bluuebunny/crossref_metadata_2025_split huggingface dataset:
Subduction in the Western Makran: the historian's contribution
Authors: Musson R.M.W. 
Published: May 2009

Abstract:
The Makran subduction zone, which runs along the southeastern coast of Iran and the southern coast of Pakistan, is a major control on the seismic hazard of the region. Whereas the eastern part of this zone has been active in recent historical times, the western part has not. This could indicate a zone currently locked, or it could be that subduction is occurring aseismically or not at all. Evidence for large thrust activity rests on one event, apparently very large, in 1483. Historical research, especially taking into consideration the political situation in the region at the end of the 15th century, suggests that this 1483 event was a moderate magnitude earthquake in the vicinity of Qeshm Island that has been misassociated with a second, later, earthquake. This interpretation removes from the earthquake catalogue any evidence for major earthquake activity along the Western Makran, and adds weight to the tectonic interpretation that major seismicity has a westerly termination at the Sonne Fault. This presents an interesting example of how a piece of obscure historical information has a significant effect on resolving a question of tectonic interpretation, and with it, influences the estimation of regional seismic hazard, including tsumani hazard in the Indian Ocean.
Risk Factors for Pituitary Tumors: A Case-control Study
Authors: Schoemaker Minouk J. , Swerdlow Anthony J. 
Published: May 2009

AbstractPituitary gland tumors are usually benign but are associated with substantial morbidity. Their etiology is largely unknown. We conducted a population-based case-control study of potential risk factors for pituitary tumors in Southeast England. Information on medical and reproductive history, female sex hormones, and cigarette smoking was collected by personal interview from 299 cases and 630 controls aged 18 to 59 years. Tumor risk was reduced in subjects reporting a past diagnosis of hay fever [odds ratio (OR), 0.7; 95% confidence interval (CI), 0.5-1.0] but not asthma or eczema. Risk was raised in women who were postmenopausal 1 year before diagnosis (OR, 3.2; 95% CI, 1.6-6.2), especially if menopause was surgically induced (OR, 6.7; 95% CI, 2.2-19.9) or occurred under age 40 years (OR, 7.5; 95% CI, 2.6-21.4). This effect remained when evaluating menopausal status 10 years before diagnosis. There was no association with parity overall, but risk was increased for first childbirth under age 20 years compared with nulliparity (OR, 3.4; 95% CI, 1.4-8.4). No significant association was observed with ever use of oral contraceptives or hormone replacement therapy, nor with cigarette smoking, past head injury, past diagnosis with epilepsy, or birth characteristics, except for an inverse association of risk with maternal age. This study suggests a raised risk of pituitary tumors in relation to surgically induced menopause, early postmenopausal age, and young age at childbirth, and possibly a reduced risk with hay fever and increasing maternal age. Reasons for these associations need further investigation, but some associations might be due to hormonal effects of an undiagnosed pituitary tumor. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1492–500)
Association of Diabetes and Body Mass Index with Levels of Prostate-Specific Antigen: Implications for Correction of Prostate-Specific Antigen Cutoff Values?
Authors: Müller Heiko , Raum Elke , Rothenbacher Dietrich , Stegmaier Christa , Brenner Hermann 
Published: May 2009

Abstract
Background: In a recent study, an inverse association between diabetes and prostate-specific antigen (PSA) levels was observed, and several studies reported lower PSA levels in groups with higher body mass index. However, all of the studies were conducted in populations with intensive PSA screening and the role of diabetes severity, duration, and therapy are yet to be explored.
Methods: Associations of diabetes duration and treatment, hemoglobin A1c, and BMI with PSA levels were assessed among 778 men ages 50 to 74 years, randomly chosen from the 2000 to 2002 baseline recruitment of a large population-based cohort study in Germany (prevalence of diabetes, 17%), using linear regression analyses.
Results: PSA values were significantly reduced in men with insulin treatment (−39%; P = 0.006) and oral diabetic medication (−24%; P = 0.030), and in men with elevated (6.1-6.9%) and highly (≥7%) elevated hemoglobin A1c values (−15%, P = 0.004 and −29%, P = 0.003, respectively). PSA reduction was not associated with duration of diabetes. Obesity was possibly associated with a reduction of PSA levels (−14%; P = 0.096).
Conclusions: Our study suggests that more severe forms of diabetes are associated with lower PSA levels and confirms the magnitude of reduction in PSA levels in diabetic men overall. The observed PSA reduction parallels reported risk reduction of prostate cancer among diabetic men. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1350–6)
Common Genetic Variation in TP53 and Risk of Human Papillomavirus Persistence and Progression to CIN3/Cancer Revisited
Authors: Koshiol Jill , Hildesheim Allan , Gonzalez Paula , Bratti M. Concepcion , Porras Carolina , Schiffman Mark , Herrero Rolando , Rodriguez Ana C. , Wacholder Sholom , Yeager Meredith , Chanock Stephen J. , Burk Robert D. , Wang Sophia S. 
Published: May 2009

