bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of BORIS in melanoma: Lack of association with MAGE‐A1 activation
Authors: Kholmanskikh Olga , Loriot Axelle , Brasseur Francis , De Plaen Etienne , De Smet Charles 
Published: October 2007

AbstractSeveral genes with specific expression in germ cells show aberrant activation in different types of tumors. These genes, termed cancer‐germline (CG) genes, encode tumor‐specific antigens, which represent potential targets for therapeutic vaccination against cancer. The germline‐specific gene BORIS (Brother Of the Regulator of Imprinted Sites), which encodes an 11‐zinc‐fingers transcriptional regulator, was recently qualified as a new CG gene, as it was found to be activated in a variety of tumor samples. Moreover, it was suggested that BORIS might be responsible for the activation of most other CG genes, including gene MAGE‐A1, in tumors. In the present study, we evaluated the frequency of BORIS activation in melanoma by quantitative RT‐PCR. BORIS activation was detected in 27% (n = 63) melanoma tissue samples. Surprisingly, many melanoma samples expressed MAGE‐A1 and other CG genes in the absence of BORIS activation, suggesting that BORIS is not an obligate factor for activation of these genes in melanoma. Consistently, forced expression of BORIS in melanoma cell lines did not induce expression of MAGE‐A1. Our results indicate that BORIS may serve as a useful target for immunotherapy of melanoma. However, it appears that BORIS is neither necessary nor sufficient for the activation of other CG genes. © 2007 Wiley‐Liss, Inc.
Screening for prostate cancer in Dutch hereditary prostate cancer families
Authors: Kiemeney Lambertus A. , Broeders Mireille J. , Pelger Marjon , Kil Paul J. , Schröder Fritz H. , Witjes Johannes A. , Vasen Hans F. 
Published: October 2007

AbstractIt is common belief that in families with hereditary prostate cancer (HPC), unaffected men should be screened periodically with PSA, but little is known about the effects of such screening. We studied test and tumor characteristics in unaffected 50–75‐year‐old screenees from HPC families. In the Netherlands, 153 verified HPC families are registered; 132 unaffected men in these families were not under surveillance for prostate cancer and gave informed consent for PSA testing by their GP and referral to a urologist in the case of a PSA level ≥ 3.0 ng/ml. Results were compared to published data from the Rotterdam and Göteborg sections of the European Randomized Study of Screening for Prostate Cancer (ERSPC). A PSA ≥ 3.0 ng/ml was found in 20 men: referral rate, 15.1% (ERSPC Rotterdam: 20.1%; ERSPC Göteborg: 12.0%). Only 3 cases of prostate cancer were diagnosed in these men: detection rate in the first screening round 2.3% (ERSPC Rotterdam: 5.3%; ERSPC Göteborg: 2.3%). Frequent opportunistic PSA testing made it impossible to estimate the detection rates in subsequent screening rounds. In the first and subsequent PSA screening rounds, 11 cases of cancer were detected. All but 1 had favorable tumor characteristics (cT1c/pT2; Gleason < 7). These results raise the question as to whether men from all HPC families should be considered at high‐risk. We suggest that the same PSA testing guidelines should apply to HPC families and the general population. A more aggressive screening policy in HPC families does not seem to be justified. © 2007 Wiley‐Liss, Inc.
Nijmegen Breakage Syndrome mutations and risk of breast cancer
Authors: Bogdanova Natalia , Feshchenko Sergei , Schürmann Peter , Waltes Regina , Wieland Britta , Hillemanns Peter , Rogov Yuri I. , Dammann Olaf , Bremer Michael , Karstens Johann H. , Sohn Christof , Varon Raymonda , Dörk Thilo 
Published: October 2007

