bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dietary Flavonoids and the Risk of Colorectal Cancer
Authors: Theodoratou Evropi , Kyle Janet , Cetnarskyj Roseanne , Farrington Susan M. , Tenesa Albert , Barnetson Rebecca , Porteous Mary , Dunlop Malcolm , Campbell Harry 
Published: April 2007

Abstract
In vitro and in vivo laboratory data point to chemoprotective effects of flavonoids on colorectal cancer. However, there has been limited epidemiologic research on the dietary intake of flavonoids and risk of colorectal cancer. Recent expansions of dietary databases to include flavonoid data now make such studies feasible. Association between the six main classes of flavonoids and the risk of colorectal cancer was examined using data from a national prospective case-control study in Scotland, including 1,456 incident cases and 1,456 population-based controls matched on age, sex, and residence area. Dietary, including flavonoid data, were obtained from a validated, self-administered food frequency questionnaire. Risk of colorectal cancer was estimated using conditional logistic regression models in the whole sample and stratified by sex, smoking status, and cancer site and adjusted for established and putative risk factors. After energy adjustment, reductions in colorectal cancer risk associated with the highest quartiles of intake (versus the lowest quartile) were 27% for flavonols [odds ratio (OR), 0.73; Ptrend = 0.012], 32% for quercetin (OR, 0.68; Ptrend = 0.001), 32% for catechin (OR, 0.68; Ptrend &lt; 0.0005); 26% for epicatechin (OR, 0.74; Ptrend = 0.019), and 22% for procyanidins (OR, 0.78; Ptrend = 0.031). The significant dose-dependent reductions in colorectal cancer risk that were associated with increased consumption of flavonols, quercetin, catechin, and epicatechin remained robust after controlling for overall fruit and vegetable consumption or for other flavonoid intake. The risk reductions were greater among nonsmokers, but no interaction beyond a multiplicative effect was present. Sex-specific or cancer-type differences were not observed. No risk reductions were associated with intake of flavones (Ptrend = 0.64), flavonones (Ptrend = 0.22), and phytoestrogens (Ptrend = 0.26). This was the first of several a priori hypotheses to be tested in this large study and showed strong and linear inverse associations of flavonoids with colorectal cancer risk. (Cancer Epidemiol Biomarkers Prev 2007;16(4):684–93)
Age at Menarche and Menopause and Breast Cancer Risk in the International BRCA1/2 Carrier Cohort Study
Authors: Chang-Claude Jenny , Andrieu Nadine , Rookus Matti , Brohet Richard , Antoniou Antonis C. , Peock Susan , Davidson Rosemarie , Izatt Louise , Cole Trevor , Noguès Catherine , Luporsi Elisabeth , Huiart Laetitia , Hoogerbrugge Nicoline , Van Leeuwen Flora E. , Osorio Ana , Eyfjord Jorunn , Radice Paolo , Goldgar David E. , Easton Douglas F. ,   Epidemiological Study of Familial Breast Cancer (EMBRACE), Gene Etude Prospective Sein Ovaire (GENEPSO), Genen Omgeving studie van de werkgroep Hereditiair Borstkanker Onderzoek Nederland (GEO-HEBON), the International BRCA1/2 Carrier Cohort Study (IBCCS) collaborators group
Published: April 2007

Abstract
Background: Early menarche and late menopause are important risk factors for breast cancer, but their effects on breast cancer risk in BRCA1 and BRCA2 carriers are unknown.
Methods: We assessed breast cancer risk in a large series of 1,187 BRCA1 and 414 BRCA2 carriers from the International BRCA1/2 Carrier Cohort Study. Rate ratios were estimated using a weighted Cox-regression approach.
Results: Breast cancer risk was not significantly related to age at menopause {hazard ratio [HR] for menopause below age 35 years, 0.60 [95% confidence interval (95% CI), 0.25-1.44]; 35 to 40 years, 1.15 [0.65-2.04]; 45 to 54 years, 1.02 [0.65-1.60]; ≥55 years, 1.12 [0.12-5.02], as compared with premenopausal women}. However, there was some suggestion of a reduction in risk after menopause in BRCA2 carriers. There was some evidence of a protective effect of oophorectomy (HR, 0.56; 95% CI, 0.29-1.09) and a significant trend of decreasing risk with increasing time since oophorectomy, but no apparent effect of natural menopause. There was no association between age at menarche and breast cancer risk, nor any apparent association with the estimated total duration of breast mitotic activity.
Conclusions: These results are consistent with other observations suggesting a protective effect of oophorectomy, similar in relative effect to that in the general population. The absence of an effect of age at natural menopause is, however, not consistent with findings in the general population and may reflect the different natural history of the disease in carriers. (Cancer Epidemiol Biomarkers Prev 2007;16(4):740–6)
Insulin Resistance-Related Genes and Advanced Left-Sided Colorectal Adenoma
Authors: Gunter Marc J. , Hayes Richard B. , Chatterjee Nilanjan , Yeager Meredith , Welch Robert , Schoen Robert E. , Yakochi Lance , Schatzkin Arthur , Peters Ulrike 
Published: April 2007

