bluuebunny/crossref_metadata_2025_split huggingface dataset:
Toll-Like Receptor 4 Genetic Variation and Advanced Prostate Cancer Risk
Authors: Cheng Iona , Plummer Sarah J. , Casey Graham , Witte John S. 
Published: February 2007

Abstract
Toll-like receptor 4 (TLR4) is a key innate immunity receptor that initiates an inflammatory response primarily against Gram-negative bacteria. Two recent publications reported that variants in TLR4 were associated with risk of prostate cancer. To further investigate the role of TLR4 in prostate cancer susceptibility, we identified six tagging single-nucleotide polymorphisms that comprehensively captured the common genetic variation of the locus and tested these polymorphisms in our case-control study of 1,012 men. Two single-nucleotide polymorphisms showed nominally statistically significant associations with prostate cancer risk, with the strongest (rs10759932) associated with a 4-fold increased risk of disease (P = 0.006). We estimated through permutation analysis that a similarly strong result would occur by chance 2.5% of the time. Our findings support previous studies and suggest that inherited differences in TLR4 influence prostate cancer risk. (Cancer Epidemiol Biomarkers Prev 2007;16(2):352–40)
Retention and Use of Breast Cancer Recurrence Risk Information from Genomic Tests: The Role of Health Literacy
Authors: Lillie Sarah E. , Brewer Noel T. , O'Neill Suzanne C. , Morrill Edward F. , Dees E. Claire , Carey Lisa A. , Rimer Barbara K. 
Published: February 2007

Abstract
Background: New genomic technology now allows physicians to provide women with individualized and highly accurate breast cancer recurrence risk estimates that are a key factor in adjuvant (after surgery) therapy decisions. Because these genomic tests are so new, little is known about how well patients understand the tests and their results.
Method: We interviewed 163 stage I or II breast cancer patients at a routine follow-up appointment. We assessed their health literacy (using the Rapid Estimate of Adult Learning in Medicine) as well as their knowledge of and attitudes towards a genomic test that identifies risk of recurrence in hormone receptor–positive, node–negative breast cancer (the OncoType Dx Recurrence Score).
Results: Women with lower health literacy recalled less of the information provided about the recurrence risk test than women with higher health literacy. Health literacy was not related to the amount of additional information women desired. Women with higher health literacy preferred to have a more active role in decisions about the test.
Implications: Health literacy may affect women's capacity to learn about the new genomic tests as well as their desire for informed participation in their medical care. (Cancer Epidemiol Biomarkers Prev 2007;16(2):249–55)
4-(Methylnitrosamino)-I-(3-Pyridyl)-1-Butanone Enhances the Expression of Apolipoprotein A-I and Clara Cell 17-kDa Protein in the Lung Proteomes of Rats Fed a Corn Oil Diet but not a Fish Oil Diet
Authors: Chang Sung Il , El-Bayoumy Karam , Sinha Indu , Trushin Neil , Stanley Bruce , Pittman Brian , Prokopczyk Bogdan 
Published: February 2007

Abstract
The nicotine-derived nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is one of the most potent lung carcinogens in rodents. Several epidemiologic studies indicated that the development of lung cancer in smokers is influenced by the type and amount of dietary polyunsaturated fatty acids. A high corn oil diet has been shown to increase lung tumor volume and to decrease tumor latency in rats treated with NNK. In this study, we investigated the effects of dietary polyunsaturated fatty acids in the form of corn oil or fish oil on lung proteomes in F344 rats treated with or without NNK. The fish oil diet contained 17% fish oil and 3% corn oil, and the corn oil diet contained 20% corn oil. Rats were sacrificed after 3 months, and lungs were excised. Whole lung tissue proteins were separated by two-dimensional liquid chromatography, and differentially expressed proteins were identified by trypsin digestion and tandem mass spectrometry. Apolipoprotein A-I and Clara cell 17-kDa protein were overexpressed in the lungs of rats fed corn oil diet, compared with fish oil diet. NNK further enhanced their expression in rats fed corn oil diet; this effect was not observed in animals fed fish oil diet. The results suggest that the elevated levels of apolipoprotein A-I and Clara cell 17-kDa protein may be involved in the development of NNK-induced lung cancer in rats fed a high corn oil diet. Therefore, we propose that both proteins may serve as potential biomarkers in future molecular epidemiologic and clinical chemoprevention intervention studies. (Cancer Epidemiol Biomarkers Prev 2007;16(2):228–35)
Serum Adiponectin Concentrations and Tissue Expression of Adiponectin Receptors Are Reduced in Patients with Prostate Cancer: A Case Control Study
Authors: Michalakis Konstantinos , Williams Catherine J. , Mitsiades Nicholas , Blakeman Jennifer , Balafouta-Tselenis Sofia , Giannopoulos Aris , Mantzoros Christos S. 
Published: February 2007

