bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of DNA damage induced by decabromodiphenyl ether (BDE‐209) in hemocytes of Dreissena polymorpha using the comet and micronucleus assays
Authors: Riva Consuelo , Binelli Andrea , Cogni Daniele , Provini Alfredo 
Published: October 2007

AbstractThe recent widespread production and use of flame retardants, polybrominated diphenyl ethers (PBDEs), is one of the reason of the increasing contamination observed worldwide. At the present, deca‐BDE mixture, in which the decabromodiphenyl ether (BDE‐209) is the major congener (98%), dominates the EU market. The potential genotoxicity of BDE‐209 was examined in the freshwater bivalve zebra mussel (Dreissena polymorpha) by means of Comet assay and micronucleus assay (MN assay). Mussels were exposed in vivo to BDE‐209 at nominal concentration of 0.1, 2, and 10 μg/l under laboratory conditions. The assays were performed on the bivalve hemocytes monitoring the levels of DNA strand breaks and the percentage of micronuclei until 168 and 96 hr of exposure, respectively. At the same time, BDE‐209 levels were measured daily in mussel soft tissues to evaluate the bioaccumulation. Results of the Comet assay showed a significant increase of DNA damages compared to controls, but a lack of dose/effect relationship probably due to the formation of less‐brominated congeners. By contrast, no significant changes in MN frequency from baseline levels were observed. These preliminary results about the potential genotoxicity of this compound in invertebrates indicated a clear BDE‐209 capability to induce DNA damage, but no irreversible effects on DNA hemocytes. Furthermore, bioaccumulation of this high‐molecular‐weight substance and its uptake mechanism in zebra mussel are also discussed. Environ. Mol. Mutagen., 2007. © 2007 Wiley‐Liss, Inc.
An exact expression for MPSK SEP
Authors: Nadarajah Saralees 
Published: October 2007

AbstractMany of the known expressions for the M ary phase shift keying (MPSK) symbol error probability (SEP) are of dubious nature because they are based on an infinite series representation that diverges. In this note, an exact and convergent expression is derived for the MPSK SEP. Some numerical comparison is provided with the known expressions. Copyright © 2007 John Wiley & Sons, Ltd.
Arylamine N‐acetyltransferase 1 expression in breast cancer cell lines: A potential marker in estrogen receptor‐positive tumors
Authors: Wakefield Larissa , Robinson James , Long Hilary , Ibbitt J. Claire , Cooke Susanna , Hurst Helen C. , Sim Edith 
Published: October 2007

AbstractThe prognosis for patients with estrogen receptor (ER)‐positive breast cancer has improved significantly with the prescription of selective ER modulators (SERMs) for ER‐positive breast cancer treatment. However, only a proportion of ER‐positive tumors respond to SERMs, and resistance to hormonal therapies is still a major problem. Detailed analysis of published microarray studies revealed a positive correlation between overexpression of the drug metabolizing enzyme arylamine N‐acetyltransferase type 1 (NAT1) and ER positivity, and increasing evidence supports a biological role for NAT1 in breast cancer progression. We have tested a range of ER‐positive and ER‐negative breast cancer cell lines for NAT1 enzyme activity, and monitored promoter and polyadenylation site usage. Amongst ER‐positive lines, NAT1 activities ranged from 202 ± 28 nmol/min/mg cellular protein (ZR‐75‐1) to 1.8 ± 0.4 nmol/min/mg cellular protein (MCF‐7). The highest levels of NAT1 activity could not be attributed to increased NAT1 gene copy number; however, we did detect differences in NAT1 promoter and polyadenylation site usage amongst the breast tumor‐derived lines. Thus, whilst all cell lines tested accumulated transcripts derived from the proximal promoter, the line expressing NAT1 most highly additionally initiated transcripts initiating at a more distal, “tissue”‐specific promoter. These data pave the way for investigating NAT1 transcripts as candidate prognostic markers in ER‐positive breast cancer. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045‐2257/suppmat. © 2007 Wiley‐Liss, Inc.
Efficacy of selegiline add on therapy to risperidone in the treatment of the negative symptoms of schizophrenia: a double‐blind randomized placebo‐controlled study
Authors: Amiri Afshar , Noorbala Ahmad‐Ali , Nejatisafa Ali‐Akbar , Ghoreishi Abolfazl , Derakhshan Mohammad‐Kamran , Khodaie‐Ardakani Mohammad‐Reza , Hajiazim Mohammad , Raznahan Maedeh , Akhondzadeh Shahin 
Published: October 2007

