bluuebunny/crossref_metadata_2025_split huggingface dataset:
A theoretical study of the possible use of electroosmotic flow to extend the read length of DNA sequencing by end‐labeled free solution electrophoresis
Authors: McCormick Laurette C. , Slater Gary W. 
Published: March 2006

AbstractEnd‐labeled free solution electrophoresis (ELFSE) provides a means of separating DNA with free‐solution CE, eliminating the need for gels and polymer solutions which increase the run time and can be difficult to load into a capillary. In free‐solution electrophoresis, DNA is normally free‐draining and all fragments reach the detector at the same time, whereas ELFSE uses an uncharged label molecule attached to each DNA fragment in order to render the electrophoretic mobility size‐dependent. With ELFSE, however, the larger molecules are not separated enough (limiting the read length in the case of ssDNA sequencing) while the smaller ones are overseparated; the larger ones are too fast while the shorter ones are too slow, which is the opposite of traditional gel‐based methods. In this article, we show how an EOF could be used to overcome these problems and extend the DNA sequencing read length of ELFSE. This counterflow would allow the larger, previously unresolved molecules more time to separate and thereby increase the read length. Through our theoretical investigation, we predict that an EOF mobility of approximately the same magnitude as that of unlabeled DNA would provide the best results for the regime where all molecules move in the same direction. Even better resolution would be possible for smaller values of EOF which allow different directions of migration; however, the migration times then would become too large. The flow would need to be well controlled since the gain in read length decreases as the magnitude of the counterflow increases; an EOF mobility double that of unlabeled DNA would no longer increase the read length, although ELFSE would still benefit from a reduction in migration time.
Silver staining method for DNA in polyacrylamide gels using eriochrome black T as a silver‐ion sensitizer
Authors: Hwang Sun‐young , Jin Li‐tai , Yoo Gyurng‐soo , Choi Jung‐Kap 
Published: March 2006

AbstractA sensitive silver staining method using eriochrome black T as a silver‐ion sensitizer for DNA detection in polyacrylamide gels was developed. The sensitivity of this staining method was significantly improved by the new silver‐ion sensitizer containing a diazo group, which has reducing power. The staining method lasted a total of approximately 15 min following a fixing step for 2×20 min. The detection limit of this staining method was 1–4 pg for ΦX174 DNA/HaeIII in both nondenaturing and denaturing polyacrylamide gels. This staining method was especially effective in low‐base pair DNA, with a sensitivity that was approximately ten‐fold higher than previously published silver staining methods.
Aflatoxin B1 and polycyclic aromatic hydrocarbon adducts, p53 mutations and p16 methylation in liver tissue and plasma of hepatocellular carcinoma patients
Authors: Zhang Yu‐Jing , Rossner Pavel , Chen Yu , Agrawal Meenakshi , Wang Qiao , Wang Lillian , Ahsan Habibul , Yu Ming‐Whei , Lee Po‐Huang , Santella Regina M. 
Published: March 2006

AbstractElevated aflatoxin B1‐albumin adducts (AFB1‐Alb) have been associated with an increased risk for HCC development. However, there are no studies in humans, correlating albumin adducts in blood with liver DNA adducts. Forty frozen tumor tissues and 39 paired plasma samples from HCC patients were collected in Taiwan, to determine the relationship between albumin adducts in blood and DNA adducts in liver tissue as well as mutations in p53 and methylation of p16. AFB1‐ and polycyclic aromatic hydrocarbon (PAH)‐DNA adducts in tissue and albumin adducts in plasma were determined by immunohistochemistry and competitive ELISA, respectively. Plasma AFB1‐Alb adducts in subjects with low, medium and high levels of AFB1‐DNA adducts in tumor tissues were 51.0 ± 36.5, 70.5 ± 48.1 and 84.9 ± 48.2 fmol/mg, respectively (ptrend = 0.05). No significant correlation was found for PAH. Fourteen of 40 (36%) tissues were positive for mutant p53 protein by immunohistochemistry; 11 of 40 tissue DNA samples (28%) were positive for p53 mutations, but not their corresponding plasma DNAs. p16 was methylated in 24 of 40 (62%) tissues and 12 of 39 (32%) plasma DNAs. Significant correlations were observed between AFB1‐Alb adducts and p53 mutations and p16 methylation. These data suggest that genetic, epigenetic and environmental exposure biomarkers in plasma may help in estimating the risk for the development of HCC. © 2006 Wiley‐Liss, Inc.
iNOS‐dependent DNA damage via NF‐κB expression in hamsters infected with Opisthorchis viverrini and its suppression by the antihelminthic drug praziquantel
Authors: Pinlaor Somchai , Hiraku Yusuke , Yongvanit Puangrat , Tada‐Oikawa Saeko , Ma Ning , Pinlaor Porntip , Sithithaworn Paiboon , Sripa Banchob , Murata Mariko , Oikawa Shinji , Kawanishi Shosuke 
Published: March 2006

