bluuebunny/crossref_metadata_2025_split huggingface dataset:
MutL-Homolog 1 Expression and Risk of Incident, Sporadic Colorectal Adenoma: Search for Prospective Biomarkers of Risk for Colorectal Cancer
Authors: Sidelnikov Eduard , Bostick Roberd M. , Flanders W. Dana , Long Qi , Cohen Vaunita L. , Dash Chiranjeev , Seabrook March E. , Fedirko Veronika 
Published: May 2009

AbstractTo characterize the expression of the mismatch repair gene MutL-homolog 1 (MLH1) in normal colorectal crypts in humans, and assess parameters of its expression as a potential biomarker of risk for colorectal neoplasms, we conducted a pilot, colonoscopy-based case-control study (51 cases, 154 controls) of incident, sporadic colorectal adenoma. Biopsies of normal-appearing rectal, sigmoid, and ascending colon mucosa were procured, immunohistochemically processed for MLH1 protein, and analyzed using custom quantitative image analysis procedures. MLH1 expression in the ascending colon was, on average, 49% proportionally lower in cases than controls (P = 0.03), but there was little evidence for case-control differences in the rectum and sigmoid colon. In cases and controls, average MLH1 expression in the ascending colon tended to be lower with increased age [by 56% (P = 0.02) and 25% (P = 0.16), respectively, for those ≥55 years], and with a history of colorectal cancer in a first-degree relative (by 22% [P = 0.56] and 34% [P = 0.16], respectively). Among cases, but not controls, average MLH1 expression tended to be higher with current alcohol consumption, regular aspirin use, and higher total intakes of calcium, vitamin D, and folate. There was little indication of similar differences in the rectum. These preliminary data suggest that lower MLH1 expression in the normal colonic mucosa, at least in the ascending colon, may be associated with increased risk of incident, sporadic colorectal adenoma, as well as with modifiable risk factors for colorectal neoplasms, thus supporting further investigation of MLH1 expression as a potential “treatable” biomarker of risk for colorectal neoplasms. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1599–609)
Racial Variation in Sex Steroid Hormones and the Insulin-Like Growth Factor Axis in Umbilical Cord Blood of Male Neonates
Authors: Rohrmann Sabine , Sutcliffe Catherine G. , Bienstock Jessica L. , Monsegue Deborah , Akereyeni Folasade , Bradwin Gary , Rifai Nader , Pollak Michael N. , Agurs-Collins Tanya , Platz Elizabeth A. 
Published: May 2009

AbstractBackground: To address whether umbilical cord blood concentrations of sex steroid hormones and the insulin-like growth factor (IGF) axis differ between African-American and White male neonates.Methods: In 2004 and 2005, venous cord blood samples were collected from 75 African-American and 38 White male full-term uncomplicated births along with birth weight, placental weight, mother's age and parity, and time of birth. Testosterone, androstanediol glucuronide, estradiol, and sex hormone binding globulin (SHBG) were measured by immunoassay, and IGF-I, IGF-2, and IGF binding protein (BP)-3 by ELISA. Crude and multivariable-adjusted geometric mean concentrations were computed.Results: Androstanediol glucuronide, estradiol, and SHBG concentrations did not differ by race; however, the molar ratio of testosterone to SHBG was higher in African-American than White male babies after adjustment (P = 0.01). Both before and after adjustment, Whites had higher concentrations of IGF-I (adjusted; White, African-American, 93.1, 71.9 ng/mL), IGF-2 (537.3-474.8 ng/mL), and IGFBP-3 (1,673-1,482 ng/mL) than African-Americans (P &lt; 0.05), although the molar ratio of IGF-I plus IGF-2 to IGFBP-3 did not differ by race.Conclusion: The higher cord blood testosterone to SHBG ratio in African-American compared with White male babies after taking into account maternal and birth factors is compatible with the hypothesis that differences in androgen levels in utero contribute to their higher prostate cancer risk, although we would have expected crude differences as well. Lower cord blood IGF-I and IGF-2 levels in African-American compared with White male babies are not consistent with the hypothesis that differences in growth factor levels contribute to their higher prostate cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1484–91)
Marijuana Smoking and the Risk of Head and Neck Cancer: Pooled Analysis in the INHANCE Consortium
Authors: Berthiller Julien , Lee Yuan-chin Amy , Boffetta Paolo , Wei Qingyi , Sturgis Erich M. , Greenland Sander , Morgenstern Hal , Zhang Zuo-Feng , Lazarus Philip , Muscat Joshua , Chen Chu , Schwartz Stephen M. , Eluf Neto José , Wünsch Filho Victor , Koifman Sergio , Curado Maria Paula , Matos Elena , Fernandez Leticia , Menezes Ana , Daudt Alexander W. , Ferro Gilles , Brennan Paul , Hashibe Mia 
Published: May 2009

