bluuebunny/crossref_metadata_2025_split huggingface dataset:
Systematic Error in Gas Chromatography-Mass Spectrometry–Based Quantification of Hydrolyzed Urinary Steroids
Authors: Moon Ju-Yeon , Ha Young Wan , Moon Myeong Hee , Chung Bong Chul , Choi Man Ho 
Published: February 2010

Abstract
Gas chromatography-mass spectrometry–based metabolite profiling can lead to an understanding of various disease mechanisms as well as to identifying new diagnostic biomarkers by comparing the metabolites related in quantification. However, the unexpected transformation of urinary steroids during enzymatic hydrolysis with Helix pomatia could result in an underestimation or overestimation of their concentrations. A comparison of β-glucurondase extracted from Escherichia coli revealed 18 conversions of 84 steroids tested as an unexpected transformation under hydrolysis with β-glucuronidase/arylsulfatase extracted from Helix pomatia. In addition to the conversion of 3β-hydroxy-5-ene steroids into 3-oxo-4-ene steroids, which has been reported, the transformation of 3β-hydroxy-5α–reduced and 3β-hydroxy-5β–reduced steroids to 3-oxo-5α–reduced and 3-oxo-5β–reduced steroids, respectively, was newly observed. The formation of by-products was in proportion to the concentration of substrates becoming saturated against the enzyme. The substances belonging to these three steroid groups were undetectable at low concentrations, whereas the corresponding by-products were overestimated. These results indicate that the systematic error in the quantification of urinary steroids hydrolyzed with Helix pomatia can lead to a misreading of the clinical implications. All these hydrolysis procedures are suitable for study purposes, and the information can help prevent false evaluations of urinary steroids in clinical studies. Cancer Epidemiol Biomarkers Prev; 19(2); 388–97
Genetic Variation in the Vitamin D Receptor (VDR) and the Vitamin D–Binding Protein (GC) and Risk for Colorectal Cancer: Results from the Colon Cancer Family Registry
Authors: Poynter Jenny N. , Jacobs Elizabeth T. , Figueiredo Jane C. , Lee Won H. , Conti David V. , Campbell Peter T. , Levine A. Joan , Limburg Paul , Le Marchand Loic , Cotterchio Michelle , Newcomb Polly A. , Potter John D. , Jenkins Mark A. , Hopper John L. , Duggan David J. , Baron John A. , Haile Robert W. 
Published: February 2010

AbstractEpidemiologic evidence supports a role for vitamin D in colorectal cancer (CRC) risk. Variants in vitamin D–related genes might modify the association between vitamin D levels and CRC risk. In this analysis, we did a comprehensive evaluation of common variants in the vitamin D receptor (VDR) and the vitamin D–binding protein (GC; group-specific component) genes using a population-based case–unaffected sibling control design that included 1,750 sibships recruited into the Colon Cancer Family Registry. We also evaluated whether any associations differed by calcium supplement use, family history of CRC, or tumor characteristics. Heterogeneity by calcium and vitamin D intake was evaluated for a subset of 585 cases and 837 sibling controls who completed a detailed food frequency questionnaire. Age- and sex-adjusted associations were estimated using conditional logistic regression. Overall, we did not find evidence for an association between any single-nucleotide polymorphism (SNP) in VDR or GC and risk for CRC (range of unadjusted P values 0.01-0.98 for VDR and 0.07-0.95 for GC). None of these associations was significant after adjustment for multiple comparisons. We also found no evidence that calcium or vitamin D intake (food and supplement) from the food frequency questionnaire modified the association estimates between VDR and GC SNPs and CRC. We did observe associations between SNPs in GC and microsatellite unstable CRC, although these results should be confirmed in additional studies. Overall, our results do not provide evidence for a role of common genetic variants in VDR or GC in susceptibility to CRC. Cancer Epidemiol Biomarkers Prev; 19(2); 525–36
Long-term Postmenopausal Hormone Therapy and Endometrial Cancer
Authors: Razavi Pedram , Pike Malcolm C. , Horn-Ross Pamela L. , Templeman Claire , Bernstein Leslie , Ursin Giske 
Published: February 2010