AbstractMutations in the NBS1 gene have been identified as disease‐causing mutations in patients with Nijmegen Breakage Syndrome (NBS), but their clinical impact on breast cancer susceptibility has remained uncertain. We determined the frequency of 2 NBS mutations, 657del5 and R215W, in two large series of breast cancer cases and controls from Northern Germany and from the Republic of Belarus. The 5‐bp‐deletion 657del5 was identified in 15/1,588 cases (0.9%) from Belarus and in 1/1,076 cases (0.1%) from Germany but in only 1/1,014 population controls from Belarus and 0/1017 German controls (p < 0.01). The missense substitution R215W was observed in 9/1,588 Byelorussian and 9/1,076 German patients (0.6% and 0.8%, respectively) but was also present in 5/1,014 Byelorussian and 2/1,017 German control individuals (adjusted OR = 1.9, 95%CI 0.8–4.6, p = 0.18). Studies of lymphoblastoid cell lines revealed that NBS1/p95 protein levels were reduced to 70% in cells from a heterozygous breast cancer patient carrying R215W and to 15% in cells from a NBS patient compound heterozygous for 657del5/R215W suggesting that the R215W substitution may be associated with protein instability. Levels of radiation‐induced phosphorylation of Nbs1/p95(Ser343) were reduced to 60% and 35% of wildtype, respectively. Neither age at diagnosis nor family history of breast cancer differed significantly between carriers and noncarriers of NBS mutations. The combined data are in line with an about 3‐fold increase in breast cancer risk for female NBS heterozygotes (OR 3.1; 95%CI 1.4–6.6) and indicate that the 657del5 deletion and perhaps the R215W substitution contribute to inherited breast cancer susceptibility in Central and Eastern Europe. © 2007 Wiley‐Liss, Inc.
Coactivator requirements for p53‐dependent transcription in the yeast Saccharomyces cerevisiae
Authors: Yousef Ahmed F. , Xu Guo Wei , Mendez Megan , Brandl Christopher J. , Mymryk Joe S. 
Published: October 2007

Abstractp53 is a sequence‐specific DNA‐binding transcription factor and key regulator of cell cycle arrest and apoptosis. p53 is mutated in most human cancers and these mutations generally impair its ability to activate transcription. When expressed in Saccharomyces cerevisiae, p53 acts as a strong transcriptional activator allowing yeast to be used as a model system to study the effects of p53 mutations on activity. However, little is known about the exact mechanisms by which p53 functions in yeast. Using 76 mutant yeast strains, we have evaluated the effect of deleting components of the ADA, COMPASS, INO80, ISW1, Mediator, RSC, SAGA, SAS, SLIK, SWI/SNF, and SWR1 transcriptional regulatory complexes on p53‐dependent transcription. In addition, we examined the role of histone H2B ubiquitylation by Rad6/Bre1 on p53 activation. Overall, our analysis indicates that there are several remarkable similarities between p53‐dependent transcription in yeast and mammalian cells, suggesting that yeast can serve as a valid model system for at least some aspects of p53 function. © 2007 Wiley‐Liss, Inc.
Genetic polymorphisms of MDM2, cumulative cigarette smoking and nonsmall cell lung cancer risk
Authors: Liu Geoffrey , Wheatley‐Price Paul , Zhou Wei , Park Sohee , Heist Rebecca S. , Asomaning Kofi , Wain John C. , Lynch Thomas J. , Su Li , Christiani David C. 
Published: October 2007

