bluuebunny/crossref_metadata_2025_split huggingface dataset:
Benign Breast Biopsy Diagnosis and Subsequent Risk of Breast Cancer
Authors: Ashbeck Erin L. , Rosenberg Robert D. , Stauber Patricia M. , Key Charles R. 
Published: March 2007

Abstract
Background: We examine benign breast biopsy diagnoses as reported by community pathologists in New Mexico and investigate associations with future breast cancer development.
Methods: Using data collected between 1992 and 2000 by the New Mexico Mammography Project and cancer data through 2003 from the New Mexico Tumor Registry, we calculated breast cancer rates following 14,602 benign breast biopsies for women ages 30 to 89 years. For comparison, we also calculated the breast cancer rate following 215,283 normal screening mammograms. Hazard ratios (HR) are presented.
Results: We identified 480 subsequent breast cancer diagnoses among 14,602 women with benign breast biopsies and 4,402 breast cancer diagnoses among 215,283 women with mammograms assigned a “negative” or “benign finding” assessment. Histologic diagnoses in absence of atypia had an age-adjusted HR of 1.95 [95% confidence interval (95% CI), 1.77-2.15]. Among low-risk histologic diagnoses, the strongest associations with subsequent breast cancer development included adenosis, apocrine metaplasia, calcifications, and ductal hyperplasia. Fibroadenoma, inflammation, and cysts did not exhibit an association with breast cancer development. Women with low-risk diagnoses and breast tissue characterized as fatty or with scattered densities had a HR of 2.09 (95% CI, 1.68-2.60), whereas women with low-risk histologic diagnoses and dense breasts had a HR of 3.36 (95% CI, 2.83-3.99).
Conclusions: The observed breast cancer occurrence contributes to evidence of increased risk following benign biopsy. The risk associated with histologic diagnoses in absence of atypia was twice the risk experienced by women with normal mammogram evaluations and may be modified by breast density. (Cancer Epidemiol Biomarkers Prev 2007;16(3):467–72)
Validity of Self-Reports of Return for Routine Repeat Screening in an Ovarian Cancer Screening Program
Authors: Lykins Emily L.B. , Pavlik Edward L. , Andrykowski Michael A. 
Published: March 2007

Abstract
Cancer screening research relies on reliable and valid measurement of cancer screening behavior. Self-reports of screening constitute a cost-effective approach to measuring screening behavior; however, demonstration of suitable validity of these self-reports is critical. We evaluated the validity of self-report of return for repeat, routine, annual transvaginal sonography (TVS) screening for ovarian cancer. Participants (n = 535) in a university-based ovarian cancer screening program for asymptomatic, average risk women completed a telephone interview 18 months following an initial, baseline TVS screening test. Self-reports of return for a repeat, routine ovarian cancer screening test since baseline were obtained and compared with objective records of repeat screening from the screening program database. Overall agreement of self-reports and objective records of ovarian cancer screening was 97.57% (κ = 0.94). Sensitivity was 0.98, specificity was 0.96, positive predictive value was 0.98, and negative predictive value was 0.96. The month of last screening was accurately identified by 80% of participants. It was concluded the validity of self-reports of TVS screening for ovarian cancer is very high and may even exceed the validity of self-reports of participation in breast, cervical, and colorectal cancer screening over similar recall periods. Consequently, self-reports of TVS screening may serve as a cost-effective substitute for more objective methods of assessing TVS screening behavior. (Cancer Epidemiol Biomarkers Prev 2007;16(3):490–3)
Statin Use and Breast Cancer Risk in a Large Population-Based Setting
Authors: Boudreau Denise M. , Yu Onchee , Miglioretti Diana L. , Buist Diana S.M. , Heckbert Susan R. , Daling Janet R. 
Published: March 2007

