bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genetic Polymorphisms in the IGFBP3 Gene: Association with Breast Cancer Risk and Blood IGFBP-3 Protein Levels among Chinese Women
Authors: Ren Zefang , Cai Qiuyin , Shu Xiao-Ou , Cai Hui , Li Chun , Yu Herbert , Gao Yu-Tang , Zheng Wei 
Published: June 2022

Abstract
Cumulative evidence suggests that insulin-like growth factors (IGF) play an important role in the etiology of breast cancer. The IGF binding proteins regulate the action of IGFs, and &gt;90% of circulating IGFs are bound to IGFBP-3. We evaluated the associations of five (A−202C, G227C, C3804G, 5606InsA, and C5827T) genetic polymorphisms in the IGFBP3 gene with breast cancer risk and the blood IGFBP-3 protein level in a population-based, case-control study conducted among Chinese women in Shanghai. Genomic DNA samples from 1,193 incident breast cancer patients and 1,310 community controls were genotyped for IGFBP3 polymorphisms. Blood IGFBP-3 levels were determined for 390 controls. A 30% to 60% elevated risk of breast cancer was found to be associated with homozygosity for the variant allele in polymorphisms A−202C, G227C, 5606InsA, and C5827T. Carrying the variant allele in C3804G was also associated with an increased risk. About 13.5% of cases and 9.7% of controls had one or more of the above risk genotypes, resulting in odds ratio [OR; 95% confidence interval (95% CI)] of 1.4 (1.0-1.9). The ORs (95% CIs) were 1.3 (1.0-1.8) and 1.7 (1.1-2.5) for women with one to two and three to five risk genotypes, respectively (P for trend &lt; 0.01). Four common haplotypes for the IGFBP3 gene were identified. Compared with the haplotype containing only the wild-type allele in the five loci, the haplotype with the variant allele in all sites was associated with an elevated risk of breast cancer (OR 1.4, 95% CI 1.0-1.9), particularly among younger women (OR 2.3, 95% CI 1.3-3.9). With the exception of C3804G, in which no homozygote was identified, the level of circulating IGFBP-3 was reduced in a dose-response manner with an increasing number of variant alleles in each of the other four polymorphic sites (P for trend &lt; 0.05). These results indicated that IGFBP3 polymorphisms may be associated with the level of blood IGFBP-3 protein and an increased risk of breast cancer.
Use of Oral Contraceptives, Alcohol, and Risk for Invasive Breast Cancer
Authors: Dumeaux Vanessa , Lund Eiliv , Hjartåker Anette 
Published: June 2022

Abstract
The aim of our study was to examine how the use of oral contraceptives (OCs) interact with alcohol on breast cancer risk within the large prospective follow-up study, Norwegian Women and Cancer Study. Between 1991 and 1997, women aged 30 to 70 years were drawn at random from the central person register and mailed an invitation. Follow-up information was collected throughout 2001 by linkage to national registries. Only women (n = 86,948) with complete information on alcohol consumption and duration of OC use were included in the present analysis. A total of 1,130 invasive breast cancers were diagnosed during 618,638 person-years of follow-up. Consumption of ≥10.0 g/d alcohol was associated with a breast cancer relative risk (95% confidence interval) of 1.69 (1.32-2.15), consistent with a linear relationship (P for trend &lt; 0.0001). Among alcohol consumers, an excess risk of breast cancer was observed for total duration of OC use only among women who consumed &lt;5 g/d alcohol (P for trend = 0.0009). We observed a negative interaction between duration of OC use and alcohol consumption effects (P for interaction = 0.01). After stratification on menopausal status, the association between high alcohol intake and breast cancer was more prominent among postmenopausal women than among premenopausal women (P for heterogeneity = 0.01). No interaction between alcohol and duration of OC use were significant after stratification on menopausal status. Our findings in conjunction with biological data imply that alcohol and OCs have antagonistic effects on breast cancer risk through a common pathway. Whether the interactive effect differs according to menopausal status remains unclear and needs further investigations.
Benzo(a)pyrene Diolepoxide (BPDE)-DNA Adduct Levels in Leukocytes of Smokers in Relation to Polymorphism of CYP1A1, GSTM1, GSTP1, GSTT1, and mEH
Authors: Lodovici Maura , Luceri Cristina , Guglielmi Francesco , Bacci Chiara , Akpan Victor , Fonnesu Maria Luisa , Boddi Vieri , Dolara Piero 
Published: June 2022

