bluuebunny/crossref_metadata_2025_split huggingface dataset:
GST, NAT, SULT1A1, CYP1B1 genetic polymorphisms, interactions with environmental exposures and bladder cancer risk in a high‐risk population
Authors: Hung Rayjean J. , Boffetta Paolo , Brennan Paul , Malaveille Christian , Hautefeuille Agnès , Donato Francesco , Gelatti Umberto , Spaliviero Massimiliano , Placidi Donatella , Carta Angela , Scotto di Carlo Antonio , Porru Stefano 
Published: April 2004

AbstractTobacco smoking and occupation are major risk factors of bladder cancer via exposure to polycyclic aromatic hydrocarbons (PAHs) and aromatic amines. Glutathione S‐transferase (GST) M1, T1 and P1 are involved in the detoxification of PAH reactive metabolites. Two N‐acetyltransferase isozymes, NAT2 and NAT1, have major roles in catalyzing the N‐acetylation and O‐acetylation of aromatic amines. Cytochrome P450 1B1 (CYP1B1) and sulfotransferase 1A1 (SULT1A1) are also involved in the metabolism of PAHs and aromatic amines. It is hypothesized that the genetic polymorphisms of these metabolic enzymes have an effect on the individual susceptibility to bladder cancer in particular by interacting with relevant environmental exposures. A hospital‐based case‐control study among men in Brescia, Northern Italy recruited 201 incidence cases and 214 controls from 1997–2000. Occupational exposures were blindly coded by occupational physicians. Genotyping of polymorphisms were carried out with PCR‐RFLP method. Unconditional multivariate logistic regression was applied to model the association between genetic polymorphisms and bladder cancer risk. Effect modifications by age of onset, smoking and occupational exposures to PAHs and aromatic amines were evaluated. We also conducted an analysis of interaction between genetic factors. GSTM1 and GSTT1 null genotype were associated with an increased risk of bladder cancer with an odds ratio (OR) of 1.69 (95% confidence interval [CI] = 1.11–2.56) and 1.74 (95% CI = 1.02–2.95), respectively. The effect of GSTM1 null was seen particularly in heavy smokers, and there was a combined effect with occupational exposure of aromatic amines (OR = 2.77, 95% CI = 1.08–7.10). We observed a trend (p‐value < 0.01) of increasing cancer risk comparing subjects with normal GSTM1 and T1 activity to subjects with one (OR = 1.82, 95% CI = 1.16–2.85) or both null genotypes (OR = 2.58, 95% CI = 1.27–5.23). NAT2 slow acetylator was associated with marginally increased risk of bladder cancer (OR = 1.50, 95% CI = 0.99–2.27), and the OR for the joint effect with occupational exposure of aromatic amines was 3.26 (95% CI = 1.06–9.95). SULT1A1 Arg213His polymorphism showed a marginal protective effect. These findings suggest that individual susceptibility to bladder cancer may be modulated by GSTM1, GSTT1 and NAT2 polymorphisms. © 2004 Wiley‐Liss, Inc.
Association between war and cervical cancer among Vietnamese women
Authors: Huynh My Linh D. , Raab Stephen S. , Suba Eric J. 
Published: April 2004

AbstractDecades ago, cervical cancer was the leading form of cancer among women in both North Vietnam and South Vietnam. Currently, cervical cancer rates are considerably lower in the northern region of the country. We performed a case‐control study to measure factors associated with the development of cervical cancer among Vietnamese women. Questionnaire‐based interviews were conducted with 202 women in southern Vietnam and 97 women in northern Vietnam. Case subjects were women hospitalized with cervical cancer. Control subjects were women hospitalized with extrauterine neoplasms. Data were analyzed using logistic regression, and odds ratios for the development of invasive cervical cancer were measured. The development of invasive cervical cancer was significantly associated with military service by husbands during the Second Indochinese War and with parity status. Odds ratio for the development of cervical cancer among southern Vietnamese women whose husbands had served in the armed forces was 2.6 (95% CI = 1.2–5.5). Odds ratio for the development of cervical cancer among northern women whose husbands had served in the armed forces was 3.9 (95% CI = 1.5–10.4) if their husbands had been stationed in South Vietnam during the war years. Northern women whose husbands had served in the military experienced no significant increase in cervical cancer risk if their husbands had been stationed in North Vietnam during the war years. Geographic and temporal variation in cervical cancer rates among Vietnamese women was associated with the movement of soldiers. These findings may be useful for cervical cancer prevention efforts in Vietnam and in other countries. © 2004 Wiley‐Liss, Inc.
Analysis of HIC‐1 methylation and transcription in human ependymomas
Authors: Waha Anke , Koch Arend , Hartmann Wolfgang , Mack Heike , Schramm Johannes , Sörensen Niels , Berthold Frank , Wiestler Otmar D. , Pietsch Torsten , Waha Andreas 
Published: April 2004