Abstract
Background: Mechanistic studies suggest that 3-hydroxy-3-methylglutaryl CoA inhibitors (statins) reduce the risk of breast cancer. Observational studies offer mixed results.
Methods: To evaluate the relation between statin use and breast cancer risk, we conducted a cohort study among women ages 45 to 89 years within an integrated health care delivery system. Information on statin use and covariates were obtained from automated databases. We identified breast cancer cases through the Surveillance, Epidemiology, and End Results registry. We used Cox proportional hazards models to estimate the hazard ratios (HR) and 95% confidence intervals (95% CI) for invasive breast cancer among statin users compared with nonusers.
Results: Among 92,788 women studied from 1990 to 2004, median follow-up time was 6.4 years, and 2,707 breast cancer cases were identified. During the study period, 7.4% of women used statins for at least 1 year, and the median duration of use was 3.1 years. We found no difference in breast cancer risk among statin users (HR, 1.07; 95% CI, 0.88-1.29) compared with nonusers. Risk of breast cancer did not differ by duration of use (1-2.9, 3-4.9, or ≥5 years) or hydrophobic statin use. We found a suggestive increased risk of breast cancer among statin users of ≥5 years (HR, 1.27; 95% CI, 0.89-1.81 for any statins and HR, 1.47; 95% CI, 0.89-2.44 for hydrophobic statins) and of estrogen receptor–negative tumors with increasing duration of statin use (1-2.9 years: HR, 1.33; 95% CI, 0.64-2.77; 3-4.9 years: HR, 1.68; 95% CI, 0.72-3.92; ≥5 years: HR, 1.81; 95% CI, 0.75-4.36).
Conclusion: This study does not support an association between statin use and breast cancer risk. (Cancer Epidemiol Biomarkers Prev 2007;16(3):416–21)
Pairwise Combinations of Estrogen Metabolism Genotypes in Postmenopausal Breast Cancer Etiology
Authors: Rebbeck Timothy R. , Troxel Andrea B. , Walker Amy H. , Panossian Saarene , Gallagher Stephen , Shatalova Ekaterina G. , Blanchard Rebecca , Norman Sandra , Bunin Greta , DeMichele Angela , Berlin Michelle , Schinnar Rita , Berlin Jesse A. , Strom Brian L. 
Published: March 2007

AbstractEstrogen exposures have been associated with breast cancer risk, and genes involved in estrogen metabolism have been reported to mediate that risk. Our goal was to better understand whether combinations of candidate estrogen metabolism genotypes are associated with breast cancer etiology. A population-based case-control study in three counties of the Philadelphia Metropolitan area was undertaken. We evaluated seven main effects and 21 first-order interactions in African Americans and European Americans for genotypes at COMT, CYP1A1, CYP1A2, CYP1B1, CYP3A4, SULT1A1, and SULT1E1 in 878 breast cancer cases and 1,409 matched random digit–dialed controls. In European Americans, we observed main effect associations of genotypes containing any CYP1A1*2C (odds ratio, 1.71; 95% confidence interval, 1.09-2.67) and breast cancer. No significant main effects were observed in African Americans. Three significant first-order interactions were observed. In European Americans, interactions between SULT1A1*2 and CYP1A1*2C genotypes (Pinteraction &lt; 0.001) and between SULT1E1 and CYP1A2*1F genotypes were observed (Pinteraction = 0.006). In African Americans, an interaction between SULT1A1*2 and CYP1B1*4 was observed (Pinteraction = 0.041). We applied the false-positive report probability approach, which suggested that these associations were noteworthy; however, we cannot rule out the possibility that chance led to these associations. Pending future confirmation of these results, our data suggest that breast cancer etiology in both European American and African American postmenopausal women may involve the interaction of a gene responsible for the generation of catecholestrogens with a gene involved in estrogen and catecholestrogen sulfation. (Cancer Epidemiol Biomarkers Prev 2007;16(3):444–50)
Ovarian Cancer Risk and Polymorphisms Involved in Estrogen Catabolism
Authors: Holt Sarah K. , Rossing Mary Anne , Malone Kathleen E. , Schwartz Stephen M. , Weiss Noel S. , Chen Chu 
Published: March 2007