Abstract
Benzo(a)pyrene [B(a)P] diolepoxide (BPDE)-DNA adducts were measured in the leukocytes of 41 healthy smokers using high-performance liquid chromatography coupled with a fluorimetric detector. The correlation between exposure to B(a)P through smoking and BPDE-DNA adduct levels was poor (r = 0.31), although subjects in the high exposure group [B(a)P &gt; 50 ng/d] had a slightly higher level of adducts compared with the less exposed group (mean ± SE, 1.70 ± 0.3 versus 1.09 ± 0.1; P = 0.057). We studied the effect on BPDE-DNA adducts of individual variations in genes controlling B(a)P metabolism, classifying subjects in “low-risk” and “high-risk” genotypes for smoking-related B(a)P DNA damage. The high-risk group included subjects characterized by a combination of increased B(a)P activation [cytochrome P450 1A1 (CYP1A1) MspI and/or exon 7 Ile462Val allele variants and microsomal epoxide hydrolase (mEH) fast activity] and decreased deactivation ability [presence of glutathione S-transferase M1 (GSTM1) null allele and wild-type glutathione S-transferase P1 (GSTP1)]. The low-risk group included smokers with lower B(a)P activation (wild-type CYP1A1, low or intermediate mEH activity) and higher deactivation capacity (active GSTM1, GSTP1 Ile105Val allele). Subjects in the low-risk group had lower levels of BPDE-DNA adducts compared with subjects in the high-risk genotype group; this difference was significant using two markers (CYP1A1 and GSTM1, median ± SD, 0.77 ± 1.16 versus 1.89 ± 0.39; P = 0.03) or three markers (CYP1A1, GSTM1, and GSTP1, median ± SD, 0.66 ± 0.93 versus 1.43 ± 1.17; P = 0.013). The discrimination between groups was reduced when including mEH as an additional marker (P = 0.085). In conclusion, CYP1A1, GSTM1, and GSTP1 genotyping seems to be a risk predictor of BPDE-DNA adduct formation in leukocytes.
Cancer Prevention Strategies That Address the Evolutionary Dynamics of Neoplastic Cells: Simulating Benign Cell Boosters and Selection for Chemosensitivity
Authors: Maley Carlo C. , Reid Brian J. , Forrest Stephanie 
Published: June 2022

AbstractCells in neoplasms evolve by natural selection. Traditional cytotoxic chemotherapies add further selection pressure to the evolution of neoplastic cells, thereby selecting for cells resistant to the therapies. An alternative proposal is a benign cell booster. Rather than trying to kill the highly dysplastic or malignant cells directly, a benign cell booster increases the fitness of the more benign cells, which may be either normal or benign clones, so that they may outcompete more advanced or malignant cells in a neoplasm. In silico simulations of benign cell boosters in neoplasms with evolving clones show benign cell boosters to be effective at destroying advanced or malignant cells and preventing relapse even when applied late in progression. These results are conditional on the benign cell boosters giving a competitive advantage to the benign cells in the neoplasm. Furthermore, the benign cell boosters must be applied over a long period of time in order for the benign cells to drive the dysplastic cells to extinction or near extinction. Most importantly, benign cell boosters based on this strategy must target a characteristic of the benign cells that is causally related to the benign state to avoid relapse. Another promising strategy is to boost cells that are sensitive to a cytotoxin, thereby selecting for chemosensitive cells, and then apply the toxin. Effective therapeutic and prevention strategies will have to alter the competitive dynamics of a neoplasm to counter progression toward invasion, metastasis, and death.
The CYP19 Gene Codon 39 Trp/Arg Polymorphism Increases Breast Cancer Risk in Subsets of Premenopausal Japanese
Authors: Hirose Kaoru , Matsuo Keitaro , Toyama Tatsuya , Iwata Hiroji , Hamajima Nobuyuki , Tajima Kazuo 
Published: June 2022

Abstract
The production of estrogen from androgen via the estrogen biosynthesis pathway is catalyzed by aromatase P450 (CYP19). To assess the association between breast cancer risk and a polymorphism at codon 39 Trp/Arg of the encoding gene, a case-control study was conducted at Aichi Cancer Center Hospital in Japan. Subjects were 248 histologically confirmed breast cancer patients and 603 hospital controls without cancer. Odds ratios (OR) and 95% confidence intervals (95% CI) were determined by logistic regression analysis. The allele frequency among controls was 3.8% for the C allele, and the OR (95% CI) of the polymorphism relative to TT genotype was 1.21 (0.69-2.14) for TC/CC genotypes combined. There was no association between CYP19 gene polymorphism and breast cancer risk in the study group as a whole, but homozygous and heterozygous carriers of the variant Arg allele showed a significantly increased risk of breast cancer among premenopausal women with a late age at first full-term pregnancy (OR 7.31, 95% CI 1.88-28.5) or a high body mass index (OR 2.77, 95% CI 1.12-6.87). Additional larger studies should be done to confirm that the rare CYP19 variant increases the risk of breast cancer among premenopausal Japanese women.
Fruits, Vegetables, and Micronutrients in Relation to Breast Cancer Modified by Menopause and Hormone Receptor Status
Authors: Gaudet Mia M. , Britton Julie A. , Kabat Geoffrey C. , Steck-Scott Susan , Eng Sybil M. , Teitelbaum Susan L. , Terry Mary Beth , Neugut Alfred I. , Gammon Marilie D. 
Published: June 2022