AbstractObjectiveIt has been reported that selegiline, a Selective Monoamine Oxidase Inhibitor B (MAOI‐B), at low doses would be helpful for treating negative symptoms in schizophrenia. Nevertheless, the results are contradictory so far. This study was designed to investigate the effect of selegiline added to risperidone as augmentation therapy in patients with chronic schizophrenia and prominent negative symptoms in an 8 week, double blind and randomized clinical trial.MethodsEligible participants in this study were 40 patients with chronic schizophrenia. All patients were inpatients and were in the active phase of the illness, and met DSM‐IV‐TR criteria for schizophrenia. Patients were allocated in a random fashion, 20 to risperidone 6 mg/day plus selegiline 10 mg/day (5 mg bid) and 20 to risperidone 6 mg/day plus placebo. The principal measure of the outcome was Positive and Negative Syndrome Scale (PANSS).ResultsAlthough both protocols significantly decreased the score of the positive, negative, and general psychopathological symptoms over the trial period, the combination of risperidone and selegiline showed a significant superiority over risperidone alone in decreasing negative symptoms and PANSS total scores.ConclusionThe present study indicates selegiline as a potential adjunctive treatment strategy for the negative symptoms of schizophrenia. Nevertheless, results of larger controlled trials are needed before recommendation for a broad clinical application can be made. Copyright © 2007 John Wiley & Sons, Ltd.
Ultrasonic measurement of suspended sediment concentrations: an experimental validation of the approach using kaolin suspensions and reservoir sediments under variable thermal conditions
Authors: Sung C. C. , Huang Y. J. , Lai J. S. , Hwang G. W. 
Published: October 2007

AbstractMultiphase suspension systems are used extensively in hydrology, biochemistry, and the food industry. Ultrasonic spectroscopy is a rapid, on‐line, non‐invasive measurement technique for suspension characterization over different particle sizes and a wide range of concentration. Although the properties of kaolin suspensions have been investigated extensively, kaolin ultrasonic attenuation properties at different temperatures and concentrations have not yet been reported. Through experimental validation in the laboratory, this study provides results from a series of measurements of kaolin ultrasonic attenuation over a wide range of concentrations (0–300 000 ppm) and practical temperatures (5–25 °C). The ultrasonic measurement of attenuation of sediment sampled from the Shihmen reservoir in Taiwan is also investigated. Results show that variations in ultrasonic attenuation are driven by concentration and temperature. Two regression functions are established to quantitatively relate attenuation to kaolin concentration and the Shihmen reservoir sample at a given temperature. An ultrasonic system is designed and manufactured for real‐time sediment concentration monitoring in the Shihmen reservoir based on these experimental ultrasonic attenuation measurements. Copyright © 2007 John Wiley & Sons, Ltd.
Hereditary nonpolyposis colorectal cancer in endometrial cancer patients
Authors: Yoon Sang Nam , Ku Ja‐Lok , Shin Young‐Kyoung , Kim Kyung‐Hee , Choi Jin‐Sung , Jang Eun‐Ja , Park Hyoung‐Chul , Kim Duck‐Woo , Kim Min A. , Kim Woo Ho , Lee Taek Sang , Kim Jae Weon , Park Noh‐Hyun , Song Yong‐Sang , Kang Soon‐Beom , Lee Hyo‐Pyo , Jeong Seung‐Yong , Park Jae‐Gahb 
Published: October 2007

AbstractEndometrial cancer is the second most common cancer in hereditary nonpolyposis colorectal cancer (HNPCC). It has often been overlooked to explore the possibility of HNPCC in endometrial cancer patients. Our study was to investigate how many HNPCC patients existed among endometrial cancer patients. Among patients who underwent hysterectomy for endometrial cancer at Seoul National University Hospital from 1996 to 2004, 113 patients were included, whose family history and clinical data could be obtained and tumor specimens were available for microsatellite instability (MSI) testing and immunohistochemical (IHC) staining of MLH1, MSH2 and MSH6 proteins. There were 4 (3.5%) clinical HNPCC patients fulfilling the Amsterdam criteria II, and 2 (2/4, 50%) of them carried MSH2 germline mutations. There were also 8 (7.1%) suspected HNPCC (s‐HNPCC) patients fulfilling the revised criteria for s‐HNPCC, and one (1/8, 12.5%) of them revealed MLH1 germline mutation. In 101 patients, who were not clinical HNPCC or s‐HNPCC, 11 patients showed both MSI‐high and loss of expression of MLH1, MSH2 or MSH6 proteins, and 2 (2/11, 18.2%) of them showed MSH6 germline mutations. In 113 patients with endometrial cancer, we could find 5 (4.4%) HNPCC patients with MMR germline mutation and 2 (1.8%) clinical HNPCC patients without identified MMR gene mutation. Family history was critical in detecting 3 HNPCC patients with MMR germline mutation, and MSI testing with IHC staining for MLH1, MSH2 and MSH6 proteins was needed in the diagnosis of 2 HNPCC patients who were not clinical HNPCC or s‐HNPCC, especially for MSH6 germline mutation. © 2007 Wiley‐Liss, Inc.
Synthesis and biological evaluation of an albumin‐binding prodrug of doxorubicin that is cleaved by prostate‐specific antigen (PSA) in a PSA‐positive orthotopic prostate carcinoma model (LNCaP)
Authors: Graeser Ralph , Chung Da‐Eun , Esser Norbert , Moor Sandra , Schächtele Christoph , Unger Clemens , Kratz Felix 
Published: October 2007