AbstractPolymorphisms within genes responsible for estrogen catabolism could alter cellular levels of genotoxic 4-hydroxylated catechol estrogens and antiangiogenic 2-methoxyestradiol, thus influencing risk of developing ovarian cancer. We carried out a population-based case-control study of 310 epithelial ovarian cancer cases and 585 controls in African-American and Caucasian women ages 35 to 54 years from Seattle, Atlanta, and Detroit metropolitan areas. Subjects were interviewed and genotyped for CYP1A1 m1, m2, m3, and m4; CYP1B1 Arg48Gly, Ala119Ser, Val432Leu, and Asn453Ser; COMT Val158Met; UGT1A1 A(TA)nTAA; and SULT1A1 Arg213His polymorphisms. Unconditional logistic regression was used to calculate odds ratios (OR). Haplotypes were inferred and analyzed using models based on expectation-maximization with progressive ligation and Bayesian coalescence theory. CYP1B1 Leu432 carriers were at increased risk of ovarian cancer, with an adjusted OR of 1.5 (95% confidence interval, 1.1-2.3) compared with Val432 homozygotes. The most common CYP1B1 haplotype was Arg48-Ala119-Val432-Asn453. All other haplotypes with frequencies &gt;5% contained the Leu432 allele. In diplotype analyses, relative to women homozygous for Arg48-Ala119-Val432-Asn453, women with diplotypes containing at least one Leu432 allele had adjusted ORs ranging from 1.3 to 2.2. Among women homozygous for COMT Met158, carriers of CYP1B1 Leu432 had a 2.6-fold increase in risk relative to CYP1B1 Val432 homozygotes (95% confidence interval, 1.1-5.9). This latter result is opposite in direction from a similar analysis conducted by other investigators in a different study population. No association of ovarian cancer risk was observed with any of the other polymorphisms examined, either alone or in combination. (Cancer Epidemiol Biomarkers Prev 2007;16(3):481–9)
Vitamin D and Reduced Risk of Breast Cancer: A Population-Based Case-Control Study
Authors: Knight Julia A. , Lesosky Maia , Barnett Heidi , Raboud Janet M. , Vieth Reinhold 
Published: March 2007

Abstract
Background: Vitamin D, antiproliferative and proapoptotic in breast cancer cell lines, can reduce the development of mammary tumors in carcinogen-exposed rats. Current evidence in humans is limited with some suggestion that vitamin D–related factors may reduce the risk of breast cancer. We conducted a population-based case-control study to assess the evidence for a relationship between sources of vitamin D and breast cancer risk.
Methods: Women with newly diagnosed invasive breast cancer were identified from the Ontario Cancer Registry. Women without breast cancer were identified through randomly selected residential telephone numbers. Telephone interviews were completed for 972 cases and 1,135 controls. Odds ratios (OR) and 95% confidence intervals (CI) for vitamin D–related variables were estimated using unconditional logistic regression with adjustment for potential confounders.
Results: Reduced breast cancer risks were associated with increasing sun exposure from ages 10 to 19 (e.g., OR, 0.65; 95% CI, 0.50-0.85 for the highest quartile of outdoor activities versus the lowest; P for trend = 0.0006). Reduced risk was also associated with cod liver oil use (OR, 0.76; 95% CI, 0.62-0.92) and increasing milk consumption (OR, 0.62 95% CI 0.45-0.86 for ≥10 glasses per week versus none; P for trend = 0.0004). There was weaker evidence for associations from ages 20 to 29 and no evidence for ages 45 to 54.
Conclusion: We found strong evidence to support the hypothesis that vitamin D could help prevent breast cancer. However, our results suggest that exposure earlier in life, particularly during breast development, maybe most relevant. These results should be confirmed. (Cancer Epidemiol Biomarkers Prev 2007;16(3):422–9)
The Common Variant rs1447295 on Chromosome 8q24 and Prostate Cancer Risk: Results from an Australian Population-Based Case-Control Study
Authors: Severi Gianluca , Hayes Vanessa M. , Padilla Emma J.D. , English Dallas R. , Southey Melissa C. , Sutherland Robert L. , Hopper John L. , Giles Graham G. 
Published: March 2007

Abstract
A recent study from deCode reported an association between common variants in the region 8q24 and prostate cancer risk. The strongest association was found with the single nucleotide polymorphism rs1447295. We genotyped 821 prostate cancer cases and 732 population controls for rs1447295 to test the association between this common variant and prostate cancer risk, and examine whether this association depends on Gleason score. Our case-control study confirmed the association between rs1447295 and prostate cancer risk (P = 0.0005). The odds ratio (OR) for prostate cancer was 1.52 [95% confidence interval (CI), 1.20-1.93] for carriers of any A allele compared with noncarriers. The OR for Gleason score 5 to 6 prostate cancer (1.48; 95% CI, 1.13-1.95) was similar to the OR for Gleason score 7 to 10 prostate cancer (1.58; 95% CI, 1.18-2.11, P for heterogeneity = 0.7). We conclude that the A allele of rs1447295 is associated with a higher risk of prostate cancer regardless of tumor aggressiveness, suggesting that such a variant, or a variant in linkage disequilibrium with it, plays a role early in prostate carcinogenesis. (Cancer Epidemiol Biomarkers Prev 2007;16(3):610–2)
Overweight and Obese Perimenopausal and Postmenopausal Women Exhibit Increased Abnormal Mammary Epithelial Cytology
Authors: Seewaldt Victoria L. , Goldenberg Vanessa , Jones Lee W. , Peace Charlotte , Broadwater Gloria , Scott Victoria , Bean Gregory R. , Wilke Lee Gravit , Zalles Carola M. , Demark-Wahnefried Wendy 
Published: March 2007