Abstract
Whether fruit, vegetable, and antioxidant micronutrient consumption is associated with a reduction in breast cancer incidence remains unresolved. To address this issue, we analyzed data from a large population-based case-control study, with consideration given to whether the associations varied with menopausal status or with clinical characteristics of the cases' disease. Study participants completed a modified Block food frequency questionnaire, which included assessment of the frequency and portion sizes of 13 fruits and fruit juices and 16 vegetables and the use of multiple and single vitamin supplements. Statistical analyses were done on 1,463 cases and 1,500 controls. Among postmenopausal women, reduced odds ratios [OR; 95% confidence intervals (95% CI)] were noted for the highest fifth, as compared with the lowest fifth, of intake of any vegetables [0.63 (0.46–0.86); P for trend &lt; 0.01] and leafy vegetables [0.66 (0.50–0.86); P for trend = 0.03] after controlling for age and energy intake. Adjusted ORs (95% CIs) were also decreased for postmenopausal breast cancer in relation to high intake of carotenoids, α-carotene, β-carotene, lutein, and particularly lycopene [0.66 (0.48–0.90); P for trend = 0.03]. Inverse associations for fruits and vegetables were stronger for postmenopausal women with estrogen receptor (ER)+ tumors (OR, 0.65; 95% CI, 0.51–0.82) than ER− tumors (OR, 0.92; 95% CI, 0.64–1.32), but results were less consistent for micronutrients. No similarly reduced associations were observed among premenopausal women. ORs did not appreciably differ by in situ or invasive breast cancer or by whether cases had begun chemotherapy. Our results support an inverse association for fruit and vegetable intake among postmenopausal but not premenopausal breast cancer, which may be more pronounced among women with ER+ tumors.
Cyclooxygenase-2 and p53 Expressions in Endometrial Cancer
Authors: Jeon Yong-Tark , Kang Sokbom , Kang Dae-Hee , Yoo Keun-Young , Park In-Ae , Bang Yung-Jue , Kim Jae Weon , Park Noh-Hyun , Kang Soon-Beom , Lee Hyo-Pyo , Song Yong-Sang 
Published: June 2022

Abstract
Cyclooxygenase-2 (COX-2) has been known to be related with various types of carcinoma, but we have insufficient knowledge about the association between COX-2 and endometrial cancer. Many have reported a close relationship between p53 expression and a poor prognosis in endometrial cancer, but it is unclear whether p53 is an independent prognostic factor. To clarify these uncertainties, we examined the expressions of COX-2 and p53 in endometrial cancer tissues. The study was carried on 152 endometrial cancer patients who had operation at Seoul National University Hospital. Paraffin-embedded tissue blocks were sectioned and immunostained using monoclonal anti-COX-2 and anti-p53 antibodies. Twenty-seven (17.8%) specimens stained as COX-2 positive. COX-2 positivity was more frequently observed in postmenopausal patients than in premenopausal patients (8.8% versus 25.0%; P = 0.009). However, COX-2 positivity did not show a statistically significant association with any other clinicopathologic characteristic (parity, body mass index, histotype, International Federation of Gynecology and Obstetrics stage, grade, lymph node metastasis, deep myometrial invasion, or p53 overexpression). Thirty-one (20.4%) specimens showed p53 overexpression and this was significantly correlated with an advanced stage (P = 0.001), poor differentiation (P &lt; 0.001), lymph node metastasis (P = 0.012), and deep myometrial invasion (P &lt; 0.001). Multivariate Cox regression analysis showed that advanced stage was an independent prognostic factor of survival, but p53 overexpression was not. COX-2 may be associated with endometrial cancer carcinogenesis during the postmenopausal period but not with tumor aggressiveness and p53 overexpression. The p53 overexpression was found to be strongly associated with endometrial cancer aggressiveness.
Hemochromatosis Gene Mutations and Distal Adenomatous Colorectal Polyps
Authors: McGlynn Katherine A. , Sakoda Lori C. , Hu Ying , Schoen Robert E. , Bresalier Robert S. , Yeager Meredith , Chanock Stephen , Hayes Richard B. , Buetow Kenneth H. 
Published: June 2022

