigated: group 1 composed of 48 healthy subjects, group 2 composed of 177 patients with previous asbestos exposure and no pleural disease, group 3 composed of 36 patients with MPM, and group 4 composed of 101 patients with previous asbestos exposure and benign pleural disease. Serum SMRP levels were determined by ELISA.
Results: Serum SMRP levels were significantly higher among group 3 than the other three groups. There were no differences in SMRP concentrations between groups 2 and 4. Subjects exposed to asbestos had higher SMRP concentrations than normal control subjects regardless of the presence of pleural disease. The area under the receiver operating characteristic curve for SMRP values was 0.75 (95% confidence interval, 0.68-0.83). The SMRP level at 0.55 nmol/L/L was determined as the most optimal cutoff value with resulting sensitivity and specificity of 72% and 72% for the diagnosis of MPM.
Conclusions: These data attest to good diagnostic sensitivity and specificity of SMRP for the diagnosis of malignant mesothelioma. We have also shown that serum SMRP levels might serve as a marker of asbestos exposure. (Cancer Epidemiol Biomarkers Prev 2009;18(2):646–50)
Telomere Length, Current Perceived Stress, and Urinary Stress Hormones in Women
Authors: Parks Christine G. , Miller Diane B. , McCanlies Erin C. , Cawthon Richard M. , Andrew Michael E. , DeRoo Lisa A. , Sandler Dale P. 
Published: February 2009

Abstract
Telomeres are repetitive DNA sequences that cap and protect the ends of chromosomes; critically short telomeres may lead to cellular senescence or carcinogenic transformation. Previous findings suggest a link between psychosocial stress, shorter telomeres, and chronic disease risk. This cross-sectional study examined relative telomere length in relation to perceived stress and urinary stress hormones in a sample of participants (n = 647) in the National Institute of Environmental Health Sciences Sister Study, a cohort of women ages 35 to 74 years who have a sister with breast cancer. Average leukocyte telomere length was determined by quantitative PCR. Current stress was assessed using the Perceived Stress Scale and creatinine-adjusted neuroendocrine hormones in first morning urines. Linear regression models estimated differences in telomere length base pairs (bp) associated with stress measures adjusted for age, race, smoking, and obesity. Women with higher perceived stress had somewhat shorter telomeres [adjusted difference of −129bp for being at or above moderate stress levels; 95% confidence interval (CI), −292 to 33], but telomere length did not decrease monotonically with higher stress levels. Shorter telomeres were independently associated with increasing age (−27bp/year), obesity, and current smoking. Significant stress-related differences in telomere length were seen in women ages 55 years and older (−289bp; 95% CI, −519 to −59), those with recent major losses (−420bp; 95% CI, −814 to −27), and those with above-average urinary catecholamines (e.g., epinephrine: −484bp; 95% CI, −709 to −259). Although current perceived stress was only modestly associated with shorter telomeres in this broad sample of women, our findings suggest the effect of stress on telomere length may vary depending on neuroendocrine responsiveness, external stressors, and age. (Cancer Epidemiol Biomarkers Prev 2009;18(2):551–60)
Nuclear Overexpression of Mitotic Regulatory Proteins in Biliary Tract Cancer: Correlation with Clinicopathologic Features and Patient Survival
Authors: Shen Ying-Chun , Hu Fu-Chang , Jeng Yung-Ming , Chang Yu-Ting , Lin Zhong-Zhe , Chang Ming-Chu , Hsu Chiun , Cheng Ann-Lii 
Published: February 2009