Abstract
High body mass index (BMI ≥ 25 kg/m2) is associated with increased postmenopausal breast cancer incidence and mortality. However, few studies have explored associations between BMI and direct measures on target tissue. Epithelial cytology was assessed in 62 high-risk perimenopausal and postmenopausal women using random periareolar fine needle aspiration. Masood cytology index scores were significantly higher among women with BMIs ≥25 kg/m2 than in women with BMIs &lt;25 kg/m2 (13.9 ± 0.42 versus 12.7 ± 0.29 kg/m2; P = 0.017). Overweight or obese women also had significantly higher random periareolar fine needle aspiration epithelial cell counts compared with those who were normal weight (1,230 ± 272 versus 521 ± 185; P = 0.028). These data suggest that overweight in perimenopausal and postmenopausal women is associated with direct cytologic abnormalities within the breast. Further research is needed to confirm these findings and to determine if this potential biomarker is responsive to changes in body weight resulting from diet and/or exercise interventions. (Cancer Epidemiol Biomarkers Prev 2007;16(3):613–6)
Direct Inhibition of Insulin-Like Growth Factor-I Receptor Kinase Activity by (−)−Epigallocatechin-3-Gallate Regulates Cell Transformation
Authors: Li Ming , He Zhiwei , Ermakova Svetlana , Zheng Duo , Tang Faqing , Cho Yong-Yeon , Zhu Feng , Ma Wei-Ya , Sham Yuk , Rogozin Evgeny A. , Bode Ann M. , Cao Ya , Dong Zigang 
Published: March 2007

Abstract
Insulin-like growth factor-I receptor (IGF-IR) has been implicated in cancer pathophysiology. Furthermore, impairment of IGF-IR signaling in various cancer cell lines caused inhibition of the transformed phenotype as determined by the inhibition of colony formation in soft agar and the inhibition of tumor formation in athymic nude mice. Thus, the IGF-IR might be an attractive target for cancer prevention. We showed that the tea polyphenol, (−)−epigallocatechin-3-gallate (EGCG), is a small-molecule inhibitor of IGF-IR activity (IC50 of 14 μmol/L). EGCG abrogated anchorage-independent growth induced by IGF-IR overexpression and also prevented human breast and cervical cancer cell phenotype expression through inhibition of IGF-IR downstream signaling. Our findings are the first to show that the IGF-IR is a novel binding protein of EGCG and thus may help explain the chemopreventive effect of EGCG on cancer development. (Cancer Epidemiol Biomarkers Prev 2007;16(3):598–605)
Infectious Agents as Causes of Non-Hodgkin Lymphoma
Authors: Engels Eric A. 
Published: March 2007

Abstract
Among exposures presently viewed as possible etiologic factors in non-Hodgkin lymphoma (NHL), infections are close to being regarded as established causes. Infectious agents causing NHL can be classified, according to mechanism, into three broad groups. First, some viruses can directly transform lymphocytes. Lymphocyte-transforming viruses include Epstein Barr virus (linked to Burkitt's lymphoma, NHLs in immunosuppressed individuals, and extranodal natural killer/T-cell NHL), human herpesvirus 8 (primary effusion lymphoma), and human T lymphotropic virus type I (adult T-cell leukemia/lymphoma). Second, human immunodeficiency virus is unique in causing profound depletion of CD4+ T lymphocytes, leading to acquired immunodeficiency syndrome and an associated high risk for some NHL subtypes. Third, recent evidence suggests that some infections increase NHL risk through chronic immune stimulation. These infections include hepatitis C virus as well as certain bacteria that cause chronic site-specific inflammation and seem to increase risk for localized mucosa-associated lymphoid tissue NHLs. Establishing that an infectious agent causes NHL depends on showing that the agent is present in persons with NHL as well as laboratory experiments elucidating the mechanisms involved. Only epidemiologic studies can provide evidence that infection is actually a risk factor by showing that infection is more frequent in NHL cases than in controls. Given the range of mechanisms by which infections could plausibly cause NHL and our growing molecular understanding of this malignancy, this field of research deserves continued attention. (Cancer Epidemiol Biomarkers Prev 2007;16(3):401–4)
Altered Immunity as a Risk Factor for Non-Hodgkin Lymphoma
Authors: Grulich Andrew E. , Vajdic Claire M. , Cozen Wendy 
Published: March 2007