Abstract
Background: Insulin resistance has been linked with colorectal neoplasia through a number of mechanistic and observational studies. Allelic variants of genes encoding components of the insulin pathway, including insulin (INS), insulin receptor (INSR), and insulin receptor substrate-1 and insulin receptor substrate-2 (IRS1 and IRS2) have been associated with hyperinsulinemia and insulin resistance and may, therefore, predict susceptibility to colorectal neoplasia.
Methods: We investigated whether single nucleotide polymorphisms (SNP) in the INS, INSR, IRS1, and IRS2 genes are associated with risk of advanced left-sided colorectal adenoma, a cancer precursor. We analyzed 20 SNPs in a largely Caucasian study population comprising 766 cases with advanced adenomas of the distal colon and 771 controls, all of whom had undergone flexible sigmoidoscopy as part of the screening arm of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.
Results: Overall, we found limited evidence for a role of gene variants of the insulin signaling pathway and prevalence of advanced colorectal adenoma. We observed a statistically significant interaction between INSR genotypes and body mass index (BMI) with colorectal adenoma prevalence (P value for global test = 0.003) and suggestion of an interaction between INSR genotypes and glycemic load (P value for global test = 0.06); however, exploration of the interaction of BMI and glycemic load with the individual SNPs in INSR did not suggest a single SNP that may explain the significance of these global tests of interaction and did not yield any consistent patterns.
Conclusion: These findings do not provide strong evidence for associations between polymorphic variation in genes of the insulin signaling pathway and advanced left-sided colorectal adenoma. Evidence for interaction between INSR variants and BMI and glycemic load for risk of advanced left-sided colorectal adenoma requires independent confirmation, and genotyping of INSR across a broader region and at greater density may be necessary to fully elucidate the nature of these interactions. (Cancer Epidemiol Biomarkers Prev 2007;16(4):703–8)
Clinical and Biological Activity of Soy Protein Powder Supplementation in Healthy Male Volunteers
Authors: Goodin Susan , Shen Francisco , Shih Weichung J. , Dave Nisha , Kane Michael P. , Medina Patrick , Lambert George H. , Aisner Joseph , Gallo Michael , DiPaola Robert S. 
Published: April 2007

Abstract
Purpose: To determine if a commonly used soy protein supplement exhibits biological activity in vivo and in vitro, we evaluated an over-the-counter soy protein powder supplement using blood from healthy male volunteers and in an estrogen receptor in vitro assay.
Subjects and Methods: We recruited healthy male volunteers 18 years of age or older that were in good health. Treatment consisted of consuming two scoops (56 g) of pure soy protein powder (Puritan's Pride, Oakdale, NY) daily for 28 days. Serum testosterone and luteinizing hormone (LH) levels were collected on days −7, 0, 14, and 28 of therapy, and day 42. A reporter estrogen receptor (ER) assay was used to determine the effect on ER-β and ER-α in vitro.
Results: Twelve subjects were enrolled with a mean age of 32.25 years (range 25 to 47). Serum testosterone decreased 19%(±22%) during the 4-week use of soy protein powder (P = 0.021) and increased within 2 weeks after we discontinued soy protein powder. Serum LH concentrations decreased during the 4-week use of soy protein powder then increased within 2 weeks after we stopped the soy protein powder, but the changes did not reach statistical significance (P = 0.20). Soy protein powder was found to induce agonist activity to ER-β using a reporter estrogen receptor assay in yeast.
Conclusion: Soy protein powder decreases serum testosterone levels in healthy men and acts as an ER-β agonist; the significance of this biological effect with respect to cancer prevention needs further study. (Cancer Epidemiol Biomarkers Prev 2007;16(4):829–33)
Mouthwash as a Low-Cost and Safe Specimen Transport Medium for Human Papillomavirus DNA Testing of Cervicovaginal Specimens
Authors: Castle Philip E. , Sadorra Mark , Garcia Francisco A.R. , Cullen Allison P. , Lorincz Attila T. , Mitchell Amy L. , Whitby Denise , Chuke Ronald , Kornegay Janet R. 
Published: April 2007