Abstract
Iron has been suggested to be a risk factor for colorectal neoplasia. Some individuals who are heterozygous for mutations in the hemochromatosis gene (HFE) have higher than average serologic measures of iron. We therefore investigated whether heterozygosity for HFE mutations was related to risk of advanced distal adenoma and whether the relationship was affected by dietary iron intake. In the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, 679 persons with advanced distal adenoma and 697 control persons were genotyped for the two major HFE mutations (C282Y and H63D), one HFE polymorphism (IVS2+4), and one polymorphism (G142S) in the transferrin receptor gene (TFRC). HFE haplotypes were also created to examine the effect of haplotype on risk. Food frequency questionnaire data were used to estimate daily iron intake. There was no relationship between any HFE genotype or haplotype and advanced adenoma. Stratification of HFE genotype by TFRC genotype did not change the results. In addition, there was no relationship between dietary iron intake and risk of adenoma or between HFE genotype and risk of adenoma, stratified by iron intake. These results do not support a relationship between HFE heterozygosity and risk of advanced distal adenoma.
Dietary Factors and Risk of Non-Hodgkin Lymphoma by Histologic Subtype: A Case-Control Analysis
Authors: Purdue Mark P. , Bassani Diego G. , Klar Neil S. , Sloan Margaret , Kreiger Nancy ,   The Canadian Cancer Registries Epidemiology Research Group
Published: June 2022

Abstract
There is speculation that etiologic heterogeneity exists among tumors classified as non-Hodgkin lymphoma (NHL), although it is not known whether diet-related associations vary between tumor subgroups. We analyzed data on 1,642 NHL cases and 5,039 controls aged 20 to 74 years from a population-based case-control study conducted in eight Canadian provinces to explore associations between dietary factors and NHL by histologic subtype. Dietary information was collected using a 69-item food frequency questionnaire. Tumors were categorized into histologic subtypes using the contents of pathology reports from the original histopathologic review of diagnostic material. Odds ratios (OR) relating consumption of dietary factors (divided into three categories) to each NHL subtype (diffuse, follicular, small lymphocytic, high grade, peripheral T cell, and unspecified lymphomas) were calculated using polytomous logistic regression. We found an increased risk of NHL with high (versus low) intake of processed meat (OR, 1.49), cheese (OR, 1.38), eggs (OR, 1.49), and dessert foods (OR, 1.24). Positive associations with NHL were also found for high consumption of total fat (OR, 1.28), saturated fat (OR, 1.29), and monounsaturated fat (OR, 1.27). Associations for consumption of some vegetables and fats were found to differ between lymphoma subtypes. Given the large number of diet/subtype comparisons done, however, the possibility that this heterogeneity arose by chance cannot be ruled out. In conclusion, these findings generally do not support the existence of etiologic heterogeneity between histologic subtypes of NHL in their associations with components of dietary intake.
Serum Oxidized Low-Density Lipoprotein Levels and Risk of Colorectal Cancer: A Case-Control Study Nested in the Japan Collaborative Cohort Study
Authors: Suzuki Koji , Ito Yoshinori , Wakai Kenji , Kawado Miyuki , Hashimoto Shuji , Toyoshima Hideaki , Kojima Masayo , Tokudome Shinkan , Hayakawa Norihiko , Watanabe Yoshiyuki , Tamakoshi Koji , Suzuki Sadao , Ozasa Kotaro , Tamakoshi Akiko ,   Japan Collaborative Cohort Study Group
Published: June 2022