AbstractInflammation‐mediated DNA damage triggered by Opisthorchis viverrini (OV) infection is a major risk factor of cholangiocarcinoma (CCA). We have recently reported that nitrative and oxidative DNA damage participates in CCA development caused by repeated infection with OV [Pinlaor et al., Carcinogenesis 2004; 25:1535–42]. Therefore, to clarify the preventive effect of the antihelminthic drug praziquantel against cholangiocarcinogenesis, we assessed the effect of this drug on nitrative and oxidative DNA damage, including the formation of 8‐nitroguanine and 8‐oxo‐7,8‐dihydro‐2′‐deoxyguanosine (8‐oxodG), and the expression of inducible nitric oxide synthase (iNOS) by immunohistochemistry in OV‐infected hamsters. We also examined the expression of nuclear factor‐κB (NF‐κB), which functions as a tumor promoter in inflammation‐associated cancer. Our results showed that although 1‐week treatment with praziquantel did not kill parasites completely in hamsters on days 14 and 30, this drug dramatically reduced inflammatory cell infiltration. Double immunofluorescence staining showed that drug treatment almost completely diminished OV‐induced 8‐nitroguanine and 8‐oxodG formation in bile duct epithelial cells. Quantitative analysis using an electrochemical detector coupled to HPLC revealed that 8‐oxodG level in the liver of OV‐infected hamsters was significantly decreased by drug treatment (p<0.05). Western blotting and immunohistochemistry revealed that the expression of NF‐κB and iNOS in bile duct epithelium was reduced by drug treatment. The amount of nitrate plus nitrite in the liver and plasma was significantly decreased after drug treatment. It is concluded that praziquantel can exhibit a preventive effect against OV‐induced cholangiocarcinoma by inhibiting iNOS‐dependent DNA damage through not only elimination of parasites but also a potential antiinflammatory effect. © 2006 Wiley‐Liss, Inc.
Small molecule drug activity in melanoma models may be dramatically enhanced with an antibody effector
Authors: Popkov Mikhail , Rader Christoph , Gonzalez Beatriz , Sinha Subhash C. , Barbas Carlos F. 
Published: March 2006

AbstractMonoclonal antibody (mAb) 38C2 belongs to a group of catalytic antibodies that were generated by reactive immunization and contains a reactive lysine. 38C2 catalyzes aldol and retro‐aldol reactions, using an enamine mechanism, and mechanistically mimics natural aldolase enzymes. In addition, mAb 38C2 can be redirected to target integrins αvβ3 and αvβ5 through the formation of a covalent bond between a β‐diketone derivative of an arginine–glycine–aspartic acid (RGD) peptidomimetic and the reactive lysine residue in the antibody combining site to provide the chemically programmed mAb cp38C2. In this study, we investigated the potential of enhancing the activity of receptor‐binding small molecule drug (SCS‐873) through antibody conjugation. Using a M21 human melanoma xenograft model in nude mice, cp38C2 inhibited the growth of the tumor by ˜81%. The chemically programmed antibody was shown to be highly active at a low concentration while SCS‐873 alone was ineffective even at dosages ˜1,000‐fold higher than those used for the chemically programmed antibody. In vitro programming of the catalytic antibody was shown to be as effective as in vivo programming. In an experimental metastasis assay, treatment with mAb cp38C2 significantly prolonged overall survival of tumor‐bearing severe combined immuno‐deficient (SCID) mice when compared to treatment with unprogrammed mAb 38C2, SCS‐873 alone or the integrin‐specific monoclonal antibody LM609. In vitro, cp38C2 inhibited human and mouse endothelial and human melanoma cell adhesion, migration and invasion. Additionally, cp38C2 inhibited human and mouse endothelial cell proliferation and was active in complement‐dependent cytotoxicity assays. These studies establish the potential of chemically programmed monoclonal antibodies as a novel and effective class of immunotherapeutics that combine the merits of traditional small molecule drug design with immunotherapy. © 2006 Wiley‐Liss, Inc.
Insulin‐like growth factor binding protein 3 as an anticancer molecule in Ewing's sarcoma
Authors: Benini Stefania , Zuntini Monia , Manara Maria Cristina , Cohen Pinchas , Nicoletti Giordano , Nanni Patrizia , Oh Youngman , Picci Piero , Scotlandi Katia 
Published: March 2006