Abstract
Purpose: Adiponectin, an adipocyte-secreted hormone with insulin-sensitizing effects, has been inversely associated with several hormonally dependent malignancies, including breast, endometrial, and colorectal cancer. Few studies have examined serum adiponectin in relation to prostate cancer, and expression of adiponectin receptors has previously not been assessed in prostate tumors.
Experimental Design: We collected plasma samples and covariate data in the context of a case-control study of 300 Greek men, including 75 prostate cancer cases, 75 patients with benign prostatic hyperplasia (BPH), and 150 healthy controls. Prostate tissue samples were taken from 72 cases and 27 noncases and examined for relative expression of adiponectin receptors AdipoR1 and AdipoR2 using immunohistochemistry.
Results: Prostate cancer patients had significantly lower plasma adiponectin concentrations as compared with men with BPH and healthy controls (7.4 ± 5.0 versus 11.5 ± 6.4 and 12.8 ± 8.0 ng/mL, respectively). Men in the top two quartiles of adiponectin had a 71% to 73% reduced risk of prostate cancer as compared with men in the lowest quartile after adjusting for age, body mass index, and additional potential confounders. We found no similar relationship between adiponectin and risk of BPH. Results from immunohistochemistry experiments show weaker expression of adiponectin receptors AdipoR1 and AdipoR2 in cancerous versus healthy prostate tissue.
Conclusions: Higher serum adiponectin is associated with a marked reduction in risk of prostate cancer, but not BPH, independently of other risk factors. Malignant prostate tissue samples have reduced expression of adiponectin receptors as compared with benign prostate tissue. These results support a role for adiponectin in the pathogenesis of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(2):308–13)
Changes in 2-Hydroxyestrone and 16α-Hydroxyestrone Metabolism with Flaxseed Consumption: Modification by COMT and CYP1B1 Genotype
Authors: McCann Susan E. , Wactawski-Wende Jean , Kufel Kari , Olson James , Ovando Bladimir , Kadlubar Susan Nowell , Davis Warren , Carter Lisa , Muti Paola , Shields Peter G. , Freudenheim Jo L. 
Published: February 2007

Abstract
Consumption of the phytoestrogen lignans, structurally similar to estrogen, has been associated with alterations in gene expression and estrogen metabolism. Furthermore, lignan consumption, subsequent changes in metabolizing enzyme expression, and genetic variability in these enzymes may alter estrogen metabolism and modify disease risk. Therefore, we investigated the effect of flaxseed on hydroxyestrone metabolite excretion by catechol-O-methyltransferase (COMT) and cytochrome P450 1B1 (CYP1B1) genotype. We conducted an intervention among 132 healthy, postmenopausal women, ages 46 to 75 years. Participants consumed 10 g ground flaxseed daily for 7 consecutive days. Blood and urine samples were collected at baseline and after the 7-day intervention. COMT Val158Met and CYP1B1 Leu432Val genotypes were determined using PCR-RFLP methods. Urinary 2-hydroxyestrone (2OHE1) and 16α-hydroxyestrone (16OHE1) were quantified by ELISA assay. The effect of genotype on intervention-related changes in estrogen metabolites was assessed with the Kruskal-Wallis test. Compared with baseline levels, postintervention levels of urinary 2OHE1 (ng/mg creatinine; mean ± SD, 16.1 ± 10.6 versus 9.3 ± 6.9, postintervention and baseline, respectively; P &lt; 0.01) and 2OHE1/16OHE1 ratios (mean ± SD, 2.73 ± 1.47 versus 1.54 ± 0.75, postintervention and baseline, respectively; P &lt; 0.01) were significantly higher. The change in 2OHE1/16OHE1 increased with increasing numbers of variant alleles for COMT (mean change: Val/Val, 0.90; Val/Met, 1.15; and Met/Met, 1.50; P = 0.17, Kruskal-Wallis) and especially CYP1B1 (mean change: Leu/Leu, 0.89; Leu/Val, 1.32; and Val/Val, 1.51; P = 0.04, Kruskal-Wallis). Our findings suggest that variation in hormone-related genes may modify the effect of dietary lignan exposures on estrogen metabolism. (Cancer Epidemiol Biomarkers Prev 2007;16(2):256–62)
Genetic Variation in the Premature Aging Gene WRN: A Case-Control Study on Breast Cancer Susceptibility
Authors: Ding Shian-ling , Yu Jyh-Cherng , Chen Shou-Tung , Hsu Giu-Cheng , Shen Chen-Yang 
Published: February 2007