AbstractAbnormalities of the tumor suppressor TP53 pathway are critical in the development of many cancers since it regulates cell cycle components and apoptosis. Murine double minute‐2 (MDM2) protein is a central node in the p53 pathway and a direct negative regulator of p53. The MDM2 SNP309 (rs2279744) polymorphism increases MDM2 RNA and protein levels, attenuating the p53 pathway. The MDM2 SNP309 polymorphism was investigated in 1,787 Caucasian nonsmall cell lung cancer (NSCLC) patients and 1,360 healthy controls. Cases and controls were analyzed for associations with genotype and adjusted for age, gender, histology and smoking history. There were no overall associations between the MDM2 genotypes and risk of lung cancer (adjusted odds ratios [AORs] = 0.82 [95% confidence interval [CI] = 0.6–1.1] for the T/G genotype and AOR = 1.32 [95% CI = 0.9–2.0] for the G/G genotype). A statistically significant interaction (p = 0.01) was found between smoking and MDM2 genotypes. Consistent with this interaction, stratified analysis by pack‐years of smoking demonstrated that the AORs of G/G vs. T/T were 1.56 (1.0–2.7), 1.46 (1.0–2.2), 0.80 (0.5–1.3) and 0.63 (0.4–1.1), respectively, for never, mild (<30 pack‐years), moderate (30–57 pack‐years) and heavy smokers (≥58 pack‐years). In conclusion, a strong gene‐smoking interaction was observed between the MDM2 SNP309 and NSCLC risk. © 2007 Wiley‐Liss, Inc.
Anticancer effects of wogonin in both estrogen receptor‐positive and ‐negative human breast cancer cell lines in vitro and in nude mice xenografts
Authors: Chung Heekyoung , Jung Young‐mi , Shin Dong‐Hui , Lee Jeong‐Yeon , Oh Mi‐Yun , Kim Hyun‐Jun , Jang Ki Seok , Jeon Su Jin , Son Kun Ho , Kong Gu 
Published: October 2007

AbstractWogonin is a plant monoflavonoid which has been reported to inhibit cell growth and/or induce apoptosis in various tumors. Herein, we investigated the in vitro and in vivo anticancer effects and associated mechanisms of wogonin in human breast cancer. Effects of wogonin were examined in estrogen receptor (ER)‐positive and ‐negative human breast cancer cells in culture for proliferation, cell cycle progression, and apoptosis. The in vivo effect of oral wogonin was examined on tumor xenograft growth in athymic nude mice. The molecular changes associated with the biological effects of wogonin were analyzed by immunoblotting. Cell growth was attenuated by wogonin (50–200 μM), independently of its ER status, in a time‐ and concentration‐dependent manner. Apoptosis was enhanced and accompanied by upregulation of PARP and Caspase 3 cleavages as well as proapoptotic Bax protein. Akt activity was suppressed and reduced phosphorylation of its substrates, GSK‐3β and p27, was observed. Suppression of Cyclin D1 expression suggested the downregulation of the Akt‐mediated canonical Wnt signaling pathway. ER expression was downregulated in ER‐positive cells, while c‐ErbB2 expression and its activity were suppressed in ER‐negative SK‐BR‐3 cells. Wogonin feeding to mice showed inhibition of tumor growth of T47D and MDA‐MB‐231 xenografts by up to 88% without any toxicity after 4 weeks of treatment. As wogonin was effective both in vitro and in vivo, our novel findings open the possibility of wogonin as an effective therapeutic and/or chemopreventive agent against both ER‐positive and ‐negative breast cancers, particularly against the more aggressive and hormonal therapy‐resistant ER‐negative types. © 2007 Wiley‐Liss, Inc.
Impact of serum total cholesterol on the incidence of gastric cancer in a population‐based prospective study: The Hisayama study
Authors: Asano Kouichi , Kubo Michiaki , Yonemoto Koji , Doi Yasufumi , Ninomiya Toshiharu , Tanizaki Yumihiro , Arima Hisatomi , Shirota Tomoko , Matsumoto Takayuki , Iida Mitsuo , Kiyohara Yutaka 
Published: October 2007

