bluuebunny/crossref_metadata_2025_split huggingface dataset:
Conditions Associated with Antibodies Against the Tumor-Associated Antigen MUC1 and Their Relationship to Risk for Ovarian Cancer
Authors: Cramer Daniel W. , Titus-Ernstoff Linda , McKolanis John R. , Welch William R. , Vitonis Allison F. , Berkowitz Ross S. , Finn Olivera J. 
Published: September 2005

AbstractMany cancers, including ovarian, overexpress epithelial mucin (MUC1) and promote anti-MUC1 antibodies that may correlate with more favorable prognosis. By extension, risk for ovarian cancer might be reduced by preexisting MUC1-specific immunity. We measured anti-MUC1 antibodies in 705 control women, identified events predicting antibodies, and estimated ovarian cancer risk by comparing profiles of events generating antibodies in controls with those in 668 ovarian cancer cases. Factors predicting antibodies included oral contraceptive use, breast mastitis, bone fracture or osteoporosis, pelvic surgeries, nonuse of talc in genital hygiene, and to a lesser extent intrauterine device use and current smoking. There was a significant increase in the likelihood of having anti-MUC1 antibodies from 24.2% in women with 0 or 1 condition, to 51.4% in those with five or more conditions. By the same index of events, the risk for ovarian cancer was inversely associated with number of conditions predisposing to anti-MUC1 antibodies. Compared with having experienced 0 or 1 event, the adjusted risk for ovarian cancer decreased progressively with relative risks (and 95% confidence limits) of 0.69 (0.52-0.92), 0.64 (0.47-0.88), 0.49 (0.34-0.72), and 0.31 (0.16-0.61), respectively for women with two, three, four, and five or more events related to the presence of antibodies (Ptrend &lt; 0.0001.) We conclude that several traditional and new risk factors for ovarian cancer may be explained by their ability to induce MUC1 immunity through exposure of MUC1 to immune recognition in the context of inflammatory or hormonal processes in various MUC1-positive tissues.
Sugar-Sweetened Soft Drink Consumption and Risk of Pancreatic Cancer in Two Prospective Cohorts
Authors: Schernhammer Eva S. , Hu Frank B. , Giovannucci Ed , Michaud Dominique S. , Colditz Graham A. , Stampfer Meir J. , Fuchs Charles S. 
Published: September 2005

Abstract
Background: A history of diabetes mellitus and a diet high in glycemic load are both potential risk factors for pancreatic cancer. Sugar-sweetened soft drinks are a prevalent source of readily absorbable sugars and have been associated with an increased risk of obesity and diabetes. We investigated whether higher consumption of sugar-sweetened soft drinks increases the risk of pancreatic cancer.
Methods: We examined the relation between consumption of sugar-sweetened soft drinks and the development of pancreatic cancer in the Nurses' Health Study and the Health Professionals Follow-up Study. Among 88,794 women and 49,364 men without cancer at baseline, we documented 379 cases of pancreatic cancer during up to 20 years of follow-up. Soft drink consumption was first assessed at baseline (1980 for the women, 1986 for the men) and updated periodically thereafter.
Results: Compared with participants who largely abstained from sugar-sweetened soft drinks, those who consumed more than three sugar-sweetened soft drinks weekly experienced overall a multivariate relative risk (RR) of pancreatic cancer of 1.13 [95% confidence interval (95% CI), 0.81-1.58; P for trend = 0.47]. Women in the highest category of sugar-sweetened soft drink intake did experience a significant increase in risk (RR, 1.57; 95% CI, 1.02-2.41; P for trend = 0.05), whereas there was no association between sweetened soft drink intake and pancreatic cancer among men. Among women, the risk associated with higher sugar-sweetened soft drink was limited to those with elevated body mass index (&gt;25 kg/m2; RR, 1.89; 95% CI, 0.96-3.72) or with low physical activity (RR, 2.02; 95% CI, 1.06-3.85). In contrast, consumption of diet soft drinks was not associated with an elevated pancreatic cancer risk in either cohort.
Conclusion: Although soft drink consumption did not influence pancreatic cancer risk among men, consumption of sugar-sweetened soft drinks may be associated with a modest but significant increase in risk among women who have an underlying degree of insulin resistance.
A Comparison of Bilateral Breast Cancers in BRCA Carriers
Authors: Weitzel Jeffrey N. , Robson Mark , Pasini Barbara , Manoukian Siranoush , Stoppa-Lyonnet Dominique , Lynch Henry T. , McLennan Jane , Foulkes William D. , Wagner Teresa , Tung Nadine , Ghadirian Parviz , Olopade Olufunmilayo , Isaacs Claudine , Kim-Sing Charmaine , Møller Pal , Neuhausen Susan L. , Metcalfe Kelly , Sun Ping , Narod Steven A. 
Published: September 2005