AbstractEpendymomas are among the most common brain tumors in children. They develop from ependymal cells lining the ventricular system of the CNS. Previous studies have demonstrated a significant rate of allelic loss at chromosome 17p13.3. The HIC‐1 putative tumor‐suppressor gene, which exhibits hypermethylation and loss of expression in various tumor entities including medulloblastomas and gliomas, maps to the affected region. In the present study, we analyzed HIC‐1 in ependymomas. Therefore, we applied methylation‐specific PCR of the 5′‐untranslated region as well as of a central region of HIC‐1 and bisulfite sequencing to determine the methylation status in 52 ependymomas of different histologic subtypes, grades and locations. In addition, we used a competitive RT‐PCR approach for sensitive assessment of HIC‐1 transcripts. Hypermethylation of at least one of the 2 analyzed regions was found in 43/52 (83%) cases. There was a significant correlation between hypermethylation of HIC‐1 and nonspinal localization (p = 0.019) as well as age. Of 27 ependymomas, 22 (81%) showed absent or low expression of HIC‐1. The elevated methylation of HIC‐1 in nonspinal ependymomas supports the hypothesis that spinal and nonspinal ependymomas represent genetically distinct entities. © 2004 Wiley‐Liss, Inc.
High fat and alcohol intakes are risk factors of postmenopausal breast cancer: A prospective study from the Malmö diet and cancer cohort
Authors: Mattisson Irene , Wirfält Elisabet , Wallström Peter , Gullberg Bo , Olsson Håkan , Berglund Göran 
Published: April 2004

AbstractAssociations between intakes of relative fat, total alcohol and alcoholic beverages and risk of breast cancer were examined in a subsample of 11,726 postmenopausal women from the MDC cohort. The MDC conducted baseline examinations from 1991 to 1996; the end of follow‐up was 31 December 2001. Data were obtained by an interview‐based diet history method, a structured questionnaire, anthropometric measurements and national and regional cancer registries. During 89,602 person‐years of follow‐up, 342 incident cases were documented. Cox regression analysis examined breast cancer risks adjusted for potential confounders. Two energy‐adjustment approaches (i.e., adjusting for total energy vs. adjusting for nonalcohol energy) were used. High total alcohol intake was associated with a nonsignificantly elevated risk. High wine intake was associated with a significantly elevated breast cancer risk (relative risk = 2.12, 95% CI 1.24–3.60). There were significant trends of increased breast cancer risk across quintiles of relative fat intake. Mutual adjustment did not affect risk estimates for total alcohol or relative fat intakes. The specific energy‐adjustment approach did not influence associations differentially. © 2004 Wiley‐Liss, Inc.
Passive smoking and breast cancer risk among non‐smoking Chinese women
Authors: Shrubsole Martha J. , Gao Yu‐Tang , Dai Qi , Shu Xiao‐Ou , Ruan Zi‐Xian , Jin Fan , Zheng Wei 
Published: April 2004

AbstractOur purpose was to evaluate whether passive exposure to cigarette smoke may be related to breast cancer risk. Data from the Shanghai Breast Cancer Study, a large population‐based study of 1,459 breast cancer cases and 1,556 controls aged 25–64 years, were analyzed. Respective response rates were 91.1% and 90.3%. Passive smoking questions were added to all face‐to‐face interviews 7 months into the study. Women were asked about exposure to their husbands' smoke at home as well as exposure in the workplace. Analyses were restricted to the 1,013 cases and 1,117 controls with passive tobacco smoke exposure data who had never actively smoked. Over 60% of controls reported some exposure to a husband's smoke and over 40% reported exposure to passive smoke in the workplace. Overall, there was no apparent association between any passive smoke exposure or exposure to a husband's smoke and breast cancer risk. There was some evidence of an elevated breast cancer risk associated with passive smoking exposure of 5 hr or more per day in the workplace (OR = 1.6, 95% confidence interval 1.0–2.4; p for trend = 0.02). This association warrants further investigation. © 2004 Wiley‐Liss, Inc.
Serologic detection of diffuse large B‐cell lymphoma‐associated antigens
Authors: Liggins Amanda P. , Guinn Barbara A. , Hatton Chris S. , Pulford Karen , Banham Alison H. 
Published: April 2004

