bluuebunny/crossref_metadata_2025_split huggingface dataset:
Vitamin D, Calcium, and Breast Cancer Risk: A Review
Authors: Cui Yan , Rohan Thomas E. 
Published: August 2006

AbstractVitamin D and calcium are metabolically interrelated and highly correlated dietary factors. Experimental studies have shown their anticarcinogenic effects due to their participation in regulating cell proliferation, differentiation, and apoptosis in normal and malignant breast cells. Given the emerging interest in their potential roles in the etiology of breast cancer, we review the current epidemiologic literature on dietary and/or supplemental intakes of vitamin D, endogenous circulating levels of vitamin D, and dietary and/or supplemental intakes of calcium in relation to breast cancer risk. To place these studies in context, we also provide a brief review of other supporting epidemiologic evidence. Despite inconsistent results from the epidemiologic studies, several lines of evidence suggest that vitamin D and calcium may be involved in the development of breast cancer. Specifically, (a) there is some epidemiologic evidence for inverse associations between vitamin D and calcium intakes and breast cancer; (b) serum, plasma, and/or blood levels of vitamin D metabolites have been inversely associated with breast cancer risk in some studies; (c) high sunlight exposure, presumably reflecting vitamin D synthesis in the skin, has been associated with a reduced risk of breast cancer; (d) vitamin D and calcium intakes have been inversely related to breast density, an intermediate end point for breast cancer; (e) calcium has been associated with a reduced risk of benign proliferative epithelial disorders of the breast, putative precursors of breast cancer; and (f) certain polymorphisms of the vitamin D receptor might modify breast cancer susceptibility. To further confirm the potential protective effects of calcium and vitamin D on breast cancer, well-designed cohort studies and clinical trials are warranted. (Cancer Epidemiol Biomarkers Prev 2006;15(8):1427-37)
Prenatal Diethylstilbestrol Exposure and Risk of Breast Cancer
Authors: Palmer Julie R. , Wise Lauren A. , Hatch Elizabeth E. , Troisi Rebecca , Titus-Ernstoff Linda , Strohsnitter William , Kaufman Raymond , Herbst Arthur L. , Noller Kenneth L. , Hyer Marianne , Hoover Robert N. 
Published: August 2006

Abstract
It has been hypothesized that breast cancer risk is influenced by prenatal hormone levels. Diethylstilbestrol (DES), a synthetic estrogen, was widely used by pregnant women in the 1950s and 1960s. Women who took the drug have an increased risk of breast cancer, but whether risk is also increased in the daughters who were exposed in utero is less clear. We assessed the relation of prenatal DES exposure to risk of breast cancer in a cohort of DES-exposed and unexposed women followed since the 1970s by mailed questionnaires. Eighty percent of both exposed and unexposed women completed the most recent questionnaire. Self-reports of breast cancer were confirmed by pathology reports. Cox proportional hazards regression was used to compute incidence rate ratios (IRR) for prenatal DES exposure relative to no exposure. During follow-up, 102 incident cases of invasive breast cancer occurred, with 76 among DES-exposed women (98,591 person-years) and 26 among unexposed women (35,046 person-years). The overall age-adjusted IRR was 1.40 [95% confidence interval (95% CI), 0.89-2.22]. For breast cancer occurring at ages ≥40 years, the IRR was 1.91 (95% CI, 1.09-3.33) and for cancers occurring at ages ≥50 years, it was 3.00 (95% CI, 1.01-8.98). Control for calendar year, parity, age at first birth, and other factors did not alter the results. These results, from the first prospective study on the subject, suggest that women with prenatal exposure to DES have an increased risk of breast cancer after age 40 years. The findings support the hypothesis that prenatal hormone levels influence breast cancer risk. (Cancer Epidemiol Biomarkers Prev 2006;15(8):1509–14)
Cancer after Total Joint Arthroplasty: A Meta-analysis
Authors: Onega Tracy , Baron John , MacKenzie Todd 
Published: August 2006