Abstract
Background: Women with breast cancer and a BRCA mutation have a high risk of developing a contralateral breast cancer. It is generally believed that the two cancers represent independent events. However, the extent of concordance between the first and second tumors with respect to hormone receptor expression and other pathologic features is unknown.
Purpose: To determine the degree of concordance of estrogen receptor (ER) status, tumor grade, and histology in tumors from women with bilateral breast cancer and a BRCA mutation.
Subjects and Methods: Women with a history of bilateral invasive breast cancers were selected from an international registry of women with BRCA1 or BRCA2 mutations. Medical records were reviewed to document the characteristics of each cancer and the treatments received.
Results: Data were available for 286 women with bilateral breast cancer and a BRCA mutation (211 BRCA1; 75 BRCA2). The mean interval between first and second tumor was 5.1 years. The two tumors were concordant more often than expected for ER status (P &lt; 0.0001) and for grade (P &lt; 0.0001), but not for histology (P = 0.55). The ER status of the first tumor was highly predictive of the ER status of the second tumor (odds ratio, 8.7; 95% confidence interval, 3.5-21.5; P &lt; 0.0001). Neither age, menopausal status, oophorectomy nor tamoxifen use was predictive of the ER status of the second tumor.
Conclusions: There is strong concordance in ER status and tumor grade between independent primary breast tumors in women with a BRCA mutation. The excess concordance may be due to common risk factors, genetic variation, or the existence of a preneoplastic lesion that is common to both tumors.
Cigarette Smoking and Risk of Non-Hodgkin's Lymphoma—A Population-Based Case-Control Study
Authors: Schöllkopf Claudia , Ekström Smedby Karin , Hjalgrim Henrik , Rostgaard Klaus , Gadeberg Ole , Roos Göran , Porwit-MacDonald Anna , Glimelius Bengt , Adami Hans-Olov , Melbye Mads 
Published: September 2005

AbstractBackground: Epidemiologic evidence of an association between tobacco smoking and non-Hodgkin's lymphoma has been conflicting. This may reflect that non-Hodgkin's lymphoma comprises several distinct disease entities with different etiologies, as some studies have indicated an association between smoking and follicular lymphoma.Objective: To investigate the association between cigarette smoking and non-Hodgkin's lymphoma risk, overall and by subtype.Methods: As part of a nationwide Danish-Swedish population-based case-control study, we interviewed 3,055 incident non-Hodgkin's lymphoma patients and 3,187 population controls. All lymphomas were uniformly classified according to the WHO classification. We used unconditional logistic regression to estimate adjusted odds ratios (OR) and 95% confidence intervals (95% CI) for the association between cigarette smoking and risk of non-Hodgkin's lymphoma.Results: Cigarette smoking was not associated with the risk of non-Hodgkin's lymphoma overall (OR, 0.97; 95% CI, 0.87-1.08) nor with the major subgroups such as diffuse large B-cell lymphoma (OR, 0.94; 95% CI, 0.79-1.10), chronic lymphocytic leukemia (OR, 0.86; 95% CI, 0.72-1.02), or follicular lymphoma (OR, 1.03; 95% CI, 0.85-1.24). Female smokers were at a marginally increased risk of follicular lymphoma (OR, 1.41; 95% CI, 1.04-1.92). Men who had ever smoked had a significantly increased risk of T-cell lymphoma (OR, 1.67; 95% CI, 1.11-2.51). No dose-response association with cigarette smoking could be established for any lymphoma subgroup.Conclusion: We found little evidence of an association between cigarette smoking and non-Hodgkin's lymphoma risk overall. Although increased risks of follicular lymphoma in female smokers and of T-cell lymphoma in male smokers were suggested, no dose-response relationship was observed, leaving limited support for causality.
Molecular Features of Adult Glioma Associated with Patient Race/Ethnicity, Age, and a Polymorphism inO6-Methylguanine-DNA-Methyltransferase
Authors: Wiencke John K. , Aldape Kenneth , McMillan Alex , Wiemels Joe , Moghadassi Michelle , Miike Rei , Kelsey Karl T. , Patoka Joe , Long Jeff , Wrensch Margaret 
Published: September 2005