Abstract
Driven by findings that human papillomavirus (HPV)-induced degradation of p53 differs by a TP53 polymorphism at codon 72 (Pro72Arg), past studies of TP53 genetic variants and cervical cancer have focused on this nonsynonymous polymorphism, with mixed results. We analyzed common single nucleotide polymorphisms (SNP) across the TP53 locus in a population-based nested case-control study in Guanacaste, Costa Rica. We evaluated 11 SNPs, including Pro72Arg (rs1042522), among 1,281 women: 465 with cervical intraepithelial neoplasia grade 3/cancer (CIN3+), 380 with HPV persistence (median, 25 months), and 436 random population controls. We combined HPV persistence and CIN3+ into one case group because they did not differ in TP53 genotypic frequencies and calculated odds ratios and 95% confidence intervals (CI) for individual SNPs and inferred haplotypes. We observed that proline at codon 72 was associated with increased risk of CIN3+/persistence compared with population controls. Relative to GG (Arg), the CG (Pro/Arg) and CC (Pro) genotypes had a 1.3-fold (95% CI, 0.99-1.6) and 1.8-fold (95% CI, 1.2-2.7) increased risk, respectively (Ptrend &lt; 0.01). rs12951053 and rs1642785 were also associated with CIN3+/persistence (P trend, 0.05 and 0.04, respectively), as was a haplotype containing the codon 72 variant (rs1042522), rs12951053, rs1642785, and rs12947788 (odds ratio, 1.6; 95% CI, 1.1-2.3 versus the most common haplotype, which comprised the major alleles for all 11 SNPs). Although genetic variation in TP53 might affect the natural history of HPV and cervical cancer, further work is needed to elucidate the possible mechanism. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1631–7)
Genetic Polymorphisms in the Catechol Estrogen Metabolism Pathway and Breast Cancer Risk
Authors: Reding Kerryn W. , Weiss Noel S. , Chen Chu , Li Christopher I. , Carlson Christopher S. , Wilkerson Hui-Wen , Farin Federico M. , Thummel Kenneth E. , Daling Janet R. , Malone Kathleen E. 
Published: May 2009

AbstractBackground: This study investigated whether single nucleotide polymorphisms (SNP) in genes within the catechol estrogen metabolism pathway altered the risk of breast cancer alone or in combination, as well as whether menopausal hormone therapy modified the effect of these SNPs on breast cancer risk.Methods: In a population-based case-control study of breast cancer, 891 cases and 878 controls were genotyped for six functional SNPs in the COMT, CYP1B1, GSTM1, GSTP1, and GSTT1 genes.Results: Women homozygous with the T allele in CYP1B1*2 (Ser119; rs1056827) were at 1.69 (95% confidence interval, 1.17-2.46) times the risk of women homozygous with the G allele; women homozygous with the G allele in GSTP1 (Val105; rs1695) were at 0.73 (95% confidence interval, 0.54-0.99) times the risk of breast cancer compared with women homozygous with the A allele. No other SNPs tested were associated with breast cancer to any appreciable degree. Potential gene-gene and gene-hormone therapy interactions were investigated.Conclusion: With the exception of GSTP1 and possibly CYP1B1*2, our findings do not provide support for the role of genetic variation in the catechol estrogen metabolism pathway and breast cancer risk in postmenopausal women. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1461–7)
Higher Prevalence of Secretory CSE1L/CAS in Sera of Patients with Metastatic Cancer
Authors: Tung Min-Che , Tsai Chin-Shaw Stella , Tung Jai-Nien , Tsao Tang-Yi , Chen Hung-Chang , Yeh Kun-Tu , Liao Ching-Fong , Jiang Ming-Chung 
Published: May 2009