Abstract
Background: Marijuana contains carcinogens similar to tobacco smoke and has been suggested by relatively small studies to increase the risk of head and neck cancer (HNC). Because tobacco is a major risk factor for HNC, large studies with substantial numbers of never tobacco users could help to clarify whether marijuana smoking is independently associated with HNC risk.
Methods: We pooled self-reported interview data on marijuana smoking and known HNC risk factors on 4,029 HNC cases and 5,015 controls from five case-control studies within the INHANCE Consortium. Subanalyses were conducted among never tobacco users (493 cases and 1,813 controls) and among individuals who did not consume alcohol or smoke tobacco (237 cases and 887 controls).
Results: The risk of HNC was not elevated by ever marijuana smoking [odds ratio (OR), 0.88; 95% confidence intervals (95% CI), 0.67-1.16], and there was no increasing risk associated with increasing frequency, duration, or cumulative consumption of marijuana smoking. An increased risk of HNC associated with marijuana use was not detected among never tobacco users (OR, 0.93; 95% CI, 0.63-1.37; three studies) nor among individuals who did not drink alcohol and smoke tobacco (OR, 1.06; 95% CI, 0.47-2.38; two studies).
Conclusion: Our results are consistent with the notion that infrequent marijuana smoking does not confer a risk of these malignancies. Nonetheless, because the prevalence of frequent marijuana smoking was low in most of the contributing studies, we could not rule out a moderately increased risk, particularly among subgroups without exposure to tobacco and alcohol. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1544–51)
Genetic Variation in the SST Gene and its Receptors in Relation to Circulating Levels of Insulin-Like Growth Factor-I, IGFBP3, and Prostate Cancer Risk
Authors: Johansson Mattias , McKay James D. , Wiklund Fredrik , Rinaldi Sabina , Hallmans Göran , Bälter Katarina , Adami Hans-Olov , Grönberg Henrik , Stattin Pär , Kaaks Rudolf 
Published: May 2009

Abstract
Background: Somatostatin (SST) and its receptors (SSTR1-5) may have a role in prostate cancer by influencing the IGFI hormone axis or through direct effects on prostate epithelia. We have investigated if genetic variation in the SST and SSTR1-5 genes influences prostate cancer risk and/or circulating IGFI and IGFBP3 hormone levels.
Materials and Methods: We analyzed 28 haplotype tagging single nucleotide polymorphisms in the SST and SSTR1-5 genes in a case-control/genetic association study to investigate the association between genetic variation and prostate cancer risk. The study included 2863 cases and 1737 controls from the Cancer Prostate in Sweden (CAPS) study. To investigate the genetic influence on circulating hormone levels, plasma concentrations of IGFI and IGFBP3 were analyzed in 874 controls of the CAPS study and 550 male subjects from the Northern Sweden Health and Disease Cohort (NSHDC).
Results: No clear association between prostate cancer risk and genetic variation of the SST and SSTR1-5 genes was identified. The SSTR5 missense single nucleotide polymorphism rs4988483 was associated with circulating IGFI (P = 0.002) and IGFBP3 (P = 0.0003) hormone levels in CAPS controls, with a per allele decrease of ∼11%. This decrease was replicated in NSHDC for circulating IGFBP3 (P = 0.01) but not for IGFI (P = 0.09). Combining CAPS and NSHDC subjects indicated evidence of association between rs4988483 and both IGFBP3 (P = 2 × 10−5) and IGFI (P = 0.0004) hormone levels.
Conclusions: Our results suggest that genetic variation in the SSTR5 gene and, particularly, the rs4988483 single nucleotide polymorphism influence circulating IGFI and IGFBP3 hormone levels with no measurable effect on prostate cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1644–50)
Serum Folate and Cancer Mortality Among U.S. Adults: Findings from the Third National Health and Nutritional Examination Survey Linked Mortality File
Authors: Yang Quanhe , Bostick Roberd M. , Friedman J.M. , Flanders W. Dana 
Published: May 2009