Abstract
Background: Some epidemiologic and laboratory studies have suggested that total joint arthroplasty could increase the risk of cancer. In this meta-analysis, we attempt to clarify the association of joint arthroplasty with subsequent cancer incidence.
Methods: We identified population-based studies reporting standardized incidence ratios (SIR) for cancer following large joint arthroplasty. After summing the observed and expected numbers of cases across all qualifying studies, we calculated SIRs for all cancers, and for those at 28 anatomic sites. Latency analysis involving 175,166 patients characterized short-term and long-term cancer associations.
Results: The analyses included 1,435,356 person-years of follow-up and 20,045 cases of cancer. Overall cancer risk among patients with arthroplasty was equal to that for the general population. The relative risk of lung cancer, reduced in the first 5 years after arthroplasty, increased significantly over time to approach that of the general population. Risks for all sites in the luminal gastrointestinal tract were significantly reduced by 10% to 20%; with relative risks that were generally stable over time. Increased risks were seen for cancer of the prostate (SIR, 1.12; 95% confidence interval, 1.08-1.16); similar relative risks were seen in each time period after the procedure. For melanoma, relative risks increased with follow-up to a SIR of 1.43 (95% confidence interval, 1.13-1.79) for 10 or more years after arthroplasty. There was a similar delayed emergence of increased risks for cancers of the urinary tract and oropharynx. The relative risk for bone cancer decreased with time after the procedure.
Conclusions: There does not seem to be an overall increased risk of cancer following total joint arthroplasty. Although the risks of prostate cancer and melanoma seem to be elevated, there is no obvious mechanism for these associations. Reductions in risk for some malignancies may not be causal. (Cancer Epidemiol Biomarkers Prev 2006;15(8):1532–7)
Associations of Ki-ras Proto-oncogene Mutation and p53 Gene Overexpression in Sporadic Colorectal Adenomas with Demographic and Clinicopathologic Characteristics
Authors: Einspahr Janine G. , Martinez Maria Elena , Jiang Ruiyun , Hsu Chiu-Hsieh , Bhattacharrya Achyut K. , Ahnen Dennis J. , Jacobs Elizabeth T. , Houlihan P. Scott , Webb C. Renee , Alberts David S. , Hamilton Stanley R. 
Published: August 2006

Abstract
In colorectal tumorigenesis, Ki-ras proto-oncogene mutation often occurs early in the adenoma-adenocarcinoma sequence, whereas mutation of the p53 gene is associated with late progression to carcinoma. We evaluated the relationship of demographic and clinicopathologic characteristics to Ki-ras mutation and p53 gene product overexpression in 1,093 baseline sporadic colorectal adenomas from 926 individuals enrolled in a phase III recurrence prevention trial. Ki-ras mutation was found in 14.7% of individuals and p53 overexpression was found in 7.0% of those tested. Multivariate analysis found older age, rectal location, and villous histology to be independently associated with Ki-ras mutation. Individuals with an advanced adenoma (≥1 cm or high-grade dysplasia or villous histology) had a 4-fold higher likelihood of Ki-ras mutation [odds ratios (OR), 3.96; 95% confidence intervals (CI), 2.54-6.18]. Ki-ras mutations in codon 12 and of the G-to-A transition type were more frequent in older individuals, whereas G-to-T transversion was more frequent in rectal adenomas than in the colon. Multivariate analysis showed that previous history of a polyp (P = 0.03) was inversely associated with p53 overexpression. Large adenoma size (≥1 cm), high-grade dysplasia, and villous histology were independently associated with p53 overexpression, with the strongest association for advanced adenomas (OR, 7.20; 95% CI, 3.01-17.22). Individuals with a Ki-ras mutated adenoma were more likely to overexpress p53 (OR, 2.46; 95% CI, 1.36-4.46), and 94.8% of adenomas with both alterations were classified as advanced (P ≤ 0.0001). Our large cross-sectional study supports the role of both Ki-ras and p53 in the progression of adenomas and shows that their molecular pathogenesis differs by anatomic location, age, and mucosal predisposition as evidenced by previous history of a polyp. (Cancer Epidemiol Biomarkers Prev 2006;15(8):1443–50)
Estrogen and α-Fetoprotein Levels in Maternal and Umbilical Cord Blood Samples in Relation to Birth Weight
Authors: Nagata Chisato , Iwasa Shinichi , Shiraki Makoto , Shimizu Hiroyuki 
Published: August 2006

Abstract
Birth weight has been associated with a subsequent risk of breast cancer. The present study examined associations between birth weight and pregnancy estrogens and α-fetoprotein (AFP). The concentrations of estradiol, estriol, and AFP were measured in maternal and umbilical cord blood samples from 194 women during pregnancy and at birth. Birth weight was significantly positively correlated with maternal serum estradiol and estriol levels in the 29th week (estradiol: r = 0.16, P = 0.03; estriol: r = 0.29, P = 0.001) and at delivery (estradiol: r = 0.20, P = 0.01; estriol: r = 0.41, P &lt; 0.0001) after controlling for covariates. The umbilical cord estriol level was moderately but significantly correlated with birth weight (r = 0.15, P = 0.049). There was no significant association between umbilical cord serum estradiol and birth weight. There was no significant association between birth weight and maternal serum AFP in any gestational week. Umbilical cord AFP was significantly inversely correlated with birth weight (r = −0.16, P = 0.04). Umbilical cord AFP was unrelated to cord levels of estradiol and estriol. The data suggested a greater exposure to estriol and a lower exposure to AFP among high birth weight babies. (Cancer Epidemiol Biomarkers Prev 2006;15(8):1469–72)
Diabetes Mellitus and Pancreatic Cancer in a Population-Based Case-Control Study in the San Francisco Bay Area, California
Authors: Wang Furong , Gupta Samir , Holly Elizabeth A. 
Published: August 2006