AbstractThe IGF/IGF‐IR system plays a major role in the pathogenesis and progression of Ewing's sarcoma. In this article, the authors evaluated whether the insulin‐like growth factor binding protein‐3 (IGFBP‐3), a molecule with growth‐inhibitory and proapoptotic activities, may be exploited for therapeutic applications in the treatment of Ewing's sarcoma (EWS). Expression of IGFBP‐3 was analyzed in a panel of EWS cell lines and clinical samples. Parameters related to malignancy (growth in anchorage‐independent conditions, migration, invasion and angiogenesis properties) were studied to establish the potential in vitro anticancer effects of exogenous IGFBP‐3. The activity of the molecule against metastasis was analyzed by taking advantage of selected clones in which IGFBP‐3 endogenous production was induced by gene transfection. The authors observed a generally low expression of IGFBP‐3 either in a panel of EWS cell lines or clinical samples. Exogenous IGFBP‐3 remarkably inhibits EWS growth, both in monolayer and anchorage‐independent conditions, and significantly reduces cell motility. Forced expression of IGFBP‐3 in TC‐71 EWS cells confirms the growth and migratory effects observed with the exogenous protein, decreases the production or activity of the matrixmetalloprotease MMP‐9 and vascular endothelial factor (VEGF)‐A and abrogates EWS metastasis ability. IGFBP‐3 acts mainly through IGF‐dependent mechanisms and the protein may therefore represent an alternative strategy to inhibit IGF‐IR functions. The data indicate IGFBP‐3 as a molecule of therapeutic potential in EWS. © 2006 Wiley‐Liss, Inc.
Chromosome 5 imbalance mapping in breast tumors from BRCA1 and BRCA2 mutation carriers and sporadic breast tumors
Authors: Johannsdottir Hrefna K. , Jonsson Goran , Johannesdottir Gudrun , Agnarsson Bjarni A. , Eerola Hannaleena , Arason Adalgeir , Heikkila Paivi , Egilsson Valgardur , Olsson Hakan , Johannsson Oskar Th. , Nevanlinna Heli , Borg Ake , Barkardottir Rosa B. 
Published: March 2006

AbstractComparative genomic hybridization (CGH) analysis has shown that chromosome 5q deletions are the most frequent aberration in breast tumors from BRCA1 mutation carriers. To map the location of putative 5q tumor suppressor gene(s), 26 microsatellite markers covering chromosome 5 were used in loss of heterozygosity (LOH) analysis of breast tumors from BRCA1 (n = 42) and BRCA2 mutation carriers (n = 67), as well as in sporadic cases (n = 65). High‐density array CGH was also used to map chromosome 5 imbalance in 10 BRCA1 tumors. A high LOH frequency was found in BRCA1 tumors (range 19–82%), as compared to BRCA2 and sporadic tumors (ranges 11–44% and 7–43%, respectively). In all, 11 distinct chromosome 5 regions with LOH were observed, the most frequent being 5q35.3 (82%), 5q14.2 (71%) and 5q33.1 (69%) in BRCA1 tumors; 5q35.3 (44%), 5q31.3 (43%) and 5q13.3 (43%) in BRCA2 tumors and 5q31.3 (43%) in sporadic tumors. Array CGH analysis confirmed the very high frequency of 5q deletions, including candidate tumor suppressor genes such as XRCC4, RAD50, RASA1, APC and PPP2R2B. In addition, 2 distinct homozygous deletions were identified, spanning regions of 0.7–1.5 Mbp on 5q12.1 and 5q12.3‐q13.1, respectively. These regions include only a few genes, most notably BRCC3/DEPDC1B (pleckstrin/G protein interacting and RhoGAP domains) and PIK3R1 (PI3 kinase P85 regulatory subunit). Significant association (p ≤ 0.05) was found between LOH at certain 5q regions and factors of poor prognosis, including negative estrogen and progesterone receptor status, high grade, large tumor size and high portion of cells in S‐phase. In conclusion, our results confirm a very high prevalence of chromosome 5q alterations in BRCA1 tumors, pinpointing new regions and genes that should be further investigated. © 2006 Wiley‐Liss, Inc.
Methodological issues in international comparison of interval breast cancers
Authors: Bulliard Jean‐Luc , Sasieni Peter , Klabunde Carrie , De Landtsheer Jean‐Pierre , Yankaskas Bonnie C. , Fracheboud Jacques 
Published: March 2006