Abstract
Metastatic markers are highly useful diagnostic and prognostic indicators of cancer metastasis. Herein, we report that secretory CSE1L/CAS, a cellular apoptosis susceptibility protein, is a new marker for metastatic cancer. CAS was colocalized with matrix metalloproteinase-2 in vesicles surrounding the outside of MCF-7 cell membranes, and the COOH-terminal domain of CAS was associated with matrix metalloproteinase-2-containing vesicles. Immunohistochemical staining for CAS was positive in the stroma and gland lumens of human metastatic cancer tissues. CAS was also detected in conditioned medium from B16-F10 melanoma cells and more frequently in the sera of patients with metastatic cancer than in sera from patients with primary cancer. Specifically, the prevalence of serum CAS in serum samples from 146 patients was 58.2% (32 of 55), 32.0% (8 of 25), and 12.1% (8 of 66) for patients with metastatic, invasive, and primary cancers, respectively. Our results suggest that CAS is a secretory protein associated with cancer metastasis, which may have clinical utility in metastatic cancer screening and diagnosis. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1570–7)
Reproductive and Hormonal Risk Factors for Ductal Carcinoma In situ of the Breast
Authors: Phillips Lynette S. , Millikan Robert C. , Schroeder Jane C. , Barnholtz-Sloan Jill S. , Levine Beverly J. 
Published: May 2009

Abstract
One-fifth of all newly diagnosed breast cancer cases are ductal carcinoma in situ (DCIS), but little is known about DCIS risk factors. Recent studies suggest that some subtypes of DCIS (high grade or comedo) share histopathologic and epidemiologic characteristics with invasive disease, whereas others (medium or low grade or non-comedo) show different patterns. To investigate whether reproductive and hormonal risk factors differ among comedo and non-comedo types of DCIS and invasive breast cancer (IBC), we used a population-based case-control study of 1,808 invasive and 446 DCIS breast cancer cases and their age and race frequency-matched controls (1,564 invasive and 458 DCIS). Three or more full-term pregnancies showed a strong inverse association with comedo-type DCIS [odds ratio (OR), 0.53; 95% confidence interval (95% CI), 0.30-0.95] and a weaker inverse association for non-comedo DCIS (OR, 0.73; 95% CI, 0.42-1.27). Several risk factors (age at first full-term pregnancy, breast-feeding, and age at menopause) showed similar associations for comedo-type DCIS and IBC but different associations for non-comedo DCIS. Ten or more years of oral contraceptive showed a positive association with comedo-type DCIS (OR, 1.31; 95% CI, 0.70-2.47) and IBC (OR, 2.33; 95% CI, 1.06-5.09) but an inverse association for non-comedo DCIS (OR, 0.51; 95% CI, 0.25-1.04). Our results support the theory that comedo-type DCIS may share hormonal and reproductive risk factors with IBC, whereas the etiology of non-comedo DCIS deserves further investigation. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1507–14)
Influence of Ovarian Cancer Risk Status on the Diagnostic Performance of the Serum Biomarkers Mesothelin, HE4, and CA125
Authors: Shah Chirag A. , Lowe Kimberly A. , Paley Pamela , Wallace Erin , Anderson Garnet L. , McIntosh Martin W. , Andersen M. Robyn , Scholler Nathalie , Bergan Lindsay A. , Thorpe Jason D. , Urban Nicole , Drescher Charles W. 
Published: May 2009

Abstract
Objective: To evaluate the effect of ovarian cancer risk on the performance of the serum biomarkers mesothelin, human epididymis protein 4 (HE4), and CA125.
Methods: We measured mesothelin, HE4, and CA125 levels from women with invasive ovarian cancer (n = 143), benign gynecologic conditions (n = 124), and controls (n = 344). Demographic, epidemiologic, reproductive, medical, and family history data were collected using a standardized questionnaire. Pedigree and BRCA 1/2 test results were used to stratify women into average and high-risk groups. The diagnostic accuracy of each biomarker was characterized using receiver operating characteristic curve methods.
Results: Baseline characteristics did not vary by risk or case status. The distribution of stage and histology was similar in average and high-risk women. All three markers discriminated ovarian cancer cases from risk-matched healthy and benign controls. Marker performance did not vary by risk status. The sensitivity at 95% specificity for discriminating cases from risk-matched healthy control women in the average and high-risk groups, respectively, was 53.9% and 39.0% for mesothelin, 80.4% and 87.8% for HE4, and 79.4% and 82.9% for CA125. The performance of the markers was not as robust when cases were compared with benign controls. Area under the curve values for cases versus healthy and benign controls did not vary by risk status.
Conclusions: The ability of serum mesothelin, HE4, and CA 125 levels to discriminate ovarian cancer cases from healthy and benign controls is not influenced by risk status. Our findings support the pursuit of additional studies evaluating the early detection potential of these markers in high-risk populations. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1365–72)
Muscular Strength and Adiposity as Predictors of Adulthood Cancer Mortality in Men
Authors: Ruiz Jonatan R. , Sui Xuemei , Lobelo Felipe , Lee Duck-chul , Morrow James R. , Jackson Allen W. , Hébert James R. , Matthews Charles E. , Sjöström Michael , Blair Steven N. 
Published: May 2009