Abstract
Background: Diabetes has been postulated to be both a risk factor and a consequence of pancreatic cancer, but the degree of risk and associated clinical factors remain unclear.
Methods: We conducted a population-based case-control study of pancreatic cancer in the San Francisco Bay Area between 1995 and 1999. Rapid case ascertainment through the Surveillance, Epidemiology and End Results registry for cases and random selection from the general population for controls were employed to identify study participants with no proxy interviews.
Results: Five hundred thirty-two cases and 1,701 controls were interviewed. Participants with pancreatic cancer were more likely to report a history of diabetes (13%) than were controls [9%; odds ratio (OR), 1.5; 95% confidence interval (95% CI), 1.1-2.1]. Compared with diabetics in the control group, diabetics in the case group had a shorter duration of diabetes (P = 0.0003) and a larger proportion of insulin users (P = 0.002). Risk for pancreatic cancer varied with duration of diabetes (OR, 2.4; 95% CI, 1.4-4.0 for 1-4 years; OR, 2.0; 95% CI, 1.2-3.4 for 5-9 years; and OR, 0.86; 95% CI, 0.52-1.4 for ≥10 years diabetes duration; Ptrend = 0.004). Among diabetics, use of oral diabetes medication or insulin for ≥5 years was not associated with pancreatic cancer, but insulin use of &lt;5 years was associated with a 6.8-fold risk for pancreatic cancer (95% CI, 3.7-12).
Conclusion: Recent-onset diabetes may be a complication or an early marker of pancreatic cancer. Diabetes of short duration with insulin use conferred a substantially elevated risk for pancreatic cancer and may reflect insulin resistance that is elicited by pancreatic cancer. (Cancer Epidemiol Biomarker Prev 2006;15(8):1458–63)
Combined Analysis of r-1,t-2,3,c-4-Tetrahydroxy-1,2,3,4-Tetrahydrophenanthrene and 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanol in Smokers' Plasma
Authors: Carmella Steven G. , Yoder Andrea , Hecht Stephen S. 
Published: August 2006

Abstract
Polycyclic aromatic hydrocarbons (PAH) and tobacco-specific nitrosamines, such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), are widely accepted to be two important types of lung carcinogens in cigarette smoke. In this study, we have developed a method to estimate individual uptake of these compounds by quantifying r-1,t-2,3,c-4-tetrahydroxy-1,2,3,4-tetrahydrophenanthrene (PheT) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in 1 mL of smokers' plasma. PheT and NNAL are biomarkers of PAH and NNK uptake, respectively. [D10]PheT and [pyridine-D4]NNAL were added to plasma as internal standards. The plasma was treated with β-glucuronidase to release any conjugated PheT and NNAL. The analytes were enriched by solid-phase extraction on a mixed mode cation exchange cartridge and the PheT fraction was further purified by high-performance liquid chromatography. The appropriate fractions were analyzed by gas chromatography-negative ion chemical ionization-mass spectrometry for PheT and liquid chromatography-electrospray ionization-mass spectrometry for NNAL. The method was sensitive (limits of quantitation: PheT, 13 fmol/mL; NNAL, 3 fmol/mL), accurate, and precise. Levels of PheT and NNAL in plasma from 16 smokers averaged 95 ± 71 and 36 ± 21 fmol/mL, respectively, which are ∼1% to 2% of the amounts found in urine. This method should be useful in molecular epidemiology studies of carcinogen uptake and lung cancer in smokers. (Cancer Epidemiol Biomarkers Prev 2006;15(8):1490–4)
MDM2 SNP309 and SNP354 Are Not Associated with Lung Cancer Risk
Authors: Pine Sharon R. , Mechanic Leah E. , Bowman Elise D. , Welsh Judith A. , Chanock Stephen C. , Shields Peter G. , Harris Curtis C. 
Published: August 2006