AbstractThe results of prospective studies that have examined the association between serum cholesterol levels and the incidence of gastric cancer remain controversial. To examine this issue in a general population, a total of 2,604 subjects aged 40 years or older were followed up prospectively for 14 years. During the follow‐up period, gastric cancer developed in 97 subjects. The age‐ and sex‐adjusted incidence of gastric cancer by quartiles of serum cholesterol level, namely, <4.06, 4.06–5.32, 5.33–6.04 and ≥6.05 mmol/L, were 3.9, 3.3, 3.1 and 2.1 per 1,000 person–years, respectively. The risk of gastric cancer increased with decreasing cholesterol level (age‐ and sex‐adjusted hazard ratio [HR], 1.22; 95% confidence interval [CI], 1.01–1.49;p= 0.04 for a decrease of 1 mmol/L in serum cholesterol level). This inverse association remained unchanged even after adjustment for other confounding factors, namely,Helicobacter pyloriinfection, atrophic gastritis, family history of malignant neoplasm, smoking habits, body mass index, hemoglobin A1c, white blood cell count and dietary factors (adjusted HR, 1.28; 95% CI, 1.03–1.58;p= 0.02). This association was significant for intestinal‐type gastric cancers, but not for diffuse‐type. As regards cancer stage, the inverse cholesterol‐cancer association was marginally significant for early gastric cancer after multivariate‐adjustment (adjusted HR, 1.25; 95% CI, 0.97–1.61;p= 0.09), but was not for advanced gastric cancer probably due to the small number of cases. In conclusion, our findings suggest that low serum cholesterol levels are an independent risk factor for developing gastric cancer, especially intestinal‐type gastric cancer. © 2007 Wiley‐Liss, Inc.
Novel production method and in‐vitro cell compatibility of porous Ti‐6Al‐4V alloy disk for hard tissue engineering
Authors: Bhattarai Shanta Raj , Khalil Khalil Abdel‐Razek , Dewidar Montasser , Hwang Pyoung Han , Yi Ho Keun , Kim Hak Yong 
Published: October 2007

AbstractPorous metals are attractive due to its unique physical, mechanical, and new bone tissue ingrowth properties. In the present study, the production of highly porous Ti‐6Al‐4V parts by powder metallurgical technology and subsequently it's uses in in vitro bone tissue engineering is described. A space‐holder method using carbamide with different particle size to produce parts with porosities between 35 and 70% were applied. The compressive strength and Young's modulus of porous Ti‐6Al‐4V were determined. Results indicated that stress and Young's modulus decrease with increasing porosity and pore size. The porous parts are characterized by scanning electron microscopy. Furthermore, study was to investigate the effects of three different porosities of porous Ti‐6Al‐4V (35, 50, and 70%) on proliferation, differentiation, and cell–matrix interaction of mouse osteoblast‐like cells, MC‐3T3. Results showed that the cell proliferation was significantly (p < 0.05) higher on 70% porous Ti‐6Al‐4V. However, synthesis of different types of extra cellular matrix proteins was also more abundant on 70% porous Ti‐6Al‐4V than 35 and 50% porous Ti‐6Al‐4V disk except some specific proteins. An increase in alkaline phosphate activity was significantly (p < 0.05) higher on 70 and 50% porous Ti‐6Al‐4V disk after 12 days of MC‐3T3 cells incubation. Above all, results indicated that porosity (nearly 70%) of porous Ti‐6Al‐4V topography affects proliferation and differentiation of osteoblast‐like MC‐3T3 cells. The results showed that this novel process is a promise to fabricate porous biomaterials for bone implants. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2008
Micelles of poly(ethylene oxide)‐b‐poly(ε‐caprolactone) as vehicles for the solubilization, stabilization, and controlled delivery of curcumin
Authors: Ma Zengshuan , Haddadi Azita , Molavi Ommoleila , Lavasanifar Afsaneh , Lai Raymond , Samuel John 
Published: October 2007