Abstract
Background: We examined the associations between muscular strength, markers of overall and central adiposity, and cancer mortality in men.
Methods: A prospective cohort study including 8,677 men ages 20 to 82 years followed from 1980 to 2003. Participants were enrolled in The Aerobics Centre Longitudinal Study, the Cooper Institute in Dallas, Texas. Muscular strength was quantified by combining 1-repetition maximal measures for leg and bench presses. Adiposity was assessed by body mass index (BMI), percent body fat, and waist circumference.
Results: Cancer death rates per 10,000 person-years adjusted for age and examination year were 17.5, 11.0, and 10.3 across incremental thirds of muscular strength (P = 0.001); 10.9, 13.4, and 20.1 across BMI groups of 18.5-24.9, 25.0-29.9, and ≥30 kg/m2, respectively (P = 0.008); 11.6 and 17.5 for normal (&lt;25%) and high percent body fat (≥25%), respectively (P = 0.006); and 12.2 and 16.7 for normal (≤102 cm) and high waist circumference (&gt;102 cm), respectively (P = 0.06). After adjusting for additional potential confounders, hazard ratios (95% confidence intervals) were 1.00 (reference), 0.65 (0.47-0.90), and 0.61 (0.44-0.85) across incremental thirds of muscular strength, respectively (P = 0.003 for linear trend). Further adjustment for BMI, percent body fat, waist circumference, or cardiorespiratory fitness had little effect on the association. The associations of BMI, percent body fat, or waist circumference with cancer mortality did not persist after further adjusting for muscular strength (all P ≥ 0.1).
Conclusions: Higher levels of muscular strength are associated with lower cancer mortality risk in men, independent of clinically established measures of overall and central adiposity, and other potential confounders. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1468–76)
Prospective Study of JC Virus Seroreactivity and the Development of Colorectal Cancers and Adenomas
Authors: Rollison Dana E. , Helzlsouer Kathy J. , Lee Ji-Hyun , Fulp William , Clipp Sandra , Hoffman-Bolton Judy A. , Giuliano Anna R. , Platz Elizabeth A. , Viscidi Raphael P. 
Published: May 2009

AbstractBackground: Infection with JC virus has been proposed as a risk factor for colorectal cancer. A nested case-control study was conducted to evaluate the association between prediagnostic JC virus antibodies and the risk of incident colorectal cancer and adenomas.Methods: Two research serum banks were established in Washington County, MD in 1974 and 1989, with the collection of blood samples from &gt;45,000 volunteers. Incident colorectal cancer cases diagnosed through 2006 (n = 611) were identified among participants by linkage to population-based cancer registries, contributing 729 pairs of observations. Cases of adenomatous polyps (n = 123) were identified from participants of the 1989 cohort who reported having a colonoscopy-detected adenoma at follow-up through 2000 with histology confirmed through medical record review. One control was matched to each case on age, sex, race, and date of blood draw, and, for adenoma controls, date of endoscopy. IgG antibodies to JC virus were measured using virus-like particle ELISA. Associations between JC virus seropositivity and colorectal cancer and adenomas were estimated using conditional logistic regression.Results: Overall, there was no association between antibodies to JC virus and colorectal cancer [odds ratio (OR), 0.91; 95% confidence interval (95% CI), 0.71-1.17]. However, a statistically significant positive association between JC virus seropositivity and subsequent adenoma diagnosis was observed among males (OR, 2.31; 95% CI, 1.20-4.46), whereas a statistically significant inverse association was observed among females (OR, 0.31; 95% CI, 0.14-0.67; P for interaction = 0.01), after adjustment for baseline smoking and body mass index.Conclusions: Overall, JC virus seropositivity was not associated with colorectal cancer development up to 31 years later. Future studies are needed to confirm the adenoma findings. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1515–23)
Dietary Acrylamide Intake and Brain Cancer Risk
Authors: Hogervorst Janneke G.F. , Schouten Leo J. , Konings Erik J.M. , Goldbohm R. Alexandra , van den Brandt Piet A. 
Published: May 2009