Abstract
Background: The relation between folate status and cancer is controversial. Several epidemiologic studies have suggested that increased folate intake is associated with reduced risk of various cancers, others have found no such associations, and a few have suggested that high folate intake might increase the risk of certain cancers.
Methods: Using data from the Third National Health and Nutrition Examination Survey (NHANES III) Mortality File, a prospective cohort study of a nationally representative sample of 14,611 U.S. adults, we conducted Cox proportional hazards regression modeling to investigate the association of baseline serum folate concentrations and all-cancer mortality determined from linked death certificate data.
Results: Relative to the lowest quintile of serum folate (&lt;3.0 ng/mL), the multivariable-adjusted hazard ratios across quintiles 2 to 5 were: 1.61 [95% confidence interval (95% CI), 1.11-2.32], 1.00 (95% CI, 0.65-1.49), 1.39 (95% CI, 0.96-2.03), and 0.85 (95% CI, 0.59-1.22). These findings did not differ substantially by age or sex, but the higher risk for those in the second quintile appeared limited to non-Hispanic whites.
Conclusion: These findings suggest that there may be a nonlinear relationship between folate status and the risk of all-cancer mortality such that persons with low, but not grossly deficient, serum blood folate concentrations may be at increased risk. Further study is needed to determine whether these findings are due to chance, and if not, to clarify their biological basis. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1439–47)
Risk of Endometrial Cancer in Relation to Medical Conditions and Medication Use
Authors: Fortuny Joan , Sima Camelia , Bayuga Sharon , Wilcox Homer , Pulick Katherine , Faulkner Shameka , Zauber Ann G. , Olson Sara H. 
Published: May 2009

AbstractWe studied the relation of medical conditions related to obesity and medications used for these conditions with endometrial cancer. We also investigated the association of other medical conditions and medications with risk. This U.S. population-based case-control study included 469 endometrial cancer cases and 467 controls. Information on putative risk factors for endometrial cancer was collected through personal interviews. We asked women about their medical history and medications used for six months or longer and the number of years each medication was taken. Risk was strongly associated with increasing obesity (P for trend &lt; 0.001). Among the conditions related to obesity, and after adjustment for age, body mass index, and other risk factors and conditions, uterine fibroids were independently related to an increased cancer risk [adjusted odds ratio (OR), 1.8; 95% confidence interval (95% CI), 1.2-2.5]. Although hypertension was not significantly related to endometrial cancer after adjustment for age and body mass index, the use of thiazide diuretics was independently associated with increased risk (OR, 1.8; 95% CI, 1.1-3.0). Anemia was associated with decreased risk (OR, 0.6; 95% CI, 0.5-0.9). Use of nonsteroidal anti-inflammatory drugs was related to a decreased risk (OR, 0.7; 95% CI, 0.5-0.97). To our knowledge, the observation about thiazide diuretics is novel and requires confirmation in other studies and populations. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1448–56)
Screening for Gastric Cancer in Korea: Population-Based Preferences for Endoscopy versus Upper Gastrointestinal Series
Authors: Choi Kui Son , Kwak Min-Son , Lee Hoo-yeon , Jun Jae Kwan , Hahm Myung-Il , Park Eun-Cheol 
Published: May 2009