Abstract
The usefulness of mouthwash as a transport medium for cervical specimens for carcinogenic human papillomavirus (HPV) DNA testing has not been evaluated. Two cervical specimens were collected from each of 34 patients, with one placed in mouthwash (Scope, Proctor and Gamble, Inc.) and the other in a liquid cytology medium commonly used for HPV DNA testing in alternating order. Paired specimens were tested by a PCR assay for carcinogenic HPV and a PCR HPV genotyping assay for 37 HPV types at 0, 3, and 6 weeks after collection; the results of the HPV genotyping assay were categorized into HPV risk groups according to cancer risk (HPV-16 &gt; HPV-18 &gt; other carcinogenic HPV types &gt; noncarcinogenic HPV types &gt; negative). After 4 months of storage, specimens were tested using a second, non-PCR test for carcinogenic HPV. We observed a ≥94% total agreement and κ values of ≥0.88 between media at each time point for PCR-detected carcinogenic HPV. We observed a ≥74% total agreement, ≥0.62 unweighted κ, and ≥0.75 linearly weighted κ between media at each time point for PCR-detected HPV cancer risk category. Finally, we observed an 88% total agreement and κ of 0.77 between media for carcinogenic HPV detection using a second test after 4 months of storage. We suggest that mouthwash might be used as a low-cost, safe, nonflammable storage and transport medium for cervical specimens for HPV DNA testing in cervical cancer screening programs. (Cancer Epidemiol Biomarkers Prev 2007;16(4):840–3)
Telomere Length, Cigarette Smoking, and Bladder Cancer Risk in Men and Women
Authors: McGrath Monica , Wong Jason Y.Y. , Michaud Dominique , Hunter David J. , De Vivo Immaculata 
Published: April 2007

Abstract
Truncated telomeres are among the defining characteristics of most carcinomas. Given the role of telomeres in tumorigenesis, we reasoned that constitutionally short telomeres might be associated with an increased risk of bladder cancer. Using quantitative real-time PCR, we measured relative telomere length in bladder cancer cases and healthy controls and evaluated the association between telomere length, cigarette smoking, and bladder cancer risk in a case-control study nested within the Health Professionals Follow-up Study and a case-control study nested within the Nurses' Health Study. Telomeres were significantly shorter in bladder cancer cases (n = 184) than in controls (n = 192). The mean relative telomere length in cases was 0.23 (SD, 0.16) versus 0.27 (SD, 0.15) in controls (P = 0.001). The adjusted odds ratio for bladder cancer was 1.88 (95% confidence interval, 1.05, 3.36) for individuals in the quartile with the shortest telomeres as compared with individuals in the quartile with the longest telomeres (Ptrend = 0.006). We observed a statistically significant difference in telomere length among men and women (P &lt; 0.001); however, the interaction between gender, telomere length, and bladder cancer risk was not significant. We also observed a significant difference in telomere length across categories of pack-years of smoking (P = 0.01). These findings suggest that truncated telomeres are associated with an increased risk of bladder cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(4):815–9)
Confirmation of a Positive Association between Prostate Cancer Risk and a Locus at Chromosome 8q24
Authors: Suuriniemi Miia , Agalliu Ilir , Schaid Daniel J. , Johanneson Bo , McDonnell Shannon K. , Iwasaki Lori , Stanford Janet L. , Ostrander Elaine A. 
Published: April 2007

Abstract
Background: Family-based linkage studies, association studies, and studies of tumors have highlighted human chromosome 8q as a genomic region of interest for prostate cancer susceptibility loci. Recently, a locus at 8q24, characterized by both a single nucleotide polymorphism (SNP) and a microsatellite marker, was shown to be associated with prostate cancer risk in Icelandic, Swedish, and U.S. samples. Although the data were provocative, the U.S. samples were not population based, which precludes assessment of the potential contribution of this locus to prostate cancer incidence in the United States.
Methods: We analyzed both markers in a population-based, case-control study of middle-aged men from King County, Washington.
Results: Overall, there was a significant positive association between the A allele of the SNP rs1447295 and prostate cancer risk [odds ratio, 1.4; 95% confidence interval (95% CI), 1.1-2.0] but no significant association with the microsatellite DG8S737. However, significant associations were observed for both markers in men with high Gleason scores. Adjusting for age, first-degree family history of prostate cancer, and prostate cancer screening history, the adjusted odds ratios were 1.4 (95% CI, 1.1-1.8) for the A allele of the SNP and 1.9 (95% CI, 1.2-2.8) for the −10 allele of the microsatellite.
Conclusions: These data suggest that the locus on chromosome 8q24 harbors a genetic variant associated with prostate cancer and that the microsatellite marker is a stronger risk factor for aggressive prostate cancers defined by poorly differentiated tumor morphology. (Cancer Epidemiol Biomarkers Prev 2007;16(4):809–14)
PECAM-1: a multifaceted regulator of megakaryocytopoiesis
Authors: Wu Yue , Welte Thomas , Michaud Michael , Madri Joseph A. 
Published: April 2007