Abstract
Oxidative stress plays an important role in carcinogenesis, but few epidemiologic studies have examined associations with risk of colorectal cancer. Relationships between serum levels of oxidized low-density lipoprotein (oxLDL) and oxLDL antibody (oLAB) and colorectal cancer risk were investigated in a case-control study nested in the Japan Collaborative Cohort Study for Evaluation of Cancer Risk. Serum samples and lifestyle information were collected at baseline from 39,242 men and women between 1988 and 1990. Of these, 161 incidents and deaths from colorectal cancer were identified through 1999, and 395 controls were matched for gender, age, and study area. Measurements were taken of serum oxLDL levels in 119 cases and 316 controls and serum oLAB levels in 153 cases and 376 controls. Odds ratios (95% confidence intervals) across quartiles, adjusted for confounding factors, were 1.55 (0.70-3.46), 1.90 (0.84-4.28), and 3.65 (1.50-8.92) for oxLDL (Ptrend = 0.004) and 0.98 (0.54-1.80), 0.75 (0.39-1.48), and 1.68 (0.90-3.13) for oLAB (Ptrend = 0.140). Further adjustment for serum total cholesterol and α-tocopherol did not materially change these associations. Odds ratio (95% confidence interval) of the highest quartile of serum oxLDL compared with the lowest quartile was 3.40 (1.09-10.58; Ptrend = 0.045). Analyses restricted to colon cancer cases and corresponding controls yielded similar relationships between serum oxLDL and oLAB levels and risk. In conclusion, higher levels of serum oxLDL may increase risk of colorectal cancer.
Effects of False-Positive Prostate Cancer Screening Results on Subsequent Prostate Cancer Screening Behavior
Authors: Ford Marvella E. , Havstad Suzanne L. , Demers Ray , Cole Johnson Christine 
Published: June 2022

Abstract
Objectives: Little is known about screening behavior following a false-positive prostate cancer screening result, which we have defined as a screening result with “abnormal/suspicious” labeling that did not result in a prostate cancer diagnosis within 14 months. The purpose of this analysis was to examine whether age, race, education, or previous false-positive prostate cancer screening results via prostate-specific antigen or digital rectal exam predict decision to obtain subsequent prostate cancer screening.
Methods: Data were drawn from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. The study sample consisted of 2,290 older men (mean age, 62.8 years; range, 55-75 years) who had false-positive (n = 318) or negative (n = 1,972) prostate-specific antigen or digital rectal exam baseline prostate cancer screening results. Multivariable logistic regression was used to assess the effect of false-positive results on subsequent prostate cancer screening behavior, adjusting for all covariates.
Results: The multivariable model showed that being African American (P = 0.016), and having a high school education or less (P = 0.007), having a previous false-positive prostate cancer screening result (P &lt; 0.001), were predictive of not returning for prostate cancer screening in the following screening trial year.
Conclusion: The study results highlight the importance of shared decision making between patients and their providers regarding the risks and benefits of prostate cancer screening, and follow-up options for abnormal prostate cancer screening results. Shared decision making may be especially important for African American men, whom prostate cancer disproportionately affects.
Polymorphism in the DNA Repair Gene XPD, Polycyclic Aromatic Hydrocarbon-DNA Adducts, Cigarette Smoking, and Breast Cancer Risk
Authors: Terry Mary Beth , Gammon Marilie D. , Zhang Fang Fang , Eng Sybil M. , Sagiv Sharon K. , Paykin Andrea B. , Wang Qiao , Hayes Sharon , Teitelbaum Susan L. , Neugut Alfred I. , Santella Regina M. 
Published: June 2022

Abstract
DNA repair is essential to an individual's ability to respond to damage caused by environmental carcinogens. Alterations in DNA repair genes may affect cancer risk by influencing individual susceptibility to environmental exposures. XPD, a gene involved in nucleotide excision repair, may influence individual DNA repair capacity particularly of bulky adducts. Using a population-based breast cancer case-control study that was specifically conducted to examine markers of environmental exposures, such as polycyclic aromatic hydrocarbons (PAH), on Long Island, NY, we examined whether XPD genotype modified the associations among PAH-DNA adducts, cigarette smoking, and breast cancer risk. Specifically, we examined the XPD polymorphism at exon 23, position 751 in 1,053 breast cancer cases and 1,102 population-based controls. The presence of at least one variant allele (Lys/Gln or Gln/Gln) was associated with a 20% increase in risk of breast cancer [odds ratio (OR), 1.21; 95% confidence interval (95% CI), 1.01-1.44]. The increase in risk for homozygosity of the variant allele (Gln/Gln) seemed limited to those with PAH-DNA adduct levels above the median(OR, 1.61; 95% CI, 0.99-2.63 for adducts above the median versus OR, 1.05; 95% CI, 0.64-1.74 for adductsbelow the median), although the multiplicative interaction was not statistically significant. The increasein risk for homozygosity of the variant allele (Gln/Gln) was only seen among current smokers (OR, 1.97; 95% CI, 1.02-3.81 for current smokers versus OR, 0.87; 95% CI, 0.57-1.32 for never smokers); the multiplicative interaction was statistically significant. Overall, this study suggests that those individuals with this polymorphism in the XPD gene may face an increased risk of breast cancer from PAH-DNA adducts and cigarette smoking.