Abstract
This study assessed the screening rates for gastric cancer by two different screening methods, upper gastrointestinal (UGI) series and endoscopy; intentions to undergo future gastric cancer screening; and the preferred method of screening. The study population was derived from the 2006 Korean National Cancer Screening Survey. The Korean National Cancer Screening Survey is an annual cross-sectional survey that uses nationally representative random sampling to investigate cancer screening rates. A total of 1,625 Koreans over 40 years of age participated in this study. Logistic regression was used to identify the factors associated with undergoing gastric cancer screening, having an intention to be screened, and preferring one of the two screening tests. Among the 1,625 subjects, 15.1% had received a UGI, 33.2% had received an endoscopy, and 43.1% had undergone either or both of the tests in the previous 2 years. About 52% of people reported the intention to be screened within the next 2 years. The odds ratio for intending to be screened was 11.8 and 6.2 higher among those who had undergone a prior UGI test and an endoscopy test within the previous 2 years, respectively, than for those who had never been screened. Among the 1,625 individuals, 67% chose endoscopy and 33% UGI for their preferred future screening method. Collectively, our results highlight the preference for endoscopy testing as a gastric cancer screening method. Providers' assessments of individuals' screening preferences in combination with intervention strategies to promote performance of the preferred test may increase patient compliance with gastric cancer screening recommendations. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1390–8)
A Decreased Ratio of Laminin-332 β3 to γ2 Subunit mRNA is Associated with Poor Prognosis in Colon Cancer
Authors: Guess Cherise M. , LaFleur Bonnie J. , Weidow Brandy L. , Quaranta Vito 
Published: May 2009

Abstract
Laminin-332 (Ln-332) is a heterotrimeric glycoprotein (α3β3γ2) unique to epithelial cells with crucial roles in signaling, adhesion, and migration. Altered localization or expression levels of Ln-332, particularly its γ2 subunit, are of prognostic value in a variety of cancers. However, the lack of standardized methodology and the limited quantification of previous study results have left unanswered questions, including the role of γ2 transcript variants and whether differential expression of this chain represents dysregulation of the whole heterotrimer. Herein, we test the hypothesis that mRNA changes in one or more Ln-332 encoding genes can be used to distinguish between early- and advanced-stage cancer specimens and shed light on mechanistic questions raised by previous studies. Statistical analyses of human microarray data from the publicly available expression project in Oncology (expO) dataset, including examination of the distributions of Ln-332 subunit mRNA levels, identified a significant decrease in the Ln-332 β3:γ2 mRNA ratio between normal (n = 10) and early-stage colon cancer (n = 29) specimens. The β3:γ2 ratio was further decreased in metastatic colon cancer (n = 41) compared with early-stage samples. Our findings raise the possibility that Ln-332 γ2 may be a therapeutic target against metastatic colon cancer because a lowered β3:γ2 ratio would reduce expression of heterotrimeric Ln-332 and increase monomeric γ2 secretion. Further, standardized, quantitative methods for patient prognosis and therapeutic choice could be developed based upon the Ln-332 mRNA changes we uncovered. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1584–90)
Common Variation in Genes Related to Innate Immunity and Risk of Adult Glioma
Authors: Rajaraman Preetha , Brenner Alina V. , Butler Mary Ann , Wang Sophia S. , Pfeiffer Ruth M. , Ruder Avima M. , Linet Martha S. , Yeager Meredith , Wang Zhaoming , Orr Nick , Fine Howard A. , Kwon Deukwoo , Thomas Gilles , Rothman Nathaniel , Inskip Peter D. , Chanock Stephen J. 
Published: May 2009

Abstract
Current evidence suggests that immune system alterations contribute to the etiology of adult glioma, the most common adult brain tumor. Although previous studies have focused on variation in candidate genes in the adaptive immune system, the innate immune system has emerged as a critical avenue for research given its known link with carcinogenesis. To identify genetic markers in pathways critical to innate immunity, we conducted an association study of 551 glioma cases and 865 matched controls of European ancestry to investigate “tag” single nucleotide polymorphisms (SNP) in 148 genetic regions. Two independent U.S. case-control studies included were as follows: a hospital-based study conducted by the National Cancer Institute (263 cases, 330 controls) and a community-based study conducted by the National Institute for Occupational Safety and Health (288 cases, 535 controls). Tag SNPs (1,397) chosen on the basis of an r2 of &gt;0.8 and minor allele frequency of &gt;5% in Caucasians in HapMap1 were genotyped. Glioma risk was estimated by odds ratios. Nine SNPs distributed across eight genetic regions (ALOX5, IRAK3, ITGB2, NCF2, NFKB1, SELP, SOD1, and STAT1) were associated with risk of glioma with P value of &lt;0.01. Although these associations were no longer statistically significant after controlling for multiple comparisons, the associations were notably consistent in both studies. Region-based tests were statistically significant (P &lt; 0.05) for SELP, SOD, and ALOX5. Analyses restricted to glioblastoma (n = 254) yielded significant associations for the SELP, DEFB126/127, SERPINI1, and LY96 genetic regions. We have identified a promising set of innate immunity-related genetic regions for further investigation. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1651–8)
Physical Activity and Health Outcomes Three Months After Completing a Physical Activity Behavior Change Intervention: Persistent and Delayed Effects
Authors: Rogers Laura Q. , Hopkins-Price Patricia , Vicari Sandy , Markwell Stephen , Pamenter Richard , Courneya Kerry S. , Hoelzer Karen , Naritoku Catherine , Edson Billie , Jones Linda , Dunnington Gary , Verhulst Steven 
Published: May 2009

