bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinical correlates of clozapine prescription for schizophrenia in China
Authors: Xiang Yu‐tao , Weng Yong‐zhen , Leung Chi‐Ming , Tang Wai‐Kwong , Ungvari Gabor Sandor 
Published: December 2006

AbstractAimsFew studies have investigated the prescription patterns of clozapine in outpatients with schizophrenia in China. It is an important issue due to clozapine's high efficacy and potentially fatal side effect profile. This study examined the use of clozapine and its correlates in China.MethodsThree hundred ninety‐eight clinically stable outpatients with schizophrenia were randomly selected and interviewed in Hong Kong (HK) and Beijing (BJ). Assessment instruments included the Structured Clinical Interview for DSM‐IV, Brief Psychiatric Rating Scale, Simpson and Angus Scale of Extrapyramidal Symptoms, Barnes Akathisia Rating Scale and the Hong Kong and Mainland China World Health Organization Quality of Life Schedule‐Brief version. Assessments were performed by the same investigator in both sites.ResultsClozapine was prescribed to 15.6% of (n = 62) patients. There was a wide inter‐site variation between HK and BJ. Use of clozapine was associated with age, age at onset, extrapyramidal side effects (EPS), having health insurance, use of depot and typical antipsychotic and anticholinergic drugs and benzodiazepines as well as history of suicidal attempts. On multiple logistic regression analysis, the number of hospitalizations, site (HK vs. BJ), use of typical antipsychotics, polypharmacy and co‐prescription with anticholinergics were significantly associated with the prescription of clozapine. No significant differences were found between the clozapine and non‐clozapine groups with regard to any of the quality of life domains.ConclusionA combination of economical and clinical factors, health policies and the characteristics of the treatment settings plays important roles in determining clozapine use. Clozapine appears to have little significant influence on quality of life in clinical stable Chinese patients with schizophrenia. Copyright © 2007 John Wiley & Sons, Ltd.
CNTO 859, a humanized anti‐tissue factor monoclonal antibody, is a potent inhibitor of breast cancer metastasis and tumor growth in xenograft models
Authors: Ngo Cam V. , Picha Kristen , McCabe Francis , Millar Hillary , Tawadros Richard , Tam Susan H. , Nakada Marian T. , Anderson G. Mark 
Published: December 2006

AbstractThromboembolic complications are frequently associated with advanced cancer. Interestingly, one of the major initiators of blood coagulation, tissue factor (TF), is reported to be overexpressed in several tumor types and can be found on both tumor cells and tumor vasculature. Although the exact mechanisms have yet to be elucidated, TF expressed on tumor cells can trigger intracellular signaling events through various pathways that can lead to tumor angiogenesis, proliferation, and metastasis. There exists preclinical evidence that disruption of TF dependent signaling can effectively inhibit tumor cell migration, metastasis, and angiogenesis. Here, we report for the first time that an antibody to tissue factor can also prevent tumor growth in vivo. Prophylactic administration of CNTO 859, a humanized anti‐human TF antibody, was shown to inhibit experimental lung metastasis of MDA‐MB‐231 human breast carcinoma cells by over 99% compared to a control antibody. Furthermore, therapeutic doses of CNTO 859 were shown to reduce tumor incidence and growth of orthotopically implanted MDA‐MB‐231 cells. © 2006 Wiley‐Liss, Inc.
Excess of cancers in Europe: A study of eleven major cancers amenable to lifestyle change
Authors: Soerjomataram Isabelle , de Vries Esther , Pukkala Eero , Coebergh Jan Willem 
Published: December 2006

AbstractWorldwide an estimated 11 million cancer cases were diagnosed in 2002, one quarter being in Europe. We estimated the potential in avoidable numbers and proportions of 11 cancers amenable to prevention (cancers of the oral cavity, oesophagus, stomach, colorectal, pancreas, laryngeal, lung, female breast, endometrium, kidney and bladder) in 28 European countries. We assumed that the aggregated rate of 3 countries with lowest incidence to be attainable throughout Europe. The difference between the age‐ and gender‐specific national cancer incidence rates and the lowest rate observed in 2002 was determined and defined as “avoidable.” Of the 1.4 million adult cases of selected cancers and countries within our study, 363,000 (59%) cancers in males and 326,000 (45%) cancers in females were hypothetically avoidable. Among men, the proportion was largest in Hungary (77%) and among women, in Belgium (54%). Assuming that differences in cancer incidence are not attributable to genetic susceptibility or diagnostic activity, about 50% of all cases of these 11 cancers could be potentially avoided, especially by decreased smoking among men. Interventions directed at reducing smoking, obesity and alcohol use as well as increasing physical activity and fruit and vegetable intake are necessary to attain lower incidence rates. It is important to recognize that the actual preventable cancer by eliminating currently known risk factors is somewhat less than we have estimated. © 2006 Wiley‐Liss, Inc.
Accurate discrimination of pancreatic ductal adenocarcinoma and chronic pancreatitis using multimarker expression data and samples obtained by minimally invasive fine needle aspiration
Authors: Chen Yian , Zheng Bin , Robbins David H. , Lewin David N. , Mikhitarian Kaidi , Graham Amanda , Rumpp Laurrie , Glenn Tammy , Gillanders William E. , Cole David J. , Lu Xinghua , Hoffman Brenda J. , Mitas Michael 
Published: December 2006