AbstractCurcumin is recognized as a potential chemotherapeutic agent against a variety of tumors. However, the clinical application of curcumin is hindered due to its poor water solubility and fast degradation. The objective of this study was to investigate amphiphilic block copolymer micelles of poly(ethylene oxide)‐b‐poly(ϵ‐caprolactone) (PEO‐PCL) as vehicles for the solubilization, stabilization, and controlled delivery of curcumin. Curcumin‐loaded PEO‐PCL micelles were prepared by a cosolvent evaporation technique. PEO‐PCL micelles were able to solubilize curcumin effectively, protect the encapsulated curcumin from hydrolytical degradation in physiological matrix, and control the release of curcumin over a few days. The characteristics of resultant micelles were found to depend on the polymerization degrees of ϵ‐caprolactone. Among different PEO‐PCL micelles, PEO5000‐PCL24500 was the most efficient in solubilizing curcumin while PEO5000‐PCL13000 was the best carrier in reducing its release rate. PEO‐PCL micelle‐encapsulated curcumin retained its cytotoxicity in B16‐F10, a mouse melanoma cell line, and SP‐53, Mino, and JeKo‐1 human mantle cell lymphoma cell lines. These results demonstrated the potential of PEO‐PCL micelles as an injectable formulation for efficient solubilization, stabilization, and controlled delivery of curcumin. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2008
Aurora‐A kinase phosphorylation of Aurora‐A kinase interacting protein (AIP) and stabilization of the enzyme‐substrate complex
Authors: Katayama Hiroshi , Sasai Kaori , Czerniak Bogdan A. , Carter Jennifer L. , Sen Subrata 
Published: October 2007

AbstractAurora‐A is an oncogenic kinase that plays essential roles in mitosis as well as cell survival. Aurora‐A interacting protein (AIP) was identified as a negative regulator of Aurora‐A with its ectopic over expression inducing destabilization of Aurora‐A protein. Here we present evidence that in human cells, contrary to the earlier report, AIP functions in stabilizing rather than destabilizing Aurora‐A. Furthermore, AIP is phosphorylated on Serine 70 by Aurora‐A but not Aurora‐B and expression of phosphorylation mimic mutant of AIP results in prolonged protein stability compared to unphosphorylatable mutant. We observed that when co‐expressed with AIP, protein levels of both Aurora‐A and Aurora‐B are markedly elevated regardless of their kinase activities and phosphorylation state of AIP. Interaction of Aurora kinases with AIP is necessary for this elevated stability. This phenomenon is commonly detected in several human cancer cell lines used in this study. Depletion of AIP by RNA interference decreased Aurora‐A but not Aurora‐B in two of the three cell lines analyzed, indicating that under physiological condition, AIP functions in stabilization of Aurora‐A but not Aurora‐B, though this regulation may be dependent on additional factors as well. Further, AIP siRNA induced cell cycle arrest at G2/M, which is consistent with anticipated loss of function of Aurora‐A in these cells. Thus, our study provides the first evidence of a role for AIP in G2/M cell cycle progression by cooperatively regulating protein stabilization of its up‐stream regulator, Aurora‐A kinase through protein–protein interaction as well as protein phosphorylation. J. Cell. Biochem. 102: 1318–1331, 2007. © 2007 Wiley‐Liss, Inc.
Molecular signaling in the regulation of mucins
Authors: Theodoropoulos George , Carraway Kermit L. 
Published: October 2007

AbstractMucins are large, highly glycosylated proteins involved in the protection of epithelia. The 20 different mucins show a diverse and highly regulated distribution among different epithelia. Most of the studies on mucin regulation done to date have been on the membrane mucins MUC1 and MUC4 and the gel‐forming mucins. Multiple mechanisms have been implicated in that regulation, including examples at the transcriptional, transcript stabilization and post‐translational levels. Several signaling pathways have been demonstrated to be involved, most frequently the canonical Erk MAP kinase pathway, but also the cytokine‐JAK‐STAT pathway and TGFβ‐SMAD pathways. Diversity in Erk signaling is achieved through multiple activation mechanisms and multiple downstream transcriptional factors that are affected. Given the still limited amount of information available on regulation of most of the mucins, other mechanisms and pathways are likely to be uncovered in the future. J. Cell. Biochem. 102: 1103–1116, 2007. © 2007 Wiley‐Liss, Inc.
On k‐domination and minimum degree in graphs
Authors: Favaron Odile , Hansberg Adriana , Volkmann Lutz 
Published: October 2007