Abstract
Estrogen-alone therapy (ET) or estrogen and progestin (EPT) as menopausal hormone therapy (HT) has been commonly used to alleviate menopausal symptoms. Treatments containing ≥10 days per month of progestin are considered relatively safe with respect to endometrial cancer risk. However, the endometrial safety of long-term EPT regimens is uncertain. We conducted a case-control study of 311 invasive endometrial cancer cases and 570 controls nested within the California Teachers Study cohort. We used unconditional logistic regression to obtain odds ratios (OR) and 95% confidence intervals (95% CI) for the association between long-term HT use and endometrial cancer risk, and to assess the modifying effect of body mass index (BMI). Long-term (≥10 years) use of ET, sequential EPT with &lt;10 days per month progestin, and continuous-combined EPT (≥25 days/month progestin) were all associated with an elevated risk of endometrial cancer (OR, 4.5; 95% CI, 2.5-8.1; OR, 4.4; 95% CI, 1.7-11.2; and OR, 2.1; 95% CI, 1.3-3.3, respectively; all Ptrend &lt; 0.001). The risk associated with short-term use was elevated only for ET preparations. The association for continuous-combined EPT was confined to thinner women (BMI, &lt;25 kg/m2; Pinteraction = 0.03). Among heavier women (BMI, ≥25 kg/m2), use of continuous-combined EPT was associated with a statistically nonsignificant reduction in risk. These findings confirm that long-term use of ET, sequential EPT, or, among normal weight women, continuous-combined EPT is associated with increased risk of endometrial cancer. Cancer Epidemiol Biomarkers Prev; 19(2); 475–83
Clinical Presentation of Endometrioid Epithelial Ovarian Cancer with Concurrent Endometriosis: A Multicenter Retrospective Study
Authors: Lim Myong Cheol , Chun Kyoung-Chul , Shin So-Jin , Lee In Ho , Lim Kyung Taek , Cho Chi Heum , Park Sang-Yoon , Nam Joo-Hyun 
Published: February 2010

Abstract
Background: Endometrioid epithelial ovarian cancer (EEOC) is frequently diagnosed in conjunction with endometriosis and is suggested to arise during the process of endometriosis. This study evaluates the clinical manifestations, including endometriosis-related symptoms and their relationships according to the coexistence of endometriosis.
Methods: Using medical records, a retrospective analysis was conducted on 221 patients treated for EEOC at four tertiary educational hospitals between 2000 and 2008. The initial presenting symptoms, particularly those related to endometriosis, were examined in relation to the coexistence of endometriosis or other clinical variables.
Results: Endometriosis was identified in 82 (37.1%) of the 221 patients with EEOC. The most common symptoms were pelvic pain followed by gastrointestinal symptoms, palpable mass, abdominal distension, vaginal bleeding, and newly developed or exacerbated dysmenorrhea (18.1%) and dyspareunia (13.6%). Notably, dysmenorrhea and dyspareunia were frequently observed in patients with endometriosis. Among 210 patients identified with pretreatment serum CA-125, 54 (25.7%) displayed normal CA-125 levels (&lt;35 units/mL) and 23.3% and 29.9% of patients without and with endometriosis had normal CA-125 levels, respectively (P = 0.381). Additionally, 32.6% of the patients with early-stage EEOC displayed normal CA-125 levels.
Conclusions: In this large series of patients with EEOC, the main presenting symptoms were pelvic pain followed by gastrointestinal symptoms, palpable mass, abdominal distension, vaginal bleeding, and newly developed or exacerbated dysmenorrhea and dyspareunia. Dyspareunia and dysmenorrhea were more frequently detected in patients with endometriosis. Normal CA-125 levels cannot be applied as a marker to exclude EEOC, particularly at the early stages. Cancer Epidemiol Biomarkers Prev; 19(2); 398–404
The Association of Metabolic Syndrome and Its Components with Serum Prostate-Specific Antigen Levels in a Korean-Screened Population
Authors: Jeong In Gab , Hwang Seung Sik , Kim Hong Kyu , Ahn Hanjong , Kim Choung-Soo 
Published: February 2010