AbstractDiffuse large B‐cell lymphoma (DLBCL) accounts for 30–40% of all adult non‐Hodgkin's lymphomas, yet the understanding of its underlying genetic abnormalities remains poor. Our present study used the serological analysis of recombinant cDNA expression libraries (SEREX) technique to identify DLBCL‐associated antigens. SEREX screening of testis libraries has previously identified cancer‐testis antigens (CTAs) that may act as disease‐specific targets for immunotherapy. Screening a testis cDNA expression library with serum from a DLBCL patient identified a total of 94 positive clones, representing 28 distinct antigens. Two of these antigens were novel, 8 were previously uncharacterised, and the remainder were proteins of known function. Screening of the antigens with sera from DLBCL (n = 10), acute myeloid leukaemia (AML, n = 10) and chronic myeloid leukaemia (CML, n = 10) patients, alongside normal healthy donor controls (n = 20), revealed that 7 of the antigens were recognised by DLBCL sera but not normal donor sera, whilst 2 of these antigens were also recognised by leukaemic sera. Some of the genes identified here were already known to be transcribed in DLBCL. The mRNA expression of the majority of the remaining antigens was confirmed in DLBCL cell lines using reverse‐transcriptase PCR (RT‐PCR). Our study identified a number of DLBCL associated antigens that may be suitable as prognostic/diagnostic markers and/or for the immunotherapy of haematologic malignancies. © 2004 Wiley‐Liss, Inc.
Low‐fat milk promotes the development of 7,12‐dimethylbenz(A)anthracene (DMBA)‐induced mammary tumors in rats
Authors: Qin Li‐Qiang , Xu Jia‐Ying , Wang Pei‐Yu , Ganmaa Davaasambuu , Li Jue , Wang Jing , Kaneko Takashi , Hoshi Kazuhiko , Shirai Tomoyuki , Sato Akio 
Published: April 2004

AbstractCommercial cow milk contains considerable amounts of estrogens. Our study assessed the effect of commercial low‐fat milk on the development of 7,12‐dimethylbenz(a)anthracene (DMBA)‐induced mammary tumors in rats. Eighty 6‐week‐old female Sprague‐Dawley rats received a single oral dose of 5 mg DMBA. Twenty‐four hours later, the animals were divided into 4 groups of 20 animals each and given 1 of 4 test solutions for 20 weeks as their drinking liquid: low‐fat (1%) milk (M), artificial milk (A), estrone sulfate solution (0.1 μg/ml, E), or tap water (W). The artificial milk was formulated to supply essentially the same calories as the milk. The low‐fat milk contained 378 pg/ml estrone sulfate. Tumor incidence, the cumulative number of tumors and the sum of tumor diameters were higher in the M and E groups than in the A or W groups. Overall, the development of mammary tumors was in the order: M = E > A = W. Whereas the plasma 17β‐estradiol concentration in the M group was the 2nd highest after the E group, the plasma level of insulin‐like growth factor (IGF‐I) was significantly higher in the M group than in the other 3 groups. In conclusion, commercially available low‐fat milk promotes the development of DMBA‐induced mammary tumors in rats. The degree of the promotion is almost comparable to that of 0.1 μg/ml estrone sulfate. The high estrogen content in the milk may be responsible for the promotional effects, acting in concert with other hormones such as IGF‐I. © 2004 Wiley‐Liss, Inc.
Definition of candidate low risk APC alleles in a Swedish population
Authors: Zhou Xiao‐Lei , Eriksson Ulrika , Werelius Barbro , Kressner Ulf , Sun Xiao‐Feng , Lindblom Annika 
Published: April 2004