AbstractThe prostate‐specific antigen (PSA) is a serine protease that is over‐expressed in prostate carcinoma and represents a molecular target for selectively releasing an anticancer agent from a prodrug formulation. We have recently investigated a macromolecular prodrug strategy for improved cancer chemotherapy based on 2 features: (i) rapid and selective binding of thiol‐reactive prodrugs to the cysteine‐34 position of endogenous albumin after intravenous administration, and (ii) enzymatic release of the albumin‐bound drug at the tumor site (Mansour et al., Cancer Res 2003, 63, 4062–4066). In this work, we describe an albumin‐binding prodrug, EMC‐Arg‐Ser‐Ser‐Tyr‐Tyr—Ser‐Arg‐DOXO [EMC: ϵ‐Maleimidocaproic acid; DOXO = doxorubicin; X = amino acid] that is cleaved by PSA. Because of the incorporation of 2 arginine residues, the prodrug exhibited excellent water‐solubility and was rapidly and selectively bound to endogenous albumin. Incubation studies with PSA and tumor homogenates from PSA‐positive tumors (LNCaP) demonstrated that the albumin‐bound form of the prodrug was efficiently cleaved by PSA at the P1–P′ 1 scissile bond releasing the doxorubicin dipeptide H‐Ser‐Arg‐DOXO, which was further degraded to doxorubicin as the final cleavage product. In cell culture experiments, the prodrug was ∼100‐fold less active against LNCaP cells than the free drug. In contrast, in a mouse model of human prostate cancer using luciferase transduced LNCaP cells orthotopically implanted in SCID mice, the prodrug showed enhanced antitumor efficacy when compared to doxorubicin. Doxorubicin treatment at a dose of 2 × 4 mg/kg caused significant weight loss and mortality (−25%), and did not result in a significant antitumor response at the end of the experiment. The prodrug at 3 × 12 mg/kg doxorubicin equivalents, however, was well tolerated and induced a significant reduction in tumor size of 62% (±25%, **p = 0.003) as well as a decrease of the metastatic burden in the lungs as detected in luciferase assays (−50%, SD ± 115%, *p = 0.038). © 2007 Wiley‐Liss, Inc.
HER‐2 status discrepancy between primary breast cancer and metastatic sites. Impact on target therapy
Authors: Santinelli Alfredo , Pisa Eleonora , Stramazzotti Daniela , Fabris Guidalberto 
Published: October 2007

AbstractIn this prospective study, we determined HER‐2 status in primary breast invasive carcinomas and in the paired lymph node metastases (synchronous and metachronous), local recurrence and metachronous distant metastases, to verify the percentage of discordant cases. HercepTest™ and Fluorescence in situ hybridization (FISH) were used to determine HER‐2 status on 119 cases of primary infiltrating breast carcinoma and paired metastases (45 cases with synchronous lymph node metastases, 9 cases with metachronous lymph node metastases, 30 cases with local recurrence, and 35 cases with metachronous distant metastases). A therapeutically significant HER‐2 status discordance was demonstrated between primary carcinoma and synchronous lymph node metastases (6.7%), local recurrence (13.3%) and metachronous distant metastases (28.6%). In the first comparison, there was a normal HER‐2 status in primary tumours and HER‐2 amplification in paired metastases, in the second the opposite phenomenon was present, and both types of discordance were evident in the third comparison. Considering the cases of local recurrences and metachronous distant metastases all together, 14 out of 65 cases (21.5%) showed a therapeutically significant discordance of HER‐2 status between the primary tumour and the paired metachronous recurrence or metastasis (p < 0.001), the 15.4% of cases showing normal HER‐2 status in the primary tumour and HER‐2 amplification in the neoplastic relapse. For the treatment of metastatic patients, the evaluation of HER‐2 status should be performed in neoplastic tissue from metastatic site, whenever possible. This procedure could be also suggested in the patients that are metastatic at the time of diagnosis. © 2007 Wiley‐Liss, Inc.
Risk of gastroesophageal cancer among smokers and users of Scandinavian moist snuff
Authors: Zendehdel Kazem , Nyrén Olof , Luo Juhua , Dickman Paul W. , Boffetta Paolo , Englund Anders , Ye Weimin 
Published: October 2007