Abstract
PECAM-1 (CD31) knockout (KO) mice exhibit excessive megakaryocytopoiesis accompanied by increased numbers of megakaryocytes associated with the stromal niche rather than the vascular niche. During earlier stages of megakaryocytopoiesis in KO marrow, an expanded Lin−Sca-1+ c-kit+ hematopoietic stem cell (HSC) population and increased quiescent Lin− progenitor pool were identified. During the later stages of megakaryocytopoiesis, CD31KO megakaryocytes exhibited abnormal adhesion/transmigration behaviors. Lastly, KO animals exhibited excessive splenic extramedullary megakaryocytopoiesis, which likely compensates for the impaired marrow megakaryocytopoiesis, resulting in normal peripheral platelet number. Thus, PECAM-1 modulates megakaryocytopoiesis in a hierarchic manner, functioning as a thermostat to “fine-tune” megakaryocytopoiesis.
Endothelial potential of human embryonic stem cells
Authors: Levenberg Shulamit , Zoldan Janet , Basevitch Yaara , Langer Robert 
Published: April 2007

Abstract
Growing interest in using endothelial cells for therapeutic purposes has led to exploring human embryonic stem cells as a potential source for endothelial progenitor cells. Embryonic stem cells are advantageous when compared with other endothelial cell origins, due to their high proliferation capability, pluripotency, and low immunogenity. However, there are many challenges and obstacles to overcome before the vision of using embryonic endothelial progenitor cells in the clinic can be realized. Among these obstacles is the development of a productive method of isolating endothelial cells from human embryonic stem cells and elucidating their differentiation pathway. This review will focus on the endothelial potential of human embryonic stem cells that is described in current studies, with respect to the differentiation of human embryonic stem cells to endothelial cells, their isolation, and their characterization.
High PR3 or ELA2 expression by CD34+ cells in advanced-phase chronic myeloid leukemia is associated with improved outcome following allogeneic stem cell transplantation and may improve PR1 peptide–driven graft-versus-leukemia effects
Authors: Yong Agnes S. M. , Rezvani Katayoun , Savani Bipin N. , Eniafe Rhoda , Mielke Stephan , Goldman John M. , Barrett A. John 
Published: April 2007

AbstractThe primary granule proteins elastase (ELA2) and proteinase 3 (PR3) both contain the nonapeptide PR1, which can induce cytotoxic T lymphocyte (CTL) responses against chronic myeloid leukemia (CML) cells. To investigate whether eradication of CML after allogeneic stem cell transplantation (SCT) was influenced by PR3 and ELA2 gene expression or PR1-specific CTL responses, we studied cells from 87 CML patients and 27 HLA-A*0201+ donors collected prior to T-cell–depleted HLA-identical sibling SCT. For patients in advanced phase (AdP), a higher expression of both PR3 and ELA2 in CD34+ progenitors before SCT was associated with a lower incidence of relapse-related death, improved leukemia-free survival (LFS), and overall survival (OS); in chronic phase patients, no differences were observed. PR1-CTL responses were detected in 7 of 27 HLA-identical sibling donors, and associated with improved LFS and OS after SCT on follow-up. PR1-CTL responses detected in 7 of 28 CML patients before transplantation were not predictive of outcome and correlated inversely with PR3 and ELA2 expression. These findings suggest that assessment of PR3 and ELA2 expression in leukemic progenitors is useful for predicting posttransplantation outcome in AdP patients undergoing SCT. The presence of a donor immune response against PR1 may be advantageous and could be exploited therapeutically.
Regulatory function of CD4+CD25+ T cells from Class II MHC-deficient mice in contact hypersensitivity responses
Authors: Kish Danielle D , Gorbachev Anton V , Fairchild Robert L 
Published: April 2007