Abstract
A single nucleotide polymorphism (SNP) in the MDM2 promoter (a T to G exchange at nucleotide 309) has been found to be associated with tumor formation. Publication of this null report is important because an association between MDM2 SNP309 and lung cancer was previously reported in two independent studies. Our findings suggest that MDM2 SNP309 is not a strong factor in lung carcinogenesis. In addition, this is the first MDM2 SNP309 report on a population consisting of Caucasians in the United States and African-Americans. A strength of the study design is that the controls consist of both population and hospital controls. (Cancer Epidemiol Biomarkers Prev 2006;15(8):1559–61)
The Prevalence of CDKN2A Germ-Line Mutations and Relative Risk for Cutaneous Malignant Melanoma: An International Population-Based Study
Authors: Berwick Marianne , Orlow Irene , Hummer Amanda J. , Armstrong Bruce K. , Kricker Anne , Marrett Loraine D. , Millikan Robert C. , Gruber Stephen B. , Anton-Culver Hoda , Zanetti Roberto , Gallagher Richard P. , Dwyer Terence , Rebbeck Timothy R. , Kanetsky Peter A. , Busam Klaus , From Lynn , Mujumdar Urvi , Wilcox Homer , Begg Colin B. ,   The GEM Study Group
Published: August 2006

Abstract
Germ-line mutations of CDKN2A have been identified as strong risk factors for melanoma in studies of multiple-case families. However, an assessment of their relative risk for melanoma in the general population has been difficult because they occur infrequently. We addressed this issue using a novel population-based case-control study design in which “cases” have incident second- or higher-order melanomas [multiple primary melanoma (MPM)] and “controls” have incident first primary melanoma [single primary melanoma (SPM)]. Participants were ascertained from nine geographic regions in Australia, Canada, Italy, and United States. In the 1,189 MPM cases and 2,424 SPM controls who were eligible and available for analysis, the relative risk of a subsequent melanoma among patients with functional mutations who have an existing diagnosis of melanoma, after adjustments for age, sex, center, and known phenotypic risk factors, is estimated to be 4.3 (95% confidence interval, 2.3-7.7). The odds ratio varied significantly depending on the type of mutation involved. The results suggest that the relative risk of mutation carriers in the population may be lower than currently believed and that different mutations on the CDKN2A gene may confer substantially different risks of melanoma. (Cancer Epidemiol Biomarkers Prev 2006;15(8)1520–5)
An Interlocker Concept of Carcinogenesis
Authors: Wattenberg Lee W. 
Published: August 2006

Abstract
A critical feature in the sequence of events occurring during carcinogenesis is the development of irreversibility. The term “Interlocker” is used here to denote a mechanism by which irreversibility is brought about. The presentation focuses on conceptualizations of such processes. Two will be described below. (Cancer Epidemiol Biomarkers Prev 2006;15(8):1425–6)
Prognostic significance of CD20 expression in childhood B-cell precursor acute lymphoblastic leukemia
Authors: Jeha Sima , Behm Frederick , Pei Deqing , Sandlund John T. , Ribeiro Raul C. , Razzouk Bassem I. , Rubnitz Jeffrey E. , Hijiya Nobuko , Howard Scott C. , Cheng Cheng , Pui Ching-Hon 
Published: August 2006

Abstract
CD20 expression is associated with inferior survival in adults with acute lymphoblastic leukemia (ALL). We analyzed the prognostic impact of CD20 expression in 353 children with B-cell precursor ALL treated in 3 consecutive St Jude Total Therapy studies. CD20 expression (> 20%) was found in 169 patients (48%) and was more frequent in patients between 1 and 10 years of age than in those younger than 1 or older than 10 years (P = .001). None of 14 patients with MLL-AF4 expressed CD20. There was no association between CD20 expression and E2A-PBX, TEL-AML1, ploidy, white blood cell count at diagnosis, or sex. In contrast to the experience in adult ALL, our patients with CD20 expression tended to have a better treatment outcome than those without the expression: 5-year event-free survival 84% ± 2.9% versus 78% ± 3.1% (P = .08). These data suggest that CD20 expression is not associated with inferior outcome in pediatric patients treated with contemporary regimens.
Reference values for exhaled nitric oxide (reveno) study
Authors: Olivieri Mario , Talamini Giorgio , Corradi Massimo , Perbellini Luigi , Mutti Antonio , Tantucci Claudio , Malerba Mario 
Published: August 2006

Abstract

Background
Despite the widespread use of fractional exhaled nitric oxide (FENO) as a biomarker of airways inflammation, there are no published papers describing normal FENO values in a large group of healthy adults.