AbstractMany families experience an apparently inherited increased risk of colorectal cancer (CRC) similar to the known syndromes familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer (HNPCC). Besides these high‐risk syndromes, approximately 10% of all CRC cases come from families with 2 affected 1st‐degree relatives, and even 1st‐degree relatives to a single case of CRC are at increased risk. Risk subjects from these families frequently show polyps at colonoscopy, which suggests the APC gene as a good candidate susceptibility gene for these attenuated polypotic syndromes. We used the sensitive DHPLC technique to search for possible predisposing germline mutations in the entire APC gene in 91 risk subjects from these high‐ and low‐risk syndromes with unknown predisposing genes. Most exons were also screened for mutations in 96 normal controls and 96 colorectal cancer cases. In our study we probably have identified the most common APC variants in a Swedish population. Among 30 germline variants identified, 1 clearly pathogenic nonsense mutation and 11 putative pathogenic variants (10 missense and one 3′ UTR) were found in 20 index patients (22%). Twelve silent as well as 5 intronic variants were considered nonpathogenic. Two of the missense variants found here, E1317Q and D1822V, have previously been related to a difference in risk of colorectal cancer. One variant, 8636C>A, located within the 3′ UTR region of the APC gene, was suggested to constitute an additional low risk allele with a similar relative risk as the Jewish I1307K mutation (OR = 1.8; 95% CI, 0.96–3.40). The question of whether all the other variants confer an increased colorectal cancer risk warrants future large association studies. © 2004 Wiley‐Liss, Inc.
In vivo administration of liposomal vincristine sensitizes drug‐resistant human solid tumors
Authors: Leonetti Carlo , Scarsella Marco , Semple Sean C. , Molinari Agnese , D'Angelo Carmen , Stoppacciaro Antonella , Biroccio Annamaria , Zupi Gabriella 
Published: April 2004

AbstractHere we evaluated the antitumor efficacy of vincristine (VCR) encapsulated in sphingomyelin/cholesterol liposomes (SM/Chol) on drug‐resistant human solid tumors. We firstly used the M14 human melanoma line and the counterpart resistant derivative, M14/R. The M14/R, selected after doxorubicin exposure, was cross resistant to VCR: the in vitro treatment with free VCR reduced the survival of M14, while M14/R line was completely resistant to VCR. Encapsulation in liposomes improved the efficacy of VCR in M14 cells and sensitized the M14/R line to the drug. Experiments in vivo confirmed these results. The treatment of M14 bearing mice with VCR resulted in marked reduction of tumor growth, while no antitumoral effect was observed in M14/R tumors. The administration of VCR encapsulated in liposomes was able to sensitize M14/R tumors to the drug, the antitumoral effect being comparable to that observed in M14 tumors after the same treatment. By injecting animals with the same dose of liposomal VCR fractionated into 3 daily injections and administering repeated cycles of treatment, to a marked improvement of the antitumor activity of liposomal VCR was observed. TUNEL assay in tumor sections indicated that the improved efficacy of liposomal VCR was related to the induction of massive necrosis and apoptosis. To confirm the efficacy of liposomal VCR on drug‐resistant tumors, MCF7 breast and LoVo colon carcinomas, sensitive and resistant to VCR treatment, were also employed. The results showed that the treatment with liposomal VCR of mice bearing breast or colon resistant tumors reduced the tumor mass and delayed the tumor regrowth to the same extent observed in the sensitive counterpart. Together, these results demonstrate the ability of VCR encapsulated in liposomes in sensitizing drug resistant tumors of different histotypes. © 2004 Wiley‐Liss, Inc.
Stromal cell‐derived factor‐1α‐induced cell proliferation and its possible regulation by CD26/dipeptidyl peptidase IV in endometrial adenocarcinoma
Authors: Mizokami Yayoi , Kajiyama Hiroaki , Shibata Kiyosumi , Ino Kazuhiko , Kikkawa Fumitaka , Mizutani Shigehiko 
Published: April 2004

AbstractCD26/dipeptidylpeptidase IV (DPPIV) is a 110 kD membrane‐bound extracellular peptidase with ubiquitous expressions, and has a variety of functional properties in the development of human malignancies as well as T‐cell biology. According to recent reports, stromal cell derived factor‐1α (SDF‐1α), which is a good substrate for CD26/DPPIV, is expressed in various solid tumors and is involved in tumor development or metastasis. We investigated the expression of SDF‐1α and its corresponding receptor, CXCR4, in human endometrial carcinoma (EMCA) tissues and the function of SDF‐1α on EMCA cells with its regulation by CD26/DPPIV. We demonstrated that SDF‐1α and CXCR4 were expressed in human EMCA, and these immunoreactivities were significantly low in Grade 3 EMCA, which was similar to that of CD26/DPPIV, compared to those in Grade 1 and Grade 2. Additionally, exogenous SDF‐1α concentration was significantly lower in CD26/DPPIV‐transfected EMCA cells than that in vector‐transfected cells. Moreover, exogenous SDF‐1α significantly stimulated cell proliferation in vector‐transfected cells in a concentration dependent manner. In contrast, in CD26/DPPIV‐transfected cells, there was no apparent effect on proliferation shown by the addition of exogenous SDF‐1α. This is the first report showing a direct link between the SDF‐1α/CXCR4 pathway with CD26/DPPIV in solid tumors, suggesting that CD26/DPPIV is likely to directly modulate various SDF‐1α induced functions. © 2004 Wiley‐Liss, Inc.
Aberrant methylation of the adenomatous polyposis coli promoter 1A in bronchial aspirates from patients with suspected lung cancer
Authors: Grote Hans J. , Schmiemann Viola , Kiel Sibylle , Böcking Alfred , Kappes Rainer , Gabbert Helmut E. , Sarbia Mario 
Published: April 2004