AbstractBackground: Risk factors for adult glioma in the San Francisco Bay Area include well-known demographic features such as age and race/ethnicity, and our previous studies indicated that these characteristics are associated with the TP53 mutation status of patients' tumors. We enlarged our study to assess the relationships of risk factors with TP53 as well as epidermal growth factor receptor (EGFR) and murine double minute-2 (MDM2) gene amplification and expression and the germ line Leu84Phe polymorphism in the DNA repair protein O6-methylguanine-DNA-methyltransferase (MGMT). MGMT expression may depend on the TP53 status of cells.Methods: Molecular analyses were carried out on 556 incident astrocytic tumors. MGMT genotype data were collected on germ line DNA from 260 of these cases.Results: The tumor data confirm the inverse relationships between TP53 mutation and MDM2 (P = 0.04) or EGFR (P = 0.004) amplification and that patients whose tumors contain TP53 mutations are younger than those without (P &lt; 0.001). Although there was little difference in age of patient by EGFR amplification or expression among glioblastoma multiforme cases, EGFR gene amplification was associated with much older age of onset of anaplastic astrocytoma; for example, EGFR-amplified anaplastic astrocytoma cases were on average 63 years old compared with 48 years for nonamplified cases (P = 0.005). An increased prevalence of TP53 mutation positive glioblastoma multiforme was noted among nonwhites (African American and Asian) compared with whites (Latino and non-Latino; P = 0.004). Carriers of the MGMT variant 84Phe allele were significantly less likely to have tumors with TP53 overexpression (odds ratio, 0.30; 95% confidence interval, 0.13-0.71) and somewhat less likely to have tumors with any TP53 mutation (odds ratio, 0.47; 95% confidence interval, 0.13-1.69) after adjusting for age, gender, and ethnicity. Interestingly, EGFR gene amplification and EGFR protein overexpression were also inversely associated with the MGMT 84Phe allele.Conclusions: Our results are consistent with ethnic variation in glioma pathogenesis. The data on MGMT show that an inherited factor involving the repair of methylation and other alkylation damage, specifically to the O6 position of guanine, may be associated with the development of tumors that proceed in their development without TP53 mutations or accumulation of TP53 protein and possibly also those that do not involve amplification of the EGFR locus.
Etiologic and Other Factors Predicting Nevus-Associated Cutaneous Malignant Melanoma
Authors: Purdue Mark P. , From Lynn , Armstrong Bruce K. , Kricker Anne , Gallagher Richard P. , McLaughlin John R. , Klar Neil S. , Marrett Loraine D. ,   for the Genes, Environment, and Melanoma Study Group
Published: September 2005

Abstract
Cutaneous malignant melanomas with histologic evidence of an associated nevus (N+) may have a different risk factor profile from that of melanomas without it (N−). To address this question, a case-only analysis of 932 people with cutaneous malignant melanoma was done to identify etiologic and other factors associated with N+ melanoma. Evidence of an associated nevus was found in 36% of melanomas. N+ melanomas were thinner (Ptrend = 0.0009) and more likely to be of the superficial spreading type than other types of melanoma. Subjects with N+ melanomas were younger (Ptrend &lt; 0.0001) and reported a higher nevus density on their skin than subjects with N− melanomas [odds ratio (OR), 3.1; 95% confidence interval (CI), 1.6-6.0, for high nevus density versus no nevi]. Indicators of high accumulated sun exposure were less prevalent among subjects with N+ melanomas (OR, 0.3; 95% CI, 0.2-0.4, for melanoma location on the head and neck versus location on trunk; OR, 0.2; 95% CI, 0.1-0.4, for severe solar elastosis adjacent to the melanoma versus no elastosis; OR, 0.2; 95% CI, 0.1-0.4, for lentigo maligna melanoma subtype versus superficial spreading subtype). With the exception of solar elastosis and age, all of the aforementioned variables remained significantly associated with N+ melanomas in multivariate analyses. No associations with self-reported measures of sun exposure, sunburn, or pigmentation phenotype were apparent. Our findings provide some support for the hypothesis of etiologically separate pathways for melanoma, with N+ melanomas appearing less likely to develop in the presence of characteristics suggesting high accumulated sun exposure than N− melanomas. However, it is possible that high UV exposure causes involution of nevi, thus reducing the density of nevi in exposed skin and thereby the probability of N+ melanoma.
Body Mass and Mortality After Breast Cancer Diagnosis
Authors: Whiteman Maura K. , Hillis Susan D. , Curtis Kathryn M. , McDonald Jill A. , Wingo Phyllis A. , Marchbanks Polly A. 
Published: September 2005