Objective
The aim of this study was to establish adult FENO reference values according to the international guidelines.

Methods
FENO was measured in 204 healthy, non-smoking adults with normal spirometry values using the on-line single-breath technique, and the results were analysed chemiluminescently.

Results
The main result of the study was the significant difference in FENO values between men and women, thus indicating that gender-based reference FENO values are necessary. The FENO levels obtained at expiratory flows of 50 ml/s ranged from 2.6 to 28.8 ppb in men, and from 1.6 to 21.5 ppb in women.

Conclusion
We propose reference FENO values for healthy adult men and women that could be used for clinical and research purposes.
Contributions of differential p53 expression in the spontaneous immortalization of a chicken embryo fibroblast cell line
Authors: Christman Shelly A , Kong Byung-Whi , Landry Megan M , Kim Hyunggee , Foster Douglas N 
Published: August 2006

Abstract

Background
The present study was carried out to determine whether the p53 pathway played a role in the spontaneous immortalization of the SC-2 chicken embryo fibroblast (CEF) cell line that has been in continuous culture for over three years.

Results
The SC-2 cell line emerged from an extended crisis period with a considerably slower growth rate than primary CEF cells. The phenotype of the SC-2 cells changed dramatically at about passage 80, appearing smaller than at earlier passages (e.g., passage 43) and possessing a small, compact morphology. This morphological change coincided with an increase in growth rate. Passage 43 SC-2 cells expressed undetectable levels of p53 mRNA, but by passage 95, the levels were elevated compared to primary passage 6 CEF cells and similar to levels in senescent CEF cells. However, the high level of p53 mRNA detected in passage 95 SC-2 cells did not correlate to functional protein activity. The expression levels of the p53-regulated p21WAF1 gene were significantly decreased in all SC-2 passages that were analyzed. Examination of the Rb pathway revealed that E2F-1 and p15INK4b expression fluctuated with increasing passages, with levels higher in passage 95 SC-2 cells compared to primary passage 6 CEF cells.

Conclusion
The present study suggests that altered expression of genes involved in the p53 and Rb pathways, specifically, p53 and p21WAF1, may have contributed to the immortalization of the SC-2 CEF cell line.
TBLR1 regulates the expression of nuclear hormone receptor co-repressors
Authors: Zhang Xin-Min , Chang Qing , Zeng Lin , Gu Judy , Brown Stuart , Basch Ross S 
Published: August 2006

AbstractBackgroundTranscription is regulated by a complex interaction of activators and repressors. The effectors of repression are large multimeric complexes which contain both the repressor proteins that bind to transcription factors and a number of co-repressors that actually mediate transcriptional silencing either by inhibiting the basal transcription machinery or by recruiting chromatin-modifying enzymes.ResultsTBLR1 [GenBank: NM024665] is a co-repressor of nuclear hormone transcription factors. A single highly conserved gene encodes a small family of protein molecules. Different isoforms are produced by differential exon utilization. Although the ORF of the predominant form contains only 1545 bp, the human gene occupies ~200 kb of genomic DNA on chromosome 3q and contains 16 exons. The genomic sequence overlaps with the putative DC42 [GenBank: NM030921] locus. The murine homologue is structurally similar and is also located on Chromosome 3. TBLR1 is closely related (79% homology at the mRNA level) to TBL1X and TBL1Y, which are located on Chromosomes X and Y. The expression of TBLR1 overlaps but is distinct from that of TBL1. An alternatively spliced form of TBLR1 has been demonstrated in human material and it too has an unique pattern of expression. TBLR1 and the homologous genes interact with proteins that regulate the nuclear hormone receptor family of transcription factors. In resting cells TBLR1 is primarily cytoplasmic but after perturbation the protein translocates to the nucleus. TBLR1 co-precipitates with SMRT, a co-repressor of nuclear hormone receptors, and co-precipitates in complexes immunoprecipitated by antiserum to HDAC3. Cells engineered to over express either TBLR1 or N- and C-terminal deletion variants, have elevated levels of endogenous N-CoR. Co-transfection of TBLR1 and SMRT results in increased expression of SMRT. This co-repressor undergoes ubiquitin-mediated degradation and we suggest that the stabilization of the co-repressors by TBLR1 occurs because of a novel mechanism that protects them from degradation. Transient over expression of TBLR1 produces growth arrest.ConclusionTBLR1 is a multifunctional co-repressor of transcription. The structure of this family of molecules is highly conserved and closely related co-repressors have been found in all eukaryotic organisms. Regulation of co-repressor expression and the consequent alterations in transcriptional silencing play an important role in the regulation of differentiation.