Abstract
Mitosis dysregulation is common in cancers. This study explored the nuclear expression patterns and prognostic significance of mitotic regulatory proteins, including Aurora kinases, survivin, and p53, in biliary tract cancer (BTC). Archival tumor samples from 161 BTC patients who underwent surgery were tested for the expression of Aurora-A, Aurora-B, survivin, and p53 by immunohistochemistry. The potential endogeneity among the clinicopathologic variables and survival outcome was assessed by a generalized simultaneous equations model. Nuclear overexpression of Aurora-A, Aurora-B, survivin, and p53 was found in 79 (49.1%), 45 (28.0%), 55 (34.2%), and 55 (34.2%) patients, respectively. Intrahepatic cholangiocarcinoma, compared with the other two subtypes, had significantly higher proportions of nuclear overexpression of Aurora-B and survivin (37.8% and 47.3%, respectively). Simultaneous overexpression of Aurora-A and Aurora-B was correlated with that of p53. Overexpression of Aurora-B was also correlated with that of survivin and tumor grade. Our data indicate that simultaneous overexpression of Aurora-A and Aurora-B, suggesting dysregulated mitosis is associated with worse survival in patients with BTC. Independent prognostic factors for poor overall survival included simultaneous overexpression of Aurora-A and Aurora-B (hazard ratio, 1.997; 95% confidence interval, 1.239-3.219; P = 0.0045) and tumor grade (hazard ratio, 2.117; 95% confidence interval, 1.339-3.348; P = 0.0013) assessed by a multivariate analysis stratified by American Joint Committee on Cancer stage and p53 overexpression. Endogeneity testing suggested that nuclear overexpression of p53 and tumor type may influence patient survival through their interactions with Aurora-A/Aurora-B expression and tumor grade. (Cancer Epidemiol Biomarkers Prev 2009;18(2):417–23)
Iron Overload Is Associated with Hepatic Oxidative Damage to DNA in Nonalcoholic Steatohepatitis
Authors: Fujita Naoki , Miyachi Hirohide , Tanaka Hideaki , Takeo Masaki , Nakagawa Naoki , Kobayashi Yoshinao , Iwasa Motoh , Watanabe Shozo , Takei Yoshiyuki 
Published: February 2009

Abstract
Several lines of evidence have suggested that oxidative stress plays an important role for the pathogenesis of nonalcoholic steatohepatitis (NASH). Therefore, by using immunohistochemical staining of liver biopsy samples, we measured hepatic 7,8-dihydro-8-oxo-2′ deoxyguanosine (8-oxodG), a DNA base-modified product generated by hydroxyl radicals, of 38 NASH patients and compared with 24 simple steatosis and 10 healthy subjects. Relation of hepatic 8-oxodG with clinical, biochemical, and histologic variables and changes after iron reduction therapy (phlebotomy plus iron–restricted diet) were also examined. Hepatic 8-oxodG levels were significantly higher in NASH compared with simple steatosis (17.5 versus 2.0 8-oxodG–positive cells/105 μm2; P &lt; 0.0001). 8-oxodG was significantly related to iron overload condition, glucose-insulin metabolic abnormality, and severities of hepatic steatosis in NASH patients. Logistic regression analysis also showed that hepatic iron deposit and insulin resistance were independent variables associated with elevated hepatic 8-oxodG. After the iron reduction therapy, hepatic 8-oxodG levels were significantly decreased (from 20.7 to 13.8 positive cells/105 μm2; P &lt; 0.01) with concomitant reductions of serum transaminase levels in NASH patients. In conclusion, iron overload may play an important role in the pathogenesis of NASH by generating oxidative DNA damage and iron reduction therapy may reduce hepatocellular carcinoma incidence in patients with NASH. (Cancer Epidemiol Biomarkers Prev 2009;18(2):424–32)
Dietary Intake of ω-6 and ω-3 Fatty Acids and Risk of Colorectal Cancer in a Prospective Cohort of U.S. Men and Women
Authors: Daniel Carrie R. , McCullough Marjorie L. , Patel Roshni C. , Jacobs Eric J. , Flanders William D. , Thun Michael J. , Calle Eugenia E. 
Published: February 2009

Abstract
Background: ω-6 and ω-3 polyunsaturated fatty acids intakes may play opposing roles in inflammation-driven colorectal carcinogenesis. We examined the relationship of these polyunsaturated fatty acids and the ratio of their intake with colorectal cancer risk in a large U.S. prospective cohort.
Design: Participants in the Cancer Prevention Study-II Nutrition Cohort completed a detailed questionnaire on diet, medical history, and lifestyle in 1999. Between 1999 and 2005, 869 incident colorectal cancer cases (452 men and 417 women) were identified among 99,080 participants (43,108 men and 55,972 women). Multivariate-adjusted rate ratios were calculated using Cox proportional hazards models.
Results: The ratio of total ω-6 to total ω-3 intake was not associated with colorectal cancer risk in either sex. Contrary to our initial hypothesis, total ω-6 intake was inversely related to colorectal cancer risk in men [multivariate relative risk (95% confidence interval) for highest to lowest quartile, 0.81 (0.61-1.07); Ptrend = 0.07], and α-linolenic acid, the primary contributor to total ω-3 intake, was associated with increased risk in women for quartiles 2 through 4 versus the lowest quartile [relative risk (95% confidence interval), 1.50 (1.12-2.01), 1.40 (1.04-1.87), and 1.38 (1.02-1.85), respectively; Ptrend = 0.13]. In women, total ω-6 and marine ω-3 intake appeared to be associated with higher and lower risk, respectively, but associations were attenuated with adjustment for other risk factors.
Conclusions: The ratio of ω-6 to ω-3 intake was not related to colorectal cancer risk in this cohort, which may be due to unexpected findings for the individual components. Differential associations by sex warrant further investigation. (Cancer Epidemiol Biomarkers Prev 2009;18(2):516–25)
Health Risk Appraisal Models for Mass Screening for Esophageal and Pharyngeal Cancer: An Endoscopic Follow-up Study of Cancer-Free Japanese Men
Authors: Yokoyama Akira , Kumagai Yoshiya , Yokoyama Tetsuji , Omori Tai , Kato Hoichi , Igaki Hiroyasu , Tsujinaka Toshimasa , Muto Manabu , Yokoyama Masako , Watanabe Hiroshi 
Published: February 2009