AbstractInternational comparisons of interval cancers (IC) are important to better understand the relationship between programmes' performance and screening practices. In this respect, differences in (i) definition, (ii) identification and (iii) quantification of IC have received little attention. To examine these 3 comparability issues and activities involving IC, an assessment was conducted among member countries of the International Breast Cancer Screening Network, and the impact of accuracy of identification and quantification practices was estimated using 1996–98 data from the Dutch breast cancer screening programme. Information was obtained from 19 screening programmes in 18 countries, 16 of which acknowledged the coexistence of opportunistic screening. IC data were collected to evaluate performance of the screening programme (100% of programmes) and the radiologists (89%); 53% of programmes had a designated review process for IC. Most programmes (84%) agreed with the European Guidelines definition of IC, but a case situation exercise evidenced substantial discrepancy in classification of cancers that occurred after a positive screen. Completeness of identification of IC appears to contribute most to international variation, and cannot be easily controlled for in methodologically rigorous comparisons. Statistically significant differences of about 4% were measured between quantification methods for IC. An operational definition of IC is proposed to enhance international comparability. Valid comparisons of IC are possible with careful attention to the definition but true differences in IC frequency across screening programmes should exceed 10% to be possibly indicative of real differences between programmes. © 2006 Wiley‐Liss, Inc.
Overexpression of RB1 transcript is significantly correlated with 13q14 allelic imbalance in colorectal carcinomas
Authors: Lai Poh‐San , Cheah Peh Yean , Kadam Priya , Chua Constance Li‐Ming , Lie Daniel Khun Hong , Li Hui‐Hua , Eu Kong‐Weng , Seow‐Choen Francis , Lee Ann Siew‐Gek 
Published: March 2006

AbstractRB1 gene expression has been reported to be upregulated in colorectal carcinomas (CRC) at both the mRNA and protein levels when compared to normal colonic mucosa. However, allelic loss at the genomic level has been detected in CRC with widely differing frequencies ranging from 11.5% to 50%. To determine whether there is indeed a correlation between RB1 allelic imbalance (AI) and expression, a consecutive series of 55 CRC from Singapore patients were analysed by microsatellite analysis, real‐time RT‐PCR and immunohistochemistry. Microsatellite analysis using 3 RB1 intragenic microsatellite markers and 2 markers flanking RB1 detected AI in 32.7% (18/55) of the cases, in at least 1 locus. The highest AI frequency (22.9%) was observed at the microsatellite marker D13S137 (Cu13), which maps 5 cM distal to RB1. AI was present in both early and late Dukes stages. Real‐time RT‐PCR revealed that all 40 cases analysed expressed RB1 mRNA, with mRNA overexpression in 37.5% (15/40) and pRB protein expression in 88.2% (30/34) of cases. Notably, a statistically significant correlation was found between AI of RB1 and mRNA overexpression of RB1 (p < 0.001, Fishers exact test). These findings provide evidence that despite AI, RB1 expression is not abrogated. Thus, our data suggests that RB1 may play a role in colorectal tumorigenesis through functional regulation of the transcript and protein rather than through its tumour suppressor role by gene inactivation. © 2006 Wiley‐Liss, Inc.
Adulthood consumption of preserved and nonpreserved vegetables and the risk of nasopharyngeal carcinoma: A systematic review
Authors: Gallicchio Lisa , Matanoski Genevieve , Tao Xuguang (Grant) , Chen Liwei , Lam Tram K. , Boyd Kristina , Robinson Karen A. , Balick Lyssa , Mickelson Stephanie , Caulfield Laura E. , Herman James G. , Guallar Eliseo , Alberg Anthony J. 
Published: March 2006