AbstractBackground: Metabolic syndrome plays a potential role in the etiology of prostate cancer and is associated with the increase in prostatic growth rate in patients with benign prostatic hyperplasia. However, the influence of metabolic syndrome on prostate-specific antigen (PSA) level remains unclear.Methods: Data were obtained from 23,601 men ages 40 years or older without a history of prostate cancer who underwent general health screening tests between 2006 and 2007 at Asan Medical Center. The criteria for metabolic syndrome were consistent with those defined by the NCEP-ATPIII-AHA/NHLBI statement. Multivariate linear regression analysis was used to determine the independent effects of age, body mass index (BMI), metabolic syndrome, and each component of metabolic syndrome, on PSA level.Results: Geometric mean PSA level increased linearly and significantly with increasing age and decreasing BMI (P &lt; 0.001). Although the geometric mean PSA levels were lower in men with metabolic syndrome than in those without the condition, metabolic syndrome no longer retained a statistically significant association with PSA after the adjustment for age and BMI (P = 0.850). Among five metabolic components, higher waist circumference and fasting plasma glucose level were significantly associated with lower PSA (P = 0.021 and P = 0.001), whereas hypertension was significantly associated with higher PSA (P &lt; 0.001), after complete adjustment for age, BMI, and other metabolic components.Conclusions: In our screened population, metabolic syndrome was not associated with PSA level. The lack of association between metabolic syndrome and PSA level may reflect the heterogeneous relationship between each metabolic risk factor and PSA level. Cancer Epidemiol Biomarkers Prev; 19(2); 371–80
Serum Vitamin D and Breast Density in Breast Cancer Survivors
Authors: Neuhouser Marian L. , Bernstein Leslie , Hollis Bruce W. , Xiao Liren , Ambs Anita , Baumgartner Kathy , Baumgartner Richard , McTiernan Anne , Ballard-Barbash Rachel 
Published: February 2010

AbstractBackground: Vitamin D influences cellular proliferation and proliferation-related breast tissue characteristics, such as mammographic breast density. Little is known about vitamin D status, assessed by serum 25-hydroxyvitamin D [25(OH)D], and its relationship to breast density in breast cancer survivors.Methods: Participants were 426 postmenopausal breast cancer survivors from the Health, Eating, Activity, and Lifestyle Study. Women from New Mexico, Los Angeles, and western Washington were enrolled postdiagnosis. Data for this report are from an examination conducted 24 months postenrollment. Participants completed health-related questionnaires, gave fasting blood samples, and completed height and weight measurements. Serum [25(OH)D] was assayed by radioimmunoabsorbant assay. Breast dense area and percent density were measured from postdiagnosis-digitized mammograms. Multivariate linear regression tested associations of serum [25(OH)D] with mammographic breast density measures.Results: Of the 426 participants, 22.8% were African-American, 11.3% were Hispanic, and 62.8% were non-Hispanic white. We observed no associations of serum [25(OH)D] with either breast density or breast dense area. Among women with vitamin D deficiency (serum [25(OH)D], &lt;16.0 ng/mL; n = 103), mean percent breast density was 8.0%, and among those with sufficient status (n = 99; serum [25(OH)D], ≥32.0 ng/mL), mean percent density was 8.5%. Breast dense area averaged 27.2 and 26.2 cm2 for women with vitamin D deficiency and sufficiency, respectively.Conclusion: Data from this multiethnic cohort of breast cancer survivors do not support the hypothesis that serum vitamin D, [25(OH)D], is associated with breast density in cancer survivors. Cancer Epidemiol Biomarkers Prev; 19(2); 412–7
Plasma Levels of Acid-Labile Subunit, Free Insulin-Like Growth Factor-I, and Prostate Cancer Risk: A Prospective Study
Authors: Mucci Lorelei A. , Stark Jennifer R. , Pollak Michael N. , Li Haojie , Kurth Tobias , Stampfer Meir J. , Ma Jing 
Published: February 2010