Abstract
Purpose: To assess the performance of our health risk appraisal (HRA) models for screening individuals at high risk of esophageal/pharyngeal squamous cell carcinoma (EPSCC).
Methods: Based on the results of our previous case-control study, we invented HRA models that enable screening for EPSCC cases in Japanese men with high sensitivity and specificity based on either their aldehyde dehydrogenase-2 genotype (HRA-G model) or alcohol flushing (HRA-F model) and drinking, smoking, and dietary habits. Follow-up endoscopy combined with esophageal iodine staining (median follow-up period: 5.0 years) was done on 404 Japanese men (50-78 years) who were registered as cancer-free controls in the previous study.
Results: The follow-up endoscopy resulted in a diagnosis of 6 esophageal SCC (Tis in 5 and T1 in 1), 1 hypopharyngeal SCC (T2), and 1 oropharyngeal SCC (T2). Seven and 6 of the 8 EPSCC cases were in the top 10% risk group at baseline according to the HRA-G and HRA-F models, respectively. The EPSCC detection rates per 100 person-years in the top 10% risk groups by the HRA-G and HRA-F models were 4.38 (95% confidence interval, 1.76-9.01) and 3.48 (95% confidence interval, 1.28-7.58), respectively. Their age-adjusted relative risk was 95.1- and 26.3-fold, respectively (P &lt; 0.0001), higher than in the bottom 90% risk groups.
Conclusions: The high detection rates for EPSCC in the top 10% risk group of this preliminary follow-up study were in good agreement with those predicted by the HRA models and thus encouraged the screening based on our HRA models in larger populations of Japanese men. (Cancer Epidemiol Biomarkers Prev 2009;18(2):651–5)
Antacid Drug Use and Risk of Esophageal and Gastric Adenocarcinomas in Los Angeles County
Authors: Duan Lei , Wu Anna H. , Sullivan-Halley Jane , Bernstein Leslie 
Published: February 2009

AbstractObjectives: Concern has been expressed that antacid drugs increase the risk of esophageal and gastric adenocarcinomas.Methods: This population-based case-control study recruited patients with incident esophageal adenocarcinoma (n = 220), gastric cardiac adenocarcinoma (n = 277), or distal gastric adenocarcinoma (n = 441) diagnosed between 1992 and 1997, and 1,356 control participants in Los Angeles County. Unconditional polychotomous multivariable logistic regression analyses were done to evaluate the association between antacid drug use and these cancers.Results: Among participants who took nonprescription acid neutralizing agents for &gt;3 years, the odds ratio for esophageal adenocarcinoma was 6.32 compared with never users (95% confidence interval, 3.14-12.69; Ptrend &lt; 0.01). Analyses stratified by history of physician diagnosed upper gastrointestinal (UGI) disorders revealed a greater increase in esophageal adenocarcinoma risk associated with nonprescription antacid use among persons with no UGI disorder than among those with an UGI disorder (homogeneity of trends P = 0.07). Regular use of nonprescription acid neutralizing agents was not associated with risk of adenocarcinomas of the gastric cardia or distal stomach. Regular use of prescription acid suppressive drugs was not associated with risk for any of these cancers.Conclusion: We found risk of esophageal adenocarcinoma was greater among long-term nonprescription acid neutralizing drugs in participants without physician-diagnosed UGI conditions than among those with these conditions; this may represent self medication for undiagnosed precursor conditions or it may be that nonprescription acid neutralizing drugs, taken without limitation on amount used when symptoms are most intense, may permit alkaline bile reflux into the lower esophagus, thereby increasing esophageal adenocarcinoma risk. (Cancer Epidemiol Biomarkers Prev 2009;18(2):526–33)