AbstractPromoter hypermethylation is a major mechanism for gene silencing and offers a promising starting point for developing molecular biomarkers. The purpose of our study was to determine aberrant methylation of the adenomatous polyposis coli (APC) gene promoter 1A with respect to its prevalence and quantitative level in bronchial aspirates from patients with suspected lung cancer. Applying quantitative methylation‐specific PCR, 155 bronchial aspirates from patients with non‐small cell cancer (NSCLC) and small cell cancer (SCLC) of the lung as well as 67 bronchial aspirates from patients diagnosed for nonneoplastic lung disease were examined in a retrospective case‐control study. Aberrant APC promoter 1A methylation was seen in 71% of NSCLCs, 38% of SCLCs and 42% of patients with nonneoplastic lung disease, being therefore not specific for the presence of primary lung cancer. In contrast, quantitative analysis showed a significantly higher methylation level of bronchial aspirates from NSCLC as compared to patients without neoplastic lung disease. Introducing a cutoff point that defined high level of APC hypermethylation NSCLC could be discriminated from cases without neoplastic disease with a specificity of 98.5% and a sensitivity of 39%. The data suggest that quantitative analysis of APC hypermethylation may serve as a biomarker of primary lung cancer. © 2004 Wiley‐Liss, Inc.
Induction of cyclooxygenase‐2 mRNA and protein expression by dentin bonding agents in human gingival fibroblasts
Authors: Huang Fu‐Mei , Chang Yu‐Chao 
Published: April 2004

AbstractAn ideal dentin bonding agent should be nonirritating to surrounding tissues. Unfortunately, all histological investigations have demonstrated that dentin bonding agents can induce mild to severe inflammatory alterations. However, there is little information on the precise mechanisms about dentin bonding agents‐induced inflammatory reaction. Cyclooxygenase‐2 (COX‐2) is an inducible enzyme believed to be responsible for prostaglandin synthesis at the site of inflammation. The aim of the present study was to investigate the effects of three dentin bonding agents, Clearfil SE Bond, Prime & Bond NT, and Single Bond on the expression of COX‐2 mRNA gene and protein in cultured human gingival fibroblasts. The exposure of quiescent human gingival fibroblasts to dentin bonding agents resulted in the induction of COX‐2 mRNA expression. The investigations of the time‐dependent on COX‐2 mRNA expression in dentin bonding agent‐treated human gingival fibroblasts revealed different patterns. The influence of COX‐2 mRNA depended on the tested materials. In addition, all dentin bonding agents also induced COX‐2 protein expression in human gingival fibroblasts. Taken together, the activation of COX‐2 expression may be one of the potential mechanisms of dentin bonding agent‐induced gingival inflammation. © 2004 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 70B: 297–302, 2004
Effect of molar mass of an experimental primer on shear bond strength to dentin
Authors: Richards Nicola D. , Söderholm Karl‐Johann , Batich Christopher D. 
Published: April 2004

AbstractA novel oligomer was synthesized in different molecular masses and used as a primer in dentin bonding. The hypothesis was that an intermediate molecular mass would optimize the conflicting needs for diffusion into etched dentin (low Mw) and high mechanical properties (high Mw). The initial oligomer synthesized was tert butylmethacrylate‐co‐maleic anhydride, which was further reacted to add hyrdoxyethyl methacrylate (HEMA) across the anhydride. The oligomer was synthesized in a series of molecular masses from ∼800–6000 amu. The oligomer with an average Mw of ∼1000 amu provided the highest bond strength (16 MPa), with both lower and higher molar mass oligomers producing lower bond strengths. A polynomial model was fitted to the data with an R2 = 0.606, while a linear model only had an R2 = 0.534. This implies that the graph of molar mass to bond strength has a maximum in the range of molar masses examined, and that an optimum molar mass can be found between 800 and 6000 amu. © 2004 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 70B: 384–388, 2004