Abstract
This review examines the association between disorders of immunity, including immune deficiency, atopy, and autoimmune disease, and non-Hodgkin lymphoma (NHL). Immune deficiency is one of the strongest known risk factors for NHL. Risk is increased whether the immune deficiency is congenital, iatrogenic, or acquired. Risk of NHL increases with degree of immune deficiency, and there is no evidence of a threshold. In the profoundly immune deficient, NHL is frequently caused by infection with the ubiquitous EBV. Whether mild, subclinical immune deficiency is related to increased NHL risk is unknown. There is inconsistent evidence that atopic conditions, such as asthma, hayfever, and eczema, characterized by an immune response that is skewed toward Th2, are associated with a decreased risk of NHL. These data come mainly from case-control studies. Concern has been expressed that the association may be due to reverse causality if early symptoms of NHL include a lessening of atopic manifestations. Case-control and cohort studies of people with autoimmune conditions have generally shown that rheumatoid arthritis, systemic lupus erythematosis, and Sjogren's disease are associated with increased NHL risk. It seems to be the intensity of the inflammatory disease rather than its treatment which is related to increased risk of NHL. The study of altered immunity as a cause of NHL in case-control studies is limited by the fact that development of NHL in itself leads to altered immunity. Cohort studies of the role of altered immunity should be a top priority in epidemiologic studies of NHL etiology. (Cancer Epidemiol Biomarkers Prev 2007;16(3):405–8)
United States China Policy
Authors: Clough Ralph N. 
Published: March 2007

Communism has taken over much of East Asia and poses a grave military and subversive threat to the free countries of the area. United States policy is aimed at counter ing this threat by deterring military aggression through a series of security pacts and the development of indigenous Free World military strength; strengthening the economies and the internal security of the free nations; and opposing any action which would contribute to Chinese Communist power to conquer or subvert. Essential to the policy of limiting the external political effectiveness of the Peiping regime is our support of the Republic of China. United States China policy has been strongly supported by the American people, but there have been expressions of doubt as to the validity of the policy for the future. A "two-Chinas" concept has sometimes been proposed as an alternative. However, the concept is vehemently op posed by both Peiping and Taipei. Even if it were practicable, its presumed advantages are highly questionable and its adop tion by the United States would seriously injure the Free World position in East Asia. This article was written just prior to the renewal of the Chi nese Communist artillery bombardment of Quemoy on August 23 and therefore does not reflect events which have taken place since then. However, it remains an authoritative exposition of United States policy towards China.
Dynamics of the Moscow-Peking Axis
Authors: Whiting Allen S. 
Published: March 2007

Alliance with Soviet Russia has served the mili tary, economic, and political interests of Communist China. The dependency of Peking upon Moscow during the Stalin period compelled suppression of ideological differences on the part of Mao Tse-tung. Growing Chinese strength, however, afforded increased leverage upon the post-Stalin leadership. In 1956, the East European crisis prompted Peking to inter vene in bloc affairs, promoting a formula which varied from the approach of Moscow. This formula called for relegation of bloc differences to secret bilateral discussions as well as for toleration of greater divergence in the domestic practices of bloc regimes. Chinese mediation between the Polish and Russian positions during 1956-57 appeared to smooth bloc relations throughout East Europe. Abandonment of this formula at the November 1957 con ference in Moscow coincided with a major shift by Mao Tse- tung on other aspects of Chinese foreign policy. This shift paralleled preconference signs from Khrushchev of a harsher line both on bloc affairs and toward the non-Communist world. Overtly the Sino-Soviet attack against "revisionism" applied to the Yugoslavs. Gomulka's position at the conference, how ever, as well as during the 1958 attack on Tito, suggested that Poland also felt pressure from the new line. The change in Peking's policy from 1956 to 1957 may have come from a reappraisal of Soviet strength resulting from intercontinental ballistic missiles (ICBM) and artificial satellite developments in the latter half of 1957. Such a reappraisal may explain the new harshness of Chinese foreign policy statements directed not only within the bloc but to other areas as well.