AbstractTo augment cytological diagnosis of pancreatic ductal adenocarcinoma (PDAC) in tissue samples obtained by minimally invasive endoscopic ultrasound‐guided fine needle aspiration, we investigated whether a small set of molecular markers could accurately distinguish PDAC from chronic pancreatitis (CP). Expression levels of 29 genes were first determined by quantitative real‐time RT‐PCR in a training set of tissues in which the final diagnosis was PDAC (n = 20) or CP (n = 10). Using receiver operator characteristic curve analysis, we determined that the single gene with the highest diagnostic accuracy for discrimination of CP vs. PDAC in the training study was urokinase plasminogen activator receptor (UPAR; AUC value = 0.895, 95% CI = 0.728–0.976). In the set of test tissues (n = 14), the accuracy of UPAR decreased to 79%. However, we observed that the addition of 6 genes (EPCAM2, MAL2, CEA5, CEA6, MSLN and TRIM29; referred to as the 6‐gene classifier) to UPAR resulted in high accuracy in both training and testing sets. Excluding 3 samples (out of 44; 7%) for which results of the UPAR/6‐gene classifier were “undefined,” the accuracy of the UPAR/6‐gene classifier was 100% in training samples (n = 29), 92% in 12 test samples (p = 0.004 that results were randomly generated; p = 0.046 that the UPAR/6‐gene classifier was comparable to UPAR alone; χ2 test), 100% in 3 samples for which the initial cytological diagnosis was “suspicious” and 98% (40/41) overall. Our results provide evidence that molecular marker expression data can be used to augment cytological analysis. © 2006 Wiley‐Liss, Inc.
Parity, tubal sterilization, hysterectomy and risk of primary fallopian tube carcinoma in Finland, 1975–2004
Authors: Riska Annika , Sund Reijo , Pukkala Eero , Gissler Mika , Leminen Arto 
Published: December 2006

AbstractWe studied the possible relationship among parity, female sterilization, hysterectomy and the risk of primary fallopian tube carcinoma (PFTC) in a case–control study in Finland in cases occurring between 1975 and 2004. A total of 573 PFTC cases were identified from the Finnish Cancer Registry, and10 age‐matched controls per case were randomly selected from the Finnish Central Population Registry. In multivariate analysis (including 189 PFTC cases and 1764 controls) parity was protective: the odds ratio (OR) for 1–2 deliveries was 0.63 (95% CI 0.44–0.91) and for ≥3 deliveries, 0.32 (95% CI 0.19–0.52). The OR for sterilization was 0.74 (95% CI 0.42–1.30) and for hysterectomy 1.27 (95% CI 0.73–2.21). Our findings suggest a possible hormonal background as regards the development of PFTC. © 2006 Wiley‐Liss, Inc.
Lack of BK virus DNA sequences in most transitional‐cell carcinomas of the bladder
Authors: Rollison Dana E. , Sexton Wade J. , Rodriguez Alejandro R. , Kang Loveleen C. , Daniel Richard , Shah Keerti V. 
Published: December 2006