AbstractAlthough Scandinavian moist snuff (“snus”), no doubt, is a safer alternative to smoking, there is limited evidence against an association with gastroesophageal cancers. In a retrospective cohort study, we investigated esophageal and stomach cancer incidence among 336,381 male Swedish construction workers who provided information on tobacco smoking and snus habits within a health surveillance program between 1971 and 1993. Essentially complete follow‐up through 2004 was accomplished through linkage to several nationwide registers. Multivariable Cox proportional hazards regression models estimated relative risks (RR) and 95% confidence intervals (CIs). Compared to never‐users of any tobacco, smokers had increased risks for adenocarcinoma (RR = 2.3, 95% CI 1.4–3.7) and squamous cell carcinoma (RR = 5.2, 95% CI 3.1–8.6) of the esophagus, as well as cardia (RR = 2.1, 95% CI 1.5–3.0) and noncardia stomach (RR = 1.3, 95% CI 1.2–1.6) cancers. We also observed excess risks for esophageal squamous cell carcinoma (RR = 3.5, 95% CI 1.6–7.6) and noncardia stomach cancer (RR = 1.4, 95% CI 1.1–1.9) among snus users who had never smoked. Although confounding by unmeasured exposures, and some differential misclassification of smoking, might have inflated the associations, our study provides suggestive evidence for an independent carcinogenic effect of snus. © 2007 Wiley‐Liss, Inc.
Identification of 2 putative critical segments of 17q gain in neuroblastoma through integrative genomics
Authors: Vandesompele Jo , Michels Evi , De Preter Katleen , Menten Björn , Schramm Alexander , Eggert Angelika , Ambros Peter F. , Combaret Valerie , Francotte Nadine , Antonacci Francesca , De Paepe Anne , Laureys Geneviève , Speleman Frank , Van Roy Nadine 
Published: October 2007

AbstractPartial gain of chromosome arm 17q is the most frequent genetic change in neuroblastoma (NB) and constitutes the strongest independent genetic factor for adverse prognosis. It is assumed that 1 or more genes on 17q contribute to NB pathogenesis by a gene dosage effect. In the present study, we applied chromosome 17 tiling path BAC arrays on a panel of 69 primary tumors and 28 NB cell lines in order to reduce the current smallest region of gain and facilitate identification of candidate dosage sensitive genes. In all tumors and cell lines with 17q gain, large distal segments were consistently present in extra copies and no interstitial gains were observed. In addition to these large regions of distal gain with breakpoints proximal to coordinate 44.3 Mb (17q21.32), smaller regions of gain (distal to coordinate 60 Mb at 17q24.1) were found superimposed on the larger region in a minority of cases. Positional gene enrichment analysis for 17q genes overexpressed in NB showed that dosage sensitive NB oncogenes are most likely located in the gained region immediately distal to the most distal breakpoint of the 2 breakpoint regions. Interestingly, comparison of gene expression profiles between primary tumors and normal fetal adrenal neuroblasts revealed 2 gene clusters on chromosome 17q that are overexpressed in NB, i.e. a region on 17q21.32 immediately distal to the most distal breakpoint (in cases with single regions of gain) and 17q24.1, a region coinciding with breakpoints leading to superimposed gain. © 2007 Wiley‐Liss, Inc.
Targeted photodynamic therapy with multiply‐loaded recombinant antibody fragments
Authors: Bhatti Manpreet , Yahioglu Gokhan , Milgrom Lionel R. , Garcia‐Maya Mitla , Chester Kerry A. , Deonarain Mahendra P. 
Published: October 2007