Abstract
Obesity is an established risk factor for some breast cancers, but less is known about its effect on breast cancer prognosis. Understanding this relationship is important, given the increasing number of women diagnosed with breast cancer and the growing prevalence of obesity. We conducted a cohort analysis of 3,924 women ages 20 to 54 with incident breast cancer enrolled between 1980 and 1982 in the Cancer and Steroid Hormone study, a case-control study. Interview data were linked to survival information from the Surveillance, Epidemiology, and End Results Program. We used proportional hazards models to examine the relationship between breast cancer mortality and adult body mass index (BMI; calculated using usual adult weight), BMI at age 18, and weight change from age 18 to adulthood. Hazard ratios (HR) were adjusted for cancer stage and other factors. During a median follow-up of 14.6 years, 1,347 women died of breast cancer. Obese women (adult BMI ≥30.00) were significantly more likely than lean women (BMI ≤22.99) to die of breast cancer [HR, 1.34; 95% confidence interval (CI), 1.09-1.65]. Women with BMIs of 25.00-29.99 (HR, 1.25; 95% CI, 1.08-1.44) or 23.00-24.99 (HR, 1.20; 95% CI, 1.04-1.39) also had higher breast cancer mortality (P for trend &lt;0.0001). BMI at age 18 and weight change were not associated with breast cancer mortality independently of other factors. Obesity could be a preventable risk factor for death among breast cancer patients. Further study is needed to determine how these findings might affect recommendations to reduce breast cancer mortality.
Increased Risk of Oral Leukoplakia and Cancer Among Mixed Tobacco Users Carrying XRCC1 Variant Haplotypes and Cancer Among Smokers Carrying Two Risk Genotypes: One on Each of Two Loci, GSTM3 and XRCC1 (Codon 280)
Authors: Majumder Mousumi , Sikdar Nilabja , Paul Ranjan Rashmi , Roy Bidyut 
Published: September 2005

Abstract
An individual's susceptibility to oral precancer and cancer depends not only on tobacco exposure but also on the genotypes/haplotypes at susceptible loci. In this hospital-based case-control study, 310 cancer patients, 197 leukoplakia patients, and 348 controls were studied to determine risk of the disease due to polymorphisms at three sites on XRCC1 and one site on XRCC3. Independently, variant genotypes on these loci did not modulate risk of leukoplakia and cancer except for the XRCC1 (codon 280) risk genotype in exclusive smokeless tobacco users with leukoplakia [odds ratios (OR), 2.4; 95% confidence intervals (CI), 1.0-5.7]. But variant haplotypes, containing one variant allele, on XRCC1 increased the risk of leukoplakia (OR, 1.3; 95% CI, 1.0-1.7). Among stratified samples, mixed tobacco users, carrying variant haplotypes, also had increased risk of both leukoplakia (OR, 2.2; 95% CI, 1.3-3.9) and cancer (OR, 1.9; 95% CI, 1.2-3.1). In a previous study on this population, it was shown that the GSTM3 (A/A) genotype increased the risk of oral leukoplakia and cancer among smokers, which has also been substantiated in this study with expanded sample sizes. The simultaneous presence of two risk genotypes in smokers, one on each of two loci, GSTM3 and XRCC1 (codon 280), increased the risk of cancer (OR, 2.4; 95% CI, 1.0-5.8). Again, smokers carrying two risk genotypes, one on each of two loci, GSTM3 and XRCC1 (codon 399), were also overrepresented in both leukoplakia and cancer populations (Ptrend = 0.02 and 0.04, respectively) but enhancement of risks were not observed; probably due to small sample sizes. Therefore, the presence of variant haplotypes on XRCC1 and two risk genotypes, one on each of two loci, GSTM3 and XRCC1, could be useful to determine the leukoplakias that might progress to cancer in a group of patients.
Endometrial Carcinoma Risks among Menopausal Estrogen plus Progestin and Unopposed Estrogen Users in a Cohort of Postmenopausal Women
Authors: Lacey James V. , Brinton Louise A. , Lubin Jay H. , Sherman Mark E. , Schatzkin Arthur , Schairer Catherine 
Published: September 2005