AbstractBK virus (BKV), a common human polyomavirus infection latent in the kidneys, can reactivate with immunosuppression to cause renal disease. Some have suggested that BKV may contribute to the development of bladder cancer, and BKV sequences have been reported from bladder tumors. To further examine the role of BKV in human bladder cancer, a series of bladder tumors was investigated for BKV genomic sequences. Fresh‐frozen specimens from 76 transitional cell carcinoma tissues and 46 paired adjacent normal urothelial tissues archived at the H. Lee Moffitt Cancer Center were studied. All tissues were histopathologically reviewed. DNA extracted from the tissues was tested by quantitative real‐time polymerase chain reaction (QPCR) assays to detect BKV DNA sequences in the VP1 coding region. Amplification of ERV‐3 was conducted separately to quantify cell copy number. Conventional PCR targeting the BKV T‐antigen (T‐Ag) coding region and immunohistochemistry for BKV T‐Ag were also conducted on all tissues that tested positive for BKV by QPCR. Seventy‐three bladder tumors yielded ≥3,000 copies of ERV‐3, 4 (5.5%) of which tested positive for BKV with average copy numbers of 7.9, 15.8, 0.4 and 0.3 per 1,000 cells. Paired normal tissue was available for 2 of these BKV‐positive tumors, 1 of which was BKV‐positive (14.6 copies/1,000 cells). No other normal tissues were BKV‐positive by QPCR. The 6 BKV‐positive tissues by QPCR were also positive by conventional PCR, but all stained negative for BKV T‐Ag by immunohistochemistry. BKV is unlikely to be involved in the etiology of most bladder tumors. © 2006 Wiley‐Liss, Inc.
The impact of epidermal growth factor receptor gene status on gefitinib‐treated Japanese patients with non‐small‐cell lung cancer
Authors: Ichihara Shuji , Toyooka Shinichi , Fujiwara Yoshiro , Hotta Katsuyuki , Shigematsu Hisayuki , Tokumo Masaki , Soh Junichi , Asano Hiroaki , Ichimura Kouichi , Aoe Keisuke , Aoe Motoi , Kiura Katsuyuki , Shimizu Kenji , Date Hiroshi , Shimizu Nobuyoshi 
Published: December 2006

AbstractWe investigated the relationships between genetic factors and clinical outcome in Japanese non‐small‐cell lung cancer (NSCLC) patients treated with gefitinib. Ninety‐eight NSCLC patients who had been treated with gefitinib, were screened for mutations in epidermal growth factor receptor (EGFR) exons 18–21, KRAS exon2, and polymorphisms including the CA simple sequence repeat in intron1 (CA‐SSR1) and single nucleotide polymorphisms in the promoter region (−216G/T and −191C/A), using a PCR‐based assay and direct sequencing. The EGFR copy number status was also evaluated using a fluorescence in situ hybridization assay. EGFR and KRAS mutations were found in 38 (38.8%) and 8 (8.2%) of the 98 patients, respectively. A high EGFR copy number status was identified in 31 (41.3%) of the 75 assessable patients. Drug‐sensitive EGFR mutations limited to exon19 deletions and L858R were independent predictive factors of a stronger sensitivity to gefitinib (p = 0.0002), the overall survival (OS) (p = 0.0036), and prolonged progression‐free survival (PFS) (p < 0.0001). The EGFR copy number status was not related to a sensitivity to gefitinib and prolonged OS and PFS. Regarding polymorphisms, patients with a short CA‐SSR1 showed a prolonged OS as compared with those with a long length in patients with a drug‐sensitive EGFR mutation, although this difference was not significant (p = 0.13). Thus, drug‐sensitive EGFR mutations predict a favorable clinical outcome and a high EGFR copy number may not be related to clinical benefits in gefitinib‐treated Japanese patients with NSCLC. Our findings also suggest that the CA‐SSR1 length may influence the clinical outcome in patients with a drug‐sensitive EGFR mutation. © 2006 Wiley‐Liss, Inc.
Specific membrane recruitment of Uso1 protein, the essential endoplasmic reticulum‐to‐Golgi tethering factor in yeast vesicular transport
Authors: Noda Yoichi , Yamagishi Tomoe , Yoda Koji 
Published: December 2006

AbstractUso1 is a yeast essential protein that functions to tether vesicles in the ER‐to‐Golgi transport. Its recruitment to the ER‐derived vesicles has been demonstrated in in vitro membrane transport systems using semi‐intact cells. Here we report that the binding of Uso1 to specific membranes can be detected through simple sucrose density block centrifugation. The purified Uso1 protein binds to slowly sedimenting membranes generated from rapidly sedimenting P10 membranes. These membranes were produced dependent on ATP hydrolysis, contained COPII vesicle components, but had neither of the coat subunits or ER proteins, which indicates that they were representative of the uncoated ER‐derived COPII vesicles. The slowly sedimenting membranes of different origins were physically linked when they were mixed in the presence of Uso1. The C‐terminal acidic region was not required in membrane binding. The presence of membranes to which Uso1 could bind in the yeast cell lysate was detected using the current method. J. Cell. Biochem. 101: 686–694, 2007. © 2006 Wiley‐Liss, Inc.
Involvement of NO/cGMP signaling in the apoptotic and anti‐angiogenic effects of β‐lapachone on endothelial cells in vitro
Authors: Kung Hsiu‐Ni , Chien Chung‐Liang , Chau Gar‐Yang , Don Ming‐Jaw , Lu Kuo‐Shyan , Chau Yat‐Pang 
Published: December 2006