AbstractCurrent photodynamic therapy (PDT) of cancer is limited by inefficiencies involved in specifically targeting photosensitizers to tumors. Although antibodies are being explored as targeting vehicles, they present significant challenges, particularly in terms of pharmacokinetics and drug‐coupling. We describe here a novel and effective system to covalently attach multiple photosensitizer molecules (both preclinical, pyropheophorbide‐a and clinically approved, verteporfin photosensitizers) to single‐chain Fvs. Further, we demonstrate that not only do the resulting photoimmunoconjugates retain photophysical functionality, they are more potent than either free photosensitizer, effectively killing tumor cells in vitro and in vivo. For example, treatment of human breast cancer xenografts with a photoimmunoconjugate comprising an anti‐HER‐2 scFv linked to 8–10 molecules of pyropheophorbide‐a leads to significant tumor regression. These results give an insight into the important features that make scFvs good carriers for PDT drugs and provide proof of concept of our unique approach to targeted photodynamic therapy (tPDT). This promises to significantly improve on current photodynamic therapies for the treatment of cancer. © 2007 Wiley‐Liss, Inc.
RBP2‐H1/JARID1B is a transcriptional regulator with a tumor suppressive potential in melanoma cells
Authors: Roesch Alexander , Mueller Andrea M. , Stempfl Thomas , Moehle Christoph , Landthaler Michael , Vogt Thomas 
Published: October 2007

AbstractThe RBP2‐H1/JARID1B nuclear protein belongs to the ARID family of DNA‐binding proteins and is a potential tumor suppressor that is lost during melanoma development. As we have recently shown, one physiological function of RBP2‐H1/JARID1B is to exert cell cycle control via maintenance of active retinoblastoma protein. We now add new evidence that RBP2‐H1/JARID1B can also directly regulate gene transcription in a reporter assay system, either alone or as part of a multimolecular complex together with the developmental transcription factors FOXG1b and PAX9. In melanoma cells, chromatin immunoprecipitation combined with promoter chip analysis (ChIP‐on‐chip) suggests a direct binding of re‐expressed RBP2‐H1/JARID1B to a multitude of human regulatory chromosomal elements (promoters, enhancers and introns). Among those, a set of 23 genes, including the melanoma relevant genes CDK6 and JAG‐1 could be confirmed by cDNA microarray analyses to be differentially expressed after RBP2‐H1/JARID1B re‐expression. In contrast, in nonmelanoma HEK 293 cells, RBP2‐H1/JARID1B overexpression only evokes a minor transcriptional response in cDNA microarray analyses. Because the transcriptional regulation in melanoma cells is accompanied by an inhibition of proliferation, an increase in caspase activity and a partial cell cycle arrest in G1/0, our data support an anti‐tumorigenic role of RBP2‐H1/JARID1B in melanocytic cells. © 2007 Wiley‐Liss, Inc.
Family history of breast or ovarian cancer modifies the risk of secondary leukemia after breast cancer: Results from a population‐based study
Authors: Verkooijen Helena M. , Fioretta Gerald , Rapiti Elisabetta , Vlastos Georges , Neyroud‐Caspar Isabelle , Chappuis Pierre O. , Bouchardy Christine 
Published: October 2007

AbstractWe evaluated the impact of a family history of breast/ovarian cancer on the risk of secondary leukemia following breast cancer. At the Geneva cancer registry, we identified 4,397 patients diagnosed with invasive breast cancer between 1990 and 2004. Patients were followed up for leukemia until the end of 2005. Family history was categorized as positive in patients with ≥1 first‐ or second‐degree relative with breast/ovarian cancer. We compared leukemia rates in patients with positive and negative family histories with those expected in the general population, generating standardized incidence ratios (SIRs). With Cox regression analysis, we calculated adjusted risks of secondary leukemia in patients with familial risks compared to those without it. Breast cancer patients had a significantly increased risk of secondary acute leukemia (SIR 3.2, 95% CI: 1.2–6.9) but not of chronic leukemia (SIR 1.6, 95% CI: 0.6–3.5). Among patients with a positive family history (n = 1.125, 25.6%), the SIRs were 5.7 (95% CI: 1.2–16.6) for acute and 5.2 (95% CI: 1.4–13.3) for chronic leukemia. Among breast cancer patients, family history was independently associated with leukemia [adjusted hazard ratio (HRadj) of 3.2, 95% CI: 1.1–9.2, among patient with vs. without family history]. The effect of family history was stronger for chronic leukemia (HRadj: 11.6, 95% CI 1.3–104.7) than for acute leukemia (HRadj 1.6, 95% CI: 0.4–6.6). Breast cancer patients with a family history of breast/ovarian have an increased risk of secondary leukemia, both compared to the general population as well as to breast cancer patients without family histories. This excess risk is largely due to the increased risk of secondary chronic leukemia. © 2007 Wiley‐Liss, Inc.