Abstract
The high risk of developing cancer seen in human genetic diseases that resemble accelerated aging provides support for a tumorigenic contribution of the mechanisms and genes responsible for regulating life span and aging. We therefore speculated that the WRN gene (encoding RECQL2, a DNA helicase), the germline mutation of which causes the progeroid disorder Werner syndrome, may be associated with breast tumorigenesis. This hypothesis was tested in this case-control study of 935 primary breast cancer patients and 1,545 healthy controls by examining single-nucleotide polymorphisms (SNPs) in WRN. We were also interested in knowing whether any identified association between WRN and breast cancer was modified by reproductive risk factors reflecting susceptibility to estrogen exposure. Our hypothesis is that because estrogen is known to promote breast cancer development via its mitogenic effect leading to cell proliferation, and because WRN is an essential gene, as its suboptimal function leads to a severe decrease in proliferation, estrogen stimulation may have a protective effect on cells harboring variant WRN, allowing them to survive and proliferate for the prolonged period needed for tumor formation. Support for this hypothesis came from the following observations: (a) one SNP in WRN was significantly associated with breast cancer risk (P = 0.002); (b) haplotype and diplotype analyses, based on different combinations of multiple SNPs in WRN, revealed a strong association with breast cancer risk; (c) this association between risk and putative high-risk genotypes was stronger and more significant in women with a longer interval between menarche and first full-term pregnancy; and (d) the protective effect conferred by having a higher number of full-term pregnancy was only significant in women with homozygous or heterozygous wild-type WRN genotypes. This study provides support for the tumorigenic role of WRN in breast cancer development, suggesting that breast cancer can be driven by the aging associated with variant WRN, the tumorigenic contribution of which might be enhanced as a result of increased cell growth due to estrogen exposure. (Cancer Epidemiol Biomarkers Prev 2007;16(2):263–9)
Interaction of Factors Related to the Metabolic Syndrome and Vitamin D on Risk of Prostate Cancer
Authors: Tuohimaa Pentti , Tenkanen Leena , Syvälä Heimo , Lumme Sonja , Hakulinen Timo , Dillner Joakim , Hakama Matti 
Published: February 2007

AbstractBackground: Factors related to the metabolic syndrome and low levels of vitamin D have been implicated as risk factors for prostate cancer. Insofar, no studies have assessed their joint effects on prostate cancer risk.Methods: We studied (a) the associations of vitamin D with the metabolic syndrome factors body mass index, systolic and diastolic blood pressure, and high-density lipoprotein cholesterol (HDL-C) and (b) the prostate cancer risk associated with these factors and especially their joint effects with vitamin D on risk of prostate cancer. We did a longitudinal nested case-control study on 132 prostate cancer cases and 456 matched controls from a cohort of 18,939 Finnish middle-aged men from the Helsinki Heart Study. The odds ratios (OR) of prostate cancer were assessed via conditional logistic regression analysis.Results: Apart from HDL-C, there was no linear association between the metabolic syndrome factors and vitamin D levels. In univariate analysis, men in the highest quartiles of body mass index (&gt;28 kg/m2) and systolic blood pressure (&gt;150 mmHg) showed a modest increase in risks of prostate cancer, with ORs of 1.37 (P = 0.16) and 1.53 (P = 0.05) when compared with the three lower quartiles, but low HDL-C entailed no prostate cancer risk. However, with all three factors present, the OR was 3.36 (P = 0.02), and jointly with low vitamin D (≤40 nmol/L), the OR was 8.03 (P = 0.005) compared with those with no metabolic syndrome factors and intermediate levels of vitamin D. There was an interaction between vitamin D and the metabolic syndrome factors so that a clustering of these factors entailed high risk of prostate cancer but only if vitamin D level was low (≤40 nmol/L). If it was at intermediate levels, the metabolic syndrome factors entailed no prostate cancer risk.Conclusions: We conclude that the prostate cancer risk associated with factors related to the metabolic syndrome is strongly conditioned by levels of vitamin D. (Cancer Epidemiol Biomarkers Prev 2007;16(2):302–7)
T cell–dependent survival of CD20+ and CD20− plasma cells in human secondary lymphoid tissue
Authors: Withers David R. , Fiorini Claudia , Fischer Randy T. , Ettinger Rachel , Lipsky Peter E. , Grammer Amrie C. 
Published: February 2007