Abstract
Background: The acid-labile subunit (ALS) acts in the insulin-like growth (IGF) system by binding circulating IGF-I in a ternary complex with binding protein (IGFBP)-3 to prevent IGF-I from crossing the endothelial barrier. Given the role of the IGF system in prostate cancer, ALS may influence carcinogenesis by modulating IGF-I levels or bioavailability.
Methods: We undertook a prospective study nested in the Physicians' Health Study to examine ALS, free IGF-I, and prostate cancer. We assayed circulating levels of ALS and IGF components among 545 incident cases and 545 matched controls. We calculated relative risks (RR) and 95% confidence intervals (95% CI) adjusted for life-style factors, total IGF-I, and IGFBP3.
Results: ALS was positively correlated with total IGF-I (r = 0.58), IGFBP3 (r = 0.68), and free IGF-I (r = 0.36). Comparing highest versus lowest quartiles, we found no association between free IGF-I and prostate cancer risk (RR, 0.9; 95% CI, 0.6-1.3). In contrast, ALS was positively associated with risk among men in the 2nd (RR, 1.5; 94% CI, 1.0-2.3), 3rd (RR, 1.6; 94% CI, 1.1-2.5), and 4th quartiles (RR, 1.4; 94% CI, 0.9-2.1) compared with lowest quartile. The association was stronger for advanced stage tumors (RR, 2.0; 94% CI, 0.8-4.6). There was a suggestion of an interaction between ALS and total IGF-I, whereby high circulating IGF-I was associated with an increased risk of advanced prostate cancer among men with low but not higher ALS levels.
Discussion: Plasma ALS is positively associated with prostate cancer risk, and may interact biologically with IGF-I to affect carcinogenesis. These data provide further support for the role of the IGF axis in prostate cancer. Cancer Epidemiol Biomarkers Prev; 19(2); 484–91
Polymorphism in the GALNT1 Gene and Epithelial Ovarian Cancer in Non-Hispanic White Women: The Ovarian Cancer Association Consortium
Authors: Phelan Catherine M. , Tsai Ya-Yu , Goode Ellen L. , Vierkant Robert A. , Fridley Brooke L. , Beesley Jonathan , Chen Xiao Qing , Webb Penelope M. , Chanock Stephen , Cramer Daniel W. , Moysich Kirsten , Edwards Robert P. , Chang-Claude Jenny , Garcia-Closas Montserrat , Yang Hannah , Wang-Gohrke Shan , Hein Rebecca , Green Adele C. , Lissowska Jolanta , Carney Michael E. , Lurie Galina , Wilkens Lynne R. , Ness Roberta B. , Pearce Celeste Leigh , Wu Anna H. , Van Den Berg David J. , Stram Daniel O. , Terry Kathryn L. , Whiteman David C. , Whittemore Alice S. , DiCioccio Richard A. , McGuire Valerie , Doherty Jennifer A. , Rossing Mary Anne , Anton-Culver Hoda , Ziogas Argyrios , Hogdall Claus , Hogdall Estrid , Krüger Kjaer Susanne , Blaakaer Jan , Quaye Lydia , Ramus Susan J. , Jacobs Ian , Song Honglin , Pharoah Paul D.P. , Iversen Edwin S. , Marks Jeffrey R. , Pike Malcolm C. , Gayther Simon A. , Cunningham Julie M. , Goodman Marc T. , Schildkraut Joellen M. , Chenevix-Trench Georgia , Berchuck Andrew , Sellers Thomas A. ,   on behalf of the Ovarian Cancer Association Consortium, Australian Cancer Study (Ovarian Cancer),   Australian Ovarian Cancer Study Group
Published: February 2010

Abstract
Aberrant glycosylation is a well-described hallmark of cancer. In a previous ovarian cancer case control study that examined polymorphisms in 26 glycosylation-associated genes, we found strong statistical evidence (P = 0.00017) that women who inherited two copies of a single-nucleotide polymorphism in the UDP-N-acetylgalactosamine:polypeptide N-acetylgalactosaminyltransferase, GALNT1, had decreased ovarian cancer risk. The current study attempted to replicate this observation. The GALNT1 single-nucleotide polymorphism rs17647532 was genotyped in 6,965 cases and 8,377 controls from 14 studies forming the Ovarian Cancer Association Consortium. The fixed effects estimate per rs17647532 allele was null (odds ratio, 0.99; 95% confidence interval, 0.92-1.07). When a recessive model was fit, the results were unchanged. Test for hetero geneity of the odds ratios revealed consistency across the 14 replication sites but significant differences compared with the original study population (P = 0.03). This study underscores the need for replication of putative findings in genetic association studies. Cancer Epidemiol Biomarkers Prev; 19(2); 600–4
Longer Relative Telomere Length in Blood from Women with Sporadic and Familial Breast Cancer Compared with Healthy Controls
Authors: Gramatges Maria M. , Telli Melinda L. , Balise Raymond , Ford James M. 
Published: February 2010