Abstract
Background: Because unopposed estrogen substantially increases endometrial carcinoma risk, estrogen plus progestin is one menopausal hormone therapy formulation for women who have not had a hysterectomy. However, endometrial carcinoma risks among estrogen plus progestin users and among former unopposed estrogen users are not firmly established.
Methods: We evaluated endometrial carcinoma risks associated with estrogen plus progestin and unopposed estrogen therapies in 30,379 postmenopausal Breast Cancer Detection Demonstration Project follow-up study participants. We ascertained hormone therapy use and other risk factors during telephone interviews and mailed questionnaires between 1979 and 1998. We identified 541 endometrial carcinomas via self-report, medical records, the National Death Index, and state cancer registries. Poisson regression generated time-dependent rate ratios (RR) and 95% confidence intervals (95% CI).
Results: Endometrial carcinoma was significantly associated with estrogen plus progestin only use (n = 68 cancers; RR, 2.6; 95% CI, 1.9-3.5), including both sequential (progestin &lt;15 days per cycle; n = 32 cancers; RR, 3.0; 95% CI, 2.0-4.6) and continuous (progestin at least 15 days per cycle; n = 15 cancers; RR, 2.3; 95% CI, 1.3-4.0) regimens. The RR increased by 0.38 (95% CI, 0.20-0.64) per year of estrogen plus progestin use, and RRs increased with increasing duration of use for both regimens. The strong association with unopposed estrogen use declined after cessation but remained significantly elevated ≥10 years after last use (RR, 1.5; 95% CI, 1.0-2.1).
Conclusions: Both estrogen plus progestin regimens significantly increased endometrial carcinoma risk in this study. Risks among unopposed estrogen users remained elevated long after last use. The prospect that all estrogen plus progestin regimens increase endometrial carcinoma risk deserves continued research.
Ethnic Difference in Daycare Attendance, Early Infections, and Risk of Childhood Acute Lymphoblastic Leukemia
Authors: Ma Xiaomei , Buffler Patricia A. , Wiemels Joseph L. , Selvin Steve , Metayer Catherine , Loh Mignon , Does Monique B. , Wiencke John K. 
Published: September 2005

Abstract
A role for infectious agents has been proposed in the etiology of childhood acute lymphoblastic leukemia (ALL), particularly for common ALL (c-ALL; ALL diagnosed in children ages 2-5 years and expressing CD10 and CD19 surface antigens). We evaluated the possible etiologic role of daycare attendance (a proxy measure for exposure to infectious agents) and infections during infancy in the Northern California Childhood Leukemia Study. A total of 294 incident ALL cases (ages 1-14 years) and 376 individually matched controls were included in this analysis. In non-Hispanic White children, daycare attendance measured by child-hours was associated with a significantly reduced risk of ALL. Compared with children who did not attend any daycare, the odds ratio (OR) for those who had &gt;5,000 child-hours during infancy was 0.42 [95% confidence interval (95% CI), 0.18-0.99] for ALL and 0.33 (95% CI, 0.11-1.01) for c-ALL. Test for trend is also significant, which supports a dose-response relationship. The magnitude of effect associated with the same number of child-hours was stronger for daycare attendance during infancy than for daycare attendance before diagnosis. In addition, self-reported ear infection during infancy was associated with a significantly reduced risk of c-ALL (OR, 0.32; 95% CI, 0.14-0.74) in non-Hispanic White children. In Hispanic children, no association was observed among daycare attendance, early infections, and risk of childhood ALL or c-ALL. These results offer indirect yet strong support for the infectious disease hypothesis in the etiology of ALL in non-Hispanic White children and highlight an important ethnic difference.
Allergies and the Risk of Pancreatic Cancer: A Meta-analysis with Review of Epidemiology and Biological Mechanisms
Authors: Gandini Sara , Lowenfels Albert B. , Jaffee Elizabeth M. , Armstrong Todd D. , Maisonneuve Patrick 
Published: September 2005

AbstractPrevious reports suggest that allergic disorders may protect against various types of cancer, but the association between history of allergy and pancreatic cancer risk has not been well studied. We did a systematic review and meta-analysis of published studies to evaluate the association of any type, and specific types, of allergy and the risk of pancreatic cancer. We did a comprehensive literature search using MEDLINE, PUBMED, and the ISI Web of Science databases to identify potential relevant case-control and cohort studies. Pooled relative risks (RR) and 95% confidence intervals (95% CI) were calculated using the fixed- and random-effects model. Fourteen population-based studies (4 cohort and 10 case-control studies) with a total of 3,040 pancreatic cancer cases fulfilled our inclusion criteria. A history of allergy was associated with a reduced risk of pancreatic cancer (RR, 0.82; 95% CI, 0.68-0.99). The risk reduction was stronger for allergies related to atopy (RR, 0.71; 95% CI, 0.64-0.80), but not for asthma (RR, 1.01; 95% CI, 0.77-1.31). There was no association between allergies related to food or drugs and pancreatic cancer (RR, 1.08; 95% CI, 0.74-1.58). Overall, there was no evidence of publication bias. Allergies, in particular those related to atopy, seem to be associated with a decreased risk of pancreatic cancer. The hyperactive immune system of allergic individuals may, therefore, in some way lead to increased surveillance and protect against pancreatic cancer development.