AbstractA subset S of vertices of a graph G is k‐dominating if every vertex not in S has at least k neighbors in S. The k‐domination number $\gamma_k(G)$ is the minimum cardinality of a k‐dominating set of G. Different upper bounds on $\gamma_{k}(G)$ are known in terms of the order n and the minimum degree $\delta$ of G. In this self‐contained article, we present an Erdös‐type result, from which some of these bounds follow. In particular, we improve the bound $\gamma_{k}(G) \le (2k- \delta - 1)n/(2k -\delta)$ for $(\delta +3)/2 \le k \le \delta - 1$, proved by Chen and Zhou in 1998. Furthermore, we characterize the extremal graphs in the inequality $\gamma_{k}(G) \le kn/(k +1)$, if $k \le \delta$, of Cockayne et al. This characterization generalizes that of graphs realizing $\gamma_1(G) = \gamma(G) = n/2$. © 2007 Wiley Periodicals, Inc. J Graph Theory 57: 33–40, 2008
Volume and morphology changes of a bdelloid rotifer species (Macrotrachela quadricornifera) during anhydrobiosis
Authors: Ricci Claudia , Caprioli Manuela , Fontaneto Diego , Melone Giulio 
Published: October 2007

AbstractFollowing a study on the changes occurring in a bdelloid species (Macrotrachela quadricornifera, Rotifera, Bdelloidea) when entering anhydrobiosis, we investigated the changes in morphology, including weight and volume during the transition from the active hydrated to the dormant anhydrobiotic state by scanning electron microscopy, confocal microscopy and light microscopy. We compared sizes and morphologies of hydrated extended, hydrated contracted and anhydrobiotic specimens. Bdelloid musculature is defined: longitudinal muscles are contracted in the hydrated contracted animal (head and foot are retracted inside the trunk), but appear loose in the anhydrobiotic animal. When anhydrobiotic, M. quadricornifera appears much smaller in size, with a volume reduction of about 60% of the hydrated volume, and its internal organization undergoes remarkable modifications. Internal body cavities, clearly distinguishable in the hydrated extended and contracted specimens, are no longer visible in the anhydrobiotic specimen. Concomitantly, M. quadricornifera loses more than 95% of its weight when anhydrobiotic; this is more than expected from the volume reduction data and could indicate the presence of space‐filling molecular species in the dehydrated animal. We estimate that the majority of body mass loss and volume reduction can be ascribed to the water loss from the body cavity during desiccation. J. Morphol., 2008. © 2007 Wiley‐Liss, Inc.
Cooperative particle swarm optimization of passive microwave devices
Authors: Mahanfar Alireza , Bila Stéphane , Aubourg Michel , Verdeyme Serge 
Published: October 2007

AbstractParticle swarm optimization (PSO) has lately become very popular in the electromagnetics domain. Although in some instances PSO shows a superior performance compared with other global optimization techniques, it is still computationally more expensive relative to classical gradient techniques. In this paper, a cooperative particle swarm optimization (CPSO) is adopted to achieve a faster convergence compared with the conventional PSO, while maintaining its main feature, which is the capability of finding global optimum. In order to deploy PSO more efficiently, the often neglected effect of the initial population on the overall convergence of PSO is discussed. It is shown that subdividing the space into grid cells and using random distribution within these cells will give the best results in terms of convergence speed. Different boundary conditions are tried on the CPSO algorithm. In order to verify the performance of the proposed algorithm, the algorithm is compared with the conventional PSO using six different objective functions. As a design example, an ultra‐wide‐band filter is designed. The results show a slightly faster convergence compared with the conventional PSO. The designed filter is fabricated and experimental results are also shown. Copyright © 2007 John Wiley & Sons, Ltd.