AbstractNeovascularization is an essential process in tumor development, it is conceivable that anti‐angiogenic treatment may block tumor growth. In angiogenesis, nitric oxide (NO) is an important factor which mediates vascular endothelial cell growth and migration. β‐Lapachone (3,4‐dihydro‐2,2‐dimethyl‐2H‐naphtho‐[1,2‐b]pyran‐5,6‐dione), a natural product extracted from the lapacho tree (Tabebuia avellanedae), has been demonstrated to possess anti‐cancer and anti‐viral effects. Whether β‐lapachone can induce endothelial cell death or has an anti‐angiogenic effect is still an enigma. We investigated the in vitro effect of β‐lapachone on endothelial cells, including human vascular endothelial cell line, EAhy926, and human umbilical vascular endothelial cells (HUVEC). Our results revealed that (1) the intracellular cGMP levels and the mitochondria membrane potential (MMP) decreased, and calpain and caspases were activated, during β‐lapachone‐induced endothelial cell death; (2) co‐treatment with calpain inhibitors (ALLM or ALLN) or the intracellular calcium chelator, BAPTA, but not the general caspase inhibitor, zVAD‐fmk, provided significant protection against apoptosis by preventing the β‐lapachone‐induced MMP decrease and cytoplasmic calcium increase; (3) addition of NO downregulated the β‐lapachone‐induced cGMP depletion and protected the cells from apoptosis by blocking the MMP decrease and the calcium increase; and (4) exogenous NO protects endothelial cells against the cell death induced by β‐lapachone, but not the anti‐angiogenic effect. From all the data above, we demonstrated that NO can attenuate the apoptotic effect of β‐lapachone on human endothelial cells and suggest that β‐lapachone may have potential as an anti‐angiogenic drug. J. Cell. Physiol. 211: 522–532, 2007. © 2006 Wiley‐Liss, Inc.
Type I interferon response against viral and non‐viral gene transfer in human tumor and primary cell lines
Authors: Rautsi Outi , Lehmusvaara Saara , Salonen Tuula , Häkkinen Katja , Sillanpää Maarit , Hakkarainen Tanja , Heikkinen Sami , Vähäkangas Elisa , Ylä‐Herttuala Seppo , Hinkkanen Ari , Julkunen Ilkka , Wahlfors Jarmo , Pellinen Riikka 
Published: December 2006

AbstractBackgroundType I interferon (IFN‐α/β) response is one of the major host defence mechanisms against viruses. Some recent reports suggest that IFNs may interfere with the efficacy of both non‐viral and virus‐vector‐mediated therapeutic gene transfer.MethodsThe type I IFN response upon different gene transfer methods in human tumor and primary cell lines was studied by analysing IFN‐β mRNA expression, secretion of type I IFNs and accumulation of IFN‐α/β‐induced MxA protein (myxovirus resistance protein A).ResultsInfection with avirulent Semliki Forest virus A7[74] induced MxA protein accumulation and increased the IFN‐β mRNA level, whereas none of the studied virus vectors (adenovirus, CRAd, lentivirus or AAV) induced IFN response. However, plasmid DNA induced the accumulation of MxA protein when transfected with several commercial transfection reagents. RNA transfection appeared to be an efficient inducer of type I IFN response: replicating alphaviral RNA, eukaryotic total RNA, or mRNA all induced both MxA protein accumulation and IFN‐β expression. siRNA transfection failed to induce MxA response.ConclusionsThe non‐viral gene transfer methods have gained more interest in recent years due to their better safety profiles when compared to their viral counterparts. However, the efficiency of non‐viral gene transfer is well below those reached by viral vector systems. The type I interferon response induced by non‐viral methods may in part contribute to this inefficiency, while most currently used viral gene transfer vectors fail to induce or are able to suppress type I IFN response. Copyright © 2006 John Wiley & Sons, Ltd.
Quality of life in patients with hepatocellular carcinoma received surgical resection
Authors: Lee Lukas Jyuhn‐Hsiarn , Chen Chien‐Hung , Yao Grace , Chung Chih‐Wen , Sheu Jin‐Chuan , Lee Po‐Huang , Tsai Yih‐Jian , Wang Jung‐Der 
Published: December 2006