Abstract
Telomeres cap the ends of chromosomes and are composed of a series of noncoding hexamer repeats. Telomeres protect the integrity of DNA coding sequences and are integral to the maintenance of genomic stability. Previous studies have shown an association between shortened lymphocyte telomeres and increased risk for specific cancers. However, the association between telomere length and breast cancer risk is less clear. We examined the relative telomere length (RTL) in blood from women with no personal or family history of cancer (controls) compared with different populations of women with breast cancer and women at high genetic risk for developing breast cancer. RTL was determined as the telomere to single gene copy number ratio assessed by quantitative PCR. Breast cancer cases (low risk, n = 40; high risk, n = 62) had significantly longer RTL compared with unaffected controls (n = 50; mean RTL = 1.11 versus 0.84; P &lt; 0.0001). The assessment of risk by RTL quartile showed an increased risk for breast cancer with each longer quartile, with the most significant risk observed in the longest quartile (odds ratio, 23.3; confidence interval, 4.4-122.3; P &lt; 0.0003). Women without breast cancer but at high risk due to family history (n = 30) also showed longer telomeres than controls (mean RTL = 1.09 versus 0.84; P &lt; 0.0001). Our analysis supports previous findings of longer RTL in breast cancer cases compared with controls, and is the first to observe longer RTL in women without breast cancer identified as high risk based on family history. Cancer Epidemiol Biomarkers Prev; 19(2); 605–13
Associations between Polymorphisms in Glucuronidation and Sulfation Enzymes and Mammographic Breast Density in Premenopausal Women in the United States
Authors: Yong Mellissa , Schwartz Stephen M. , Atkinson Charlotte , Makar Karen W. , Thomas Sushma S. , Newton Katherine M. , Aiello Bowles Erin J. , Holt Victoria L. , Leisenring Wendy M. , Lampe Johanna W. 
Published: February 2010

Abstract
Objective: Sex hormones are metabolized to less active compounds via (a) glucuronidation catalyzed by UDP-glucuronosyltransferases (UGT) and (b) sulfation catalyzed by sulfotransferases (SULT). Functional UGT and SULT polymorphisms can affect clearance of sex hormones, thereby influencing exposure in hormone-sensitive tissues, such as the breast. We assessed relationships between functional polymorphisms in the UGT and SULT genes and breast density in premenopausal women.
Methods: One hundred seventy-five women ages 40 to 45 years, who had a screening mammogram taken within the previous year, provided a genomic DNA sample. Mammograms were digitized to obtain breast density measures. Using generalized linear regression, we assessed associations between percent breast density and polymorphisms in the UGT1A and UGT2B families, SULT1A1, and SULT1E1.
Results: Women with the SULT1A1(H213/H213) genotype had 16% lower percent breast density compared with women with the SULT1A1(R213/R213) genotype after controlling for ethnicity (P = 0.001). Breast density was 5% lower among women carrying at least one copy of the UGT1A1(TA7)-UGT1A3(R11)-UGT1A3(A47) haplotype compared with the UGT1A1(TA6)-UGT1A3(W11R)-UGT1A3(V47A) haplotype (P = 0.07). No associations were observed between polymorphisms in the UGT2B family or SULT1E1 and breast density.
Conclusion: Polymorphisms in SULT1A1 and the UGT1A locus may influence percent breast density in premenopausal women. Cancer Epidemiol Biomarkers Prev; 19(2); 537–46
210Pb: A Predictive Biomarker of Retrospective Cigarette Smoke Exposure
Authors: Schayer Stephen R. , Qu Qingshan , Wang Yanling , Cohen Beverly S. 
Published: February 2010

Abstract
Although cigarette smoking continues to occur worldwide, there are few methods available to assess a person's retrospective exposure to mainstream smoke. The tobacco of cigarettes contains trace quantities of radioactive 210Pb and 210Po, which are volatilized and inhaled when a cigarette is smoked. It was hypothesized that urinary 210Pb and 210Po activity concentrations could be used as biomarkers of exposure to mainstream tobacco smoke. Human subjects (n = 250) were recruited from Beijing, China, and reported their smoking habits. Each subject provided a 24-hour urine sample, which was assayed for its 210Pb and 210Po activity concentrations. Although the urinary 210Po activity from smoking was very low compared with background levels, the urinary 210Pb activity correlated with the number of cigarettes smoked per day (CPD; ρ = 0.38, P &lt; 0.001) and the urinary cotinine concentration (ρ = 0.52, P &lt; 0.001). In a linear regression model, a 1-unit increase in CPD was associated with an increase of 0.13 mBq in urinary 210Pb activity. In a logistic regression model, a 1-unit increase in urinary 210Pb activity was associated with an estimated 25% increase in the odds of being a smoker. These data were modeled using the respiratory, gastrointestinal, and biokinetic models of the International Commission on Radiological Protection. When the final model was applied for a long-term smoker (20 CPD) that suddenly quits, the predicted urinary activity decreased to 50% of the steady-state activity in about 90 days. Based on this half-time estimate and the regression results, urinary 210Pb can be used to assess the probability of having smoked in the past months. Cancer Epidemiol Biomarkers Prev; 19(2); 338–50