Abstract
Background: Acrylamide is a probable human carcinogen, which is present in several heat-treated foods. In epidemiologic studies, positive associations with endometrial, ovarian, and renal cell cancer risk have been observed. The incidence of central nervous system tumors was increased upon acrylamide administration in drinking water to rats. In the current study, the association between dietary acrylamide intake and human brain cancer risk was investigated for the first time.
Methods: In 1986, 120,852 persons (ages 55-69 years) were included in the Netherlands Cohort Study on diet and cancer. At baseline, a random subcohort of 5,000 participants was randomly selected from the total cohort for a case-cohort approach. Acrylamide intake was assessed with a food frequency questionnaire at baseline and based on acrylamide analyses in relevant Dutch foods. Hazard ratios (HR) were calculated using Cox proportional hazards analysis. Subgroup analyses were done for microscopically verified brain cancer, astrocytic gliomas, high-grade astrocytic gliomas, and never-smokers. The acrylamide risk estimates were adjusted for possible brain cancer risk factors.
Results: After 16.3 years of follow-up, 216 brain cancer cases were available for analysis. The multivariable-adjusted HR per 10 μg/d increment of acrylamide intake was 1.02 (95% confidence interval, 0.89-1.16). HRs were not significantly increased either when dietary acrylamide intake was analyzed as a categorical variable. Also, there was no association in the subgroups based on histology and smoking.
Conclusion: In this prospective cohort study, acrylamide intake was not associated with brain cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1663–6)
Reproductive History and Pancreatic Cancer Incidence and Mortality in a Cohort of Postmenopausal Women
Authors: Stevens Richard J. , Roddam Andrew W. , Green Jane , Pirie Kirstin , Bull Diana , Reeves Gillian K. , Beral Valerie ,   on behalf of the Million Women Study Collaborators
Published: May 2009

Abstract
There is inconsistent evidence about the effect of reproductive history on women's risk of pancreatic cancer. In the Million Women Study, a prospective cohort of middle-aged women in the United Kingdom, we examined associations between reproductive history and pancreatic cancer incidence and mortality, controlling for age, socioeconomic status, geographic region, body mass index, smoking, and history of diabetes. During 7.1 million person-years of follow-up in 995,192 postmenopausal women, there were 1,182 incident pancreatic cancers. Pancreatic cancer incidence and mortality did not vary significantly with age at menarche, number of children, age at first birth, breast-feeding, type of menopause, age at menopause, or time since menopause. Any effect of reproductive history and pancreatic cancer risk in women is likely to be weak, if it exists at all. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1457–60)
Established Prostate Cancer Susceptibility Variants are not Associated with Disease Outcome
Authors: Wiklund Fredrik E. , Adami Hans-Olov , Zheng Sigun L. , Stattin Pär , Isaacs William B. , Grönberg Henrik , Xu Jianfeng 
Published: May 2009

Abstract
Recent genome-wide association studies have been successful in identifying common sequence variants associated with prostate cancer risk; however, their importance in prostate cancer prognosis remains unknown. To assess confirmed prostate cancer susceptibility variants with prostate cancer prognosis, we genotyped 16 established susceptibility variants in a Swedish cohort of 2,875 prostate cancer cases, ascertained between 2001 and 2003, with complete follow-up regarding vital status through January 2008. Cox regression models, adjusted for age, clinical stage, pathologic grade, nodal or distant metastases, and diagnostic serum levels of prostate-specific antigen level, were used to assess association between risk variants and prostate cancer–specific survival. During follow-up, 626 men died, and of those, 440 had prostate cancer classified as their underlying cause of death. We found no association between any of the explored sequence variants and prostate cancer–specific mortality, either in exploring individual variants or in assessing the cumulative effect of all variants. We conclude that hitherto established prostate cancer susceptibility variants are not associated with the lethal potential of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1659–62)