AbstractContact hypersensitivity (CHS) is a CD8+ T cell-mediated, inflammatory response to hapten sensitization and challenge of the skin. During sensitization, the magnitude and duration of hapten-specific CD8+ T cell expansion in the skin-draining lymph nodes (LN) are restricted by CD4+CD25+ T regulatory cells (Treg). The regulation of hapten-specific CD8+ T cell priming in Class II MHC-deficient (MHC–/–) mice was investigated. Although hapten-specific CD8+ T cell priming and CHS responses were elevated in Class II MHC–/– versus wild-type mice, presensitization depletion of CD4+ or CD25+ cells in Class II MHC–/– mice further increased CD8+ T cell priming and the elicited CHS response. Flow cytometry analyses of LN cells from Class II MHC–/– mice revealed a population of CD4+ T cells with a majority expressing CD25. Forkhead box p3 mRNA was expressed in LN cells from Class II MHC–/– and was reduced to background levels by depletion of CD4+ or CD25+ cells. Isolated CD4+CD25+ T cells from wild-type and Class II MHC–/– mice limited in vitro proliferation of alloantigen- and hapten-specific T cells to antigen-presenting stimulator cells. These results identify functional CD4+CD25+ Treg in Class II MHC–/– mice, which restrict hapten-specific CD8+ T cell priming and the magnitude of CHS responses.
Circulating CD14−CD36+ peripheral blood mononuclear cells constitutively produce interleukin-10
Authors: Barrett Lisa , Dai Chunming , Gamberg Jane , Gallant Maureen , Grant Michael 
Published: April 2007

AbstractThe impact of immune regulatory imbalance covers surprising physiological breadth. Although dominance of anti-inflammatory cytokines such as IL-10 is associated with reduced immune responsiveness and susceptibility to persistent infection, conditions such as cardiovascular disease and diabetes are linked to chronic inflammation and lower IL-10 levels. An appropriate threshold for immune activation is critical for optimal protection from infection and conversely, from short- and long-term side-effects of immune effector mechanisms. To assess the possibility that IL-10 plays a role in setting this threshold and that healthy maintenance of immune silence may involve low-level immune suppression, we sought out and characterized human peripheral blood cells constitutively producing the immunosuppressive cytokine IL-10. We determined the surface phenotype of circulating PBMC constitutively producing IL-10 by surface and intracellular flow cytometry and visualized their ultrastructure by electron microscopy. The frequency of IL-10-producing and -secreting cells was estimated by ELISPOT and flow cytometry. Up to 1% of PBMC constitutively produce IL-10. These CD14−CD36+CD61+ nonadherent cells expressed general markers of hematopoietic and progenitor cells (CD45 and CD7) but no stem cell, T cell, B cell, NK cell, monocytes or dendritic cell markers. Inflammation-associated TLRs were also absent. The IL-10-producing cells had prominent nuclei, multiple mitochondria, and abundant rough endoplasmic reticulum. Healthy individuals have PBMC constitutively producing IL-10. Although the lineage of these cells remains unclear, their properties and frequency suggest a potential role in homeostatic or innate immune suppression.
Understanding of Prognosis Among Parents of Children With Cancer: Parental Optimism and the Parent-Physician Interaction
Authors: Mack Jennifer W. , Cook E. Francis , Wolfe Joanne , Grier Holcombe E. , Cleary Paul D. , Weeks Jane C. 
Published: April 2007

Purpose Patients often overestimate their chances of surviving cancer. Factors that contribute to accurate understanding of prognosis are not known. We assessed understanding of likelihood of cure and functional outcome among parents of children with cancer and sought to identify factors that place parents at risk for overly optimistic beliefs about prognosis. Patients and Methods We conducted a cross-sectional survey of 194 parents of children with cancer (response rate, 70%) who were treated at the Dana-Farber Cancer Institute and Children's Hospital in Boston, MA, and the children's physicians. Parent and physician expectations for likelihood of cure and functional outcome were compared. In 152 accurate or optimistic parents, we determined factors associated with accurate understanding of likelihood of cure compared with optimism. Results The majority of parents (61%) were more optimistic than physicians about the likelihood of cure. Parents' beliefs about other outcomes of cancer treatment were similar (quality-of-life impairment, P = .70) or more pessimistic (physical impairment, P = .01; intellectual impairment, P = .01) than physicians' beliefs. Parents and physicians were more likely to agree about chances of cure when physicians had confidence in knowledge of prognosis (odds ratio [OR] = 2.55, P = .004) and allowed parents to take their preferred decision-making role (OR = 1.89, P = .019). Conclusion Parents of children with cancer are overly optimistic about chances of cure but not about other outcomes of cancer therapy. Parents tend to be overly optimistic about cure when physicians have little confidence and when the decision-making process does not meet parents' preferences. These findings suggest that physicians are partly responsible for parents' unrealistic expectations about cure.