AbstractThe incidence rates of nasopharyngeal carcinoma (NPC) are dramatically higher in certain regions of Asia compared to the rest of the world. Few risk factors for NPC are known; however, in contrast to the hypothesized health benefits of nonpreserved vegetables, it is thought that preserved vegetable intake may play a role in contributing to the higher incidence of NPC in high‐risk regions. Therefore, the purpose of this study was to systematically review the epidemiologic evidence on the associations between adulthood intake of preserved and nonpreserved vegetables and NPC risk. A search of the epidemiological literature from 1966 to 2004 was performed using several bibliographic databases, including PubMed and the Chinese Biomedical Literature Database System. There were no language restrictions. Meta‐analysis was conducted to obtain pooled odds ratios (ORs) for the highest‐versus‐lowest categories of preserved and nonpreserved vegetable intake. A total of 16 case‐control studies were identified in the search. Results showed that highest‐versus‐lowest preserved vegetable intake was associated with a 2‐fold increase in the risk of NPC (Random Effects Odds Ratio (RE OR) 2.04; 95% Confidence Limits (CL) 1.43, 2.92). Conversely, high nonpreserved vegetable intake was associated with 36% decrease in the risk of NPC (RE OR 0.64; 95% CL 0.48, 0.85). Findings for both preserved and nonpreserved vegetables were consistent across vegetable type and by country of study. Further research in high‐risk areas to gain insight into the risk associated with preserved vegetables and protection associated with nonpreserved vegetables may advance understanding of NPC and yield clues for prevention. © 2006 Wiley‐Liss, Inc.
Brain cancer mortality and potential occupational exposure to lead: Findings from the National Longitudinal Mortality Study, 1979–1989
Authors: van Wijngaarden Edwin , Dosemeci Mustafa 
Published: March 2006

AbstractWe evaluated the association between potential occupational lead exposure and the risk of brain cancer mortality in the National Longitudinal Mortality Study (NLMS), which is a prospective census‐based cohort study of mortality among the noninstitutionalized United States population (1979–1989). The present study was limited to individuals for whom occupation and industry were available (n = 317,968). Estimates of probability and intensity of lead exposure were assigned using a job‐exposure matrix (JEM). Risk estimates for the impact of lead on brain cancer mortality were computed using standardized mortality ratio (SMR) and proportional hazards and Poisson regression techniques, adjusting for the effects of age, gender and several other covariates. Brain cancer mortality rates were greater among individuals in jobs potentially involving lead exposure as compared to those unexposed (age‐ and gender‐adjusted hazard ratio (HR) = 1.5; 95% confidence interval (CI) = 0.9–2.3) with indications of an exposure–response trend (probability: low HR = 0.7 (95% CI = 0.2–2.2), medium HR = 1.4 (95% CI = 0.8–2.5), high HR = 2.2 (95% CI = 1.2–4.0); intensity: low HR = 1.2 (95% CI = 0.7–2.1), medium/high HR = 1.9 (95% CI = 1.0–3.4)). Brain cancer risk was greatest among individuals with the highest levels of probability and intensity (HR = 2.3; 95% CI = 1.3–4.2). These findings provide further support for an association between occupational lead exposure and brain cancer mortality, but need to be interpreted cautiously due to the consideration of brain cancer as one disease entity and the absence of biological measures of lead exposure. © 2006 Wiley‐Liss, Inc.
Nicotine induces the fragile histidine triad methylation in human esophageal squamous epithelial cells
Authors: Soma Toshiya , Kaganoi Junichi , Kawabe Atsushi , Kondo Kan , Imamura Masayuki , Shimada Yutaka 
Published: March 2006

AbstractThe fragile histidine triad (FHIT) gene has been proposed to have an important role in very early carcinogenesis. Methylation of the FHIT gene is associated with transcriptional inactivation in esophageal squamous cell carcinoma, and FHIT inactivation has been linked to smoking‐related carcinogenesis. In this study, we confirmed methylation of the FHIT gene in human esophageal squamous epithelial cells (HEECs) and examined whether nicotine induced alteration of FHIT. Methylation status in the promoter region of the FHIT gene and p16INK4A gene was determined by methylation‐specific PCR in HEECs exposed to nicotine under various conditions. Methylation status of the FHIT gene was confirmed by DNA‐sequencing analysis. Protein expression of Fhit and the DNA methyltransferases (DNMTs) DNMT1 and DNMT3a were assessed by immunoblot analysis. In the absence of nicotine, methylation of the FHIT gene and attenuation of Fhit protein were not detected in HEECs. Nicotine induced the methylation of FHIT gene and attenuated Fhit protein in association with increased expression of DNMT3a. Reexpression of Fhit protein in HEECs was found after cessation of moderate‐ to long‐term exposure to nicotine. Our results show that nicotine induces methylation of the FHIT gene followed by loss of Fhit protein expression in HEECs. Continuous smoking may thus increase the risk of esophageal cancer. © 2006 Wiley‐Liss, Inc.