AbstractThe signals mediating human plasma cell survival in vivo, particularly within secondary lymphoid tissue, are unclear. Human tonsils grafted into immunodeficient mice were therefore used to delineate the mechanisms promoting the survival of plasma cells. Tonsillar plasma cells were maintained within the grafts and the majority were nonproliferating, indicating a long-lived phenotype. A significant depletion of graft plasma cells was observed after anti-CD20 treatment, consistent with the expression of CD20 by most of the cells. Moreover, anti-CD52 treatment caused the complete loss of all graft lymphocytes, including plasma cells. Unexpectedly, anti-CD3, but not anti-CD154, treatment caused the complete loss of plasma cells, indicating an essential role for T cells, but not CD40-CD154 interactions in plasma cell survival. The in vitro coculture of purified tonsillar plasma cells and T cells revealed a T-cell survival signal requiring cell contact. Furthermore, immunofluorescence studies detected a close association between human plasma cells and T cells in vivo. These data reveal that human tonsil contains long-lived plasma cells, the majority of which express CD20 and can be deleted with anti-CD20 therapy. In addition, an important role for contact-dependent interactions with T cells in human plasma cell survival within secondary lymphoid tissue was identified.
Monosomy 7 and deletion 7q in children and adolescents with acute myeloid leukemia: an international retrospective study
Authors: Hasle Henrik , Alonzo Todd A. , Auvrignon Anne , Behar Catherine , Chang Myron , Creutzig Ursula , Fischer Alexandra , Forestier Erik , Fynn Alcira , Haas Oskar A. , Harbott Jochen , Harrison Christine J. , Heerema Nyla A. , van den Heuvel-Eibrink Marry M. , Kaspers Gertjan J. L. , Locatelli Franco , Noellke Peter , Polychronopoulou Sophia , Ravindranath Yaddanapudi , Razzouk Bassem , Reinhardt Dirk , Savva Natalia N. , Stark Batia , Suciu Stefan , Tsukimoto Ichiro , Webb David K. , Wojcik Dorora , Woods William G. , Zimmermann Martin , Niemeyer Charlotte M. , Raimondi Susana C. 
Published: February 2007

AbstractMonosomy 7 (−7) and deletion 7q \del(7q)] are rare in childhood acute myeloid leukemia (AML). We retrospectively collected data on 258 children with AML or refractory anemia with excess blasts in transformation (RAEB-T) and −7 or del(7q) with or without other cytogenetic aberrations \± other]. Karyotypes included −7 (n = 90), −7 other (n = 82), del(7q) (n = 21), and del(7q) other (n = 65). Complete remission (CR) was achieved in fewer patients with −7 ± other compared with del(7q) ± other (61% versus 89%, P < .001). Overall, the 5-year survival rate was 39% (SE, 3%). Survival was superior in del(7q) ± other compared with −7 ± other (51% versus 30%, P < .01). Cytogenetic aberrations considered favorable in AML \t(8;21)(q22;q22), inv(16)(p13q22), t(15;17)(q22;q21), t(9;11)(p22;q23)] (n = 24) were strongly associated with del(7q) and a higher 5-year survival rate compared with del(7q) without favorable cytogenetics (75% versus 46%, P = .03). Patients with −7 and inv(3),−5/del(5q), or + 21 had a 5-year survival rate of 5%. Stem cell transplantation analyzed as a time-dependent variable had no impact on overall survival. However, patients not achieving CR had a 31% survival rate after stem cell transplantation. Childhood AML with chromosome 7 aberrations represents a heterogeneous group of disorders with additional cytogenetic aberrations having a major prognostic impact which should be reflected in future risk-group stratification.
Bortezomib enhances dendritic cell (DC)–mediated induction of immunity to human myeloma via exposure of cell surface heat shock protein 90 on dying tumor cells: therapeutic implications
Authors: Spisek Radek , Charalambous Anna , Mazumder Amitabha , Vesole David H. , Jagannath Sundar , Dhodapkar Madhav V. 
Published: February 2007