Abstract
Purpose: We previously reported the effectiveness of a 12-week physical activity behavior change intervention for breast cancer survivors postintervention with this report, aiming to determine delayed and/or persistent effects 3 months after intervention completion.
Methods: Forty-one sedentary women with stage I, II, or IIIA breast cancer currently receiving hormonal therapy were randomly assigned to receive the 12-week Better Exercise Adherence after Treatment for Cancer intervention or usual care. Assessments occurred at baseline, postintervention, and 3 months postintervention.
Results: Weekly minutes of greater than or equal to moderate intensity physical activity measured by accelerometer showed a significant group by time interaction (F = 3.51; P = 0.035; between group difference in the mean change from baseline to 3 months postintervention, 100.1 minute, P = 0.012). Significant group by time interactions also showed sustained improvements from baseline to 3 months postintervention in strength (F = 3.82; P = 0.027; between group difference, 11.2 kg; P = 0.026), waist-to-hip ratio (F = 3.36; P = 0.041; between group difference, −0.04; P = 0.094), and social well-being (F = 4.22; P = 0.023; between group difference, 3.9; P = 0.039). A delayed reduction in lower extremity dysfunction 3 months postintervention was noted (F = 3.24; P = 0.045; between group difference in the mean change from postintervention to 3 months follow-up; P = −7.6; P = 0.015). No group by time effect was noted for fitness, body mass index, percent fat, bone density, total quality of life (Functional Assessment of Cancer Therapy-General), fatigue, endocrine symptoms, cognitive function, or sleep.
Conclusions: The intervention resulted in sustained improvements in physical activity, strength, central adiposity, and social well-being with lower extremity function benefits appearing 3 months after intervention completion. Testing translation in a multisite study is warranted. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1410–8)
No Effect of Aspirin on Mammographic Density in a Randomized Controlled Clinical Trial
Authors: McTiernan Anne , Wang C.Y. , Sorensen Bess , Xiao Liren , Buist Diana S.M. , Aiello Bowles Erin J. , White Emily , Rossing Mary Anne , Potter John , Urban Nicole 
Published: May 2009

AbstractBackground: Epidemiologic studies suggest a reduced risk of breast cancer among women who regularly use aspirin; a plausible mechanism is through aspirin effect on mammographic breast density, a breast cancer risk factor, possibly mediated through aspirin interference with estrogen synthesis.Methods: In a 2-arm randomized placebo-controlled clinical trial, we evaluated the effects of 6-month administration of 325 mg/day aspirin on total mammographic breast dense area and percent of the mammographic breast image occupied by dense areas (% density) in 143 postmenopausal women. Eligible women, recruited from 2005 to 2007, were healthy, not taking hormone therapy, with elevated mammographic breast density (American College of Radiology Breast Imaging Reporting and Data System density category 2, 3, or 4) within 6 months before enrollment.Results: Women were a mean (SD) 59.5 (5.5) years. Geometric mean baseline percent density was 17.6% (95% confidence interval, 14.8-20.9) in women randomized to aspirin and 19.2% (95% confidence interval, 16.3-22.7) in women randomized to placebo. Percent density decreased in women randomized to aspirin by an absolute 0.8% versus an absolute decrease of 1.2% in controls (P = 0.84). Total breast area and dense area decreased to a similar degree in women assigned to aspirin and in those assigned to placebo, with no statistically significant differences between trial arms.Conclusions: A single daily administration of adult-dose aspirin for 6 months had no effect on mammographic density in postmenopausal women. If aspirin affects breast cancer risk in postmenopausal women, it may do so through alternative pathways than mammographic breast density. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1524–30)