AbstractBackgroundHepatocellular carcinoma (HCC) is one the most common malignancies in the world. As the prognosis for HCC patients is poor, the quality of life (QOL) is becoming more important on the outcome assessments. The aim of this study was to evaluate QOL in HCC patients.MethodsA total of 161 patients with HCC were enrolled at a university hospital. Most of these patients received surgical resections. They were assessed with Taiwan versions of WHOQOL‐BREF, EORTC QLQ‐C30, and utility measures. The WHOQOL‐BREF domain scores for the HCC patients were compared to healthy normative Taiwan population, using general linear models controlling for gender and age. Multiple logistic regressions were applied to explore association between a better QOL and clinical/sociodemographic variables.ResultsCompared with healthy people, the HCC patients had reduced QOL in physical domains, but better environmental QOL. After controlling gender, age, education, and employment, duration of HCC more than 1 year was associated with better QOL scores. WHOQOL‐BREF could be cross‐validated with EORTC QLQ‐C30.ConclusionsSurvival over 1 year was associated with better QOL in HCC patients. WHOQOL‐BREF could be a valid QOL instrument for the assessments of QOL in HCC patients. J. Surg. Oncol. 2007;95:34–39. © 2006 Wiley‐Liss, Inc.
Influence of epidermal growth factor receptor (EGFR) gene mutations on the expression of EGFR, phosphoryl‐Akt, and phosphoryl‐MAPK, and on the prognosis of patients with non‐small cell lung cancer
Authors: Sonobe Makoto , Nakagawa Masatsugu , Takenaka Kazumasa , Katakura Hiromichi , Adachi Masashi , Yanagihara Kazuhiro , Otake Yosuke , Wada Hiromi , Tanaka Fumihiro 
Published: December 2006

AbstractBackground and ObjectivesIn this paper we examined the influence of epidermal growth factor receptor (EGFR) gene mutations on EGFR expression, downstream mediators, and survival in patients with non‐small cell lung cancer (NSCLC).MethodsWe retrospectively analyzed the tumors of 53 patients with completely resected pathological stage I–IIIA NSCLC for the presence of EGFR gene mutations, the expression of EGFR mRNA and protein, phosphoryl‐Akt, and phosphoryl‐mitogen‐activated protein kinase (MAPK) using immunostaining, and patients' prognosis.ResultsEGFR mutations were associated with elevations in EGFR mRNA (P = 0.004) and protein (P = 0.029) expression, but not with the expression of phosphoryl‐Akt or phosphoryl‐MAPK. The 5‐year survival rate for all patients who exhibited an EGFR mutation was similar to those who were free of such mutations (71% vs. 56%, P = 0.252). However, the 5‐year survival rate of patients with either a stage I adenocarcinoma or large cell carcinoma who had an EGFR mutation was significantly greater than for those who did not have such a mutation (92% vs. 57%, P = 0.037).ConclusionsEGFR gene mutations were significantly associated with higher EGFR expression, but not with p‐Akt or p‐MAPK status. In early stage NSCLC, the presence of an EGFR gene mutation bode well for the patient's prognosis. J. Surg. Oncol. 2007;95:63–69. © 2006 Wiley‐Liss, Inc.
Hedgehog signaling pathway is a possible therapeutic target for gastric cancer
Authors: Yanai Kosuke , Nagai Shuntaro , Wada Junji , Yamanaka Naoki , Nakamura Masafumi , Torata Nobuhiro , Noshiro Hirokazu , Tsuneyoshi Masazumi , Tanaka Masao , Katano Mitsuo 
Published: December 2006

AbstractBackground and ObjectivesIt has been shown that the hedgehog (Hh) signaling pathway is activated in gastric cancer. To investigate the viability of the Hh pathway as a therapeutic target, we analyzed activation of the Hh pathway in gastric cancer.MethodsSurgically resected gastric carcinoma specimens and lymph nodes were analyzed immunohistochemically. We used the percentage of cancer cells with nuclear translocation of Gli1 as a marker of Hh pathway activation.ResultsNuclear localization of Gli1 was higher in 28 undifferentiated‐type tumors than in 30 differentiated‐type tumors. Eighteen of the fifty‐eight cancer specimens consisted of a mixture of a histologically predominant part and a small area with different histology. In these 18 tumors, the percentage of cells showing nuclear staining of Gli1 was higher in the undifferentiated‐type part than in the differentiated‐type part. Nuclear staining of Gli1 in primary tumors was positively correlated with lymph node metastasis. The Gli1 nuclear staining percentage of metastatic lymph nodes correlated closely with that of each primary carcinoma. Cyclopamine, a Hh pathway inhibitor, suppressed the growth of gastric cancer cells in vitro.ConclusionsThe Hh pathway may be a useful therapeutic target for such as undifferentiated‐type gastric cancer with lymph node metastasis. J. Surg. Oncol. 2007;95:55–62. © 2006 Wiley‐Liss, Inc.