AbstractMost anticancer chemotherapies are immunosuppressive and induce nonimmunogenic tumor cell death. Bortezomib, a specific inhibitor of 26S proteasome, has shown clinical activity in several human tumors, including myeloma. Here we show that the uptake of human myeloma cells by dendritic cells (DCs) after tumor cell death by bortezomib, but not γ irradiation or steroids, leads to the induction of antitumor immunity, including against primary tumor cells, without the need for any additional adjuvants. The delivery of activating signal from bortezomib-killed tumor cells to DCs depends on cell-cell contact between DCs and dying tumor cells and is mediated by bortezomib-induced exposure of heat shock protein 90 (hsp90) on the surface of dying cells. The combination of bortezomib and geldanamycin (an hsp90 inhibitor) leads to greater apoptosis of tumor cells but abrogates their immunogenicity. These data identify drug-induced exposure of endogenous heat shock proteins on the surface of dying cells as a mechanism of immunogenic death of human tumors. Specific targeting of bortezomib to tumors may enhance their immunogenicity and the induction of antitumor immunity.
Black tea prevents cigarette smoke-induced apoptosis and lung damage
Authors: Banerjee Shuvojit , Maity Palas , Mukherjee Subhendu , Sil Alok K , Panda Koustubh , Chattopadhyay Dhrubajyoti , Chatterjee Indu B 
Published: February 2007

Abstract

Background
Cigarette smoking is a major cause of lung damage. One prominent deleterious effect of cigarette smoke is oxidative stress. Oxidative stress may lead to apoptosis and lung injury. Since black tea has antioxidant property, we examined the preventive effect of black tea on cigarette smoke-induced oxidative damage, apoptosis and lung injury in a guinea pig model.

Methods
Guinea pigs were subjected to cigarette smoke exposure from five cigarettes (two puffs/cigarette) per guinea pig/day for seven days and given water or black tea to drink. Sham control guinea pigs were exposed to air instead of cigarette smoke. Lung damage, as evidenced by inflammation and increased air space, was assessed by histology and morphometric analysis. Protein oxidation was measured through oxyblot analysis of dinitrophenylhydrazone derivatives of the protein carbonyls of the oxidized proteins. Apoptosis was evidenced by the fragmentation of DNA using TUNEL assay, activation of caspase 3, phosphorylation of p53 as well as over-expression of Bax by immunoblot analyses.

Results
Cigarette smoke exposure to a guinea pig model caused lung damage. It appeared that oxidative stress was the initial event, which was followed by inflammation, apoptosis and lung injury. All these pathophysiological events were prevented when the cigarette smoke-exposed guinea pigs were given black tea infusion as the drink instead of water.

Conclusion
Cigarette smoke exposure to a guinea pig model causes oxidative damage, inflammation, apoptosis and lung injury that are prevented by supplementation of black tea.
Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 cooperatively contribute to the cutaneous Arthus reaction
Authors: Orito Hidemitsu , Fujimoto Manabu , Ishiura Nobuko , Yanaba Koichi , Matsushita Takashi , Hasegawa Minoru , Ogawa Fumihide , Takehara Kazuhiko , Sato Shinichi 
Published: February 2007

AbstractImmune complex (IC)-induced inflammation is mediated by inflammatory cell infiltration, a process that is highly regulated by expression of multiple adhesion molecules. The roles and interactions of ICAM-1 and VCAM-1, the major regulators of leukocyte firm adhesion, were examined in the cutaneous reverse-passive Arthus reaction using ICAM-1-deficient (ICAM-1−/−) mice and blocking mAb against VCAM-1. Within 8 h, IC challenge of wild-type mice induced edema, hemorrhage, interstitial accumulation of neutrophils and mast cells, as well as production of TNF-α and IL-6. All of these inflammatory parameters were reduced significantly in ICAM-1−/− mice. The blockade of VCAM-1 in wild-type mice did not affect any inflammatory parameters. In contrast, ICAM-1−/− mice treated with anti-VCAM-1 mAb had significantly reduced edema, hemorrhage, and neutrophil infiltration. Furthermore, VCAM-1 blockade in ICAM-1−/− mice suppressed cutaneous TNF-α and IL-6 production. Thus, VCAM-1 plays a complementary role to ICAM-1 in the cutaneous Arthus reaction by regulating leukocyte accumulation and proinflammatory cytokine production.