bluuebunny/crossref_metadata_2025_split huggingface dataset:
Flood simulation using the gauge‐adjusted radar rainfall and physics‐based distributed hydrologic model
Authors: Sik Kim Byung , Kyung Kim Bo , Soo Kim Hung 
Published: October 2008

AbstractThis paper reports the results of an investigation into flood simulation by areal rainfall estimated from the combination of gauged and radar rainfalls and a rainfall–runoff model on the Anseong‐cheon basin in the southern part of Korea. The spatial and temporal characteristics and behaviour of rainfall are analysed using various approaches combining radar and rain gauges: (1) using kriging of the rain gauge alone; (2) using radar data alone; (3) using mean field bias (MFB) of both radar and rain gauges; and (4) using conditional merging technique (CM) of both radar and rain gauges. To evaluate these methods, statistics and hyetograph for rain gauges and radar rainfalls were compared using hourly radar rainfall data from the Imjin‐river, Gangwha, rainfall radar site, Korea. Then, in order to evaluate the performance of flood estimates using different rainfall estimation methods, rainfall–runoff simulation was conducted using the physics‐based distributed hydrologic model, Vflo™. The flood runoff hydrograph was used to compare the calculated hydrographs with the observed one. Results show that the rainfall field estimated by CM methods improved flood estimates, because it optimally combines rainfall fields representing actual spatial and temporal characteristics of rainfall. Copyright © 2008 John Wiley & Sons, Ltd.
Social differences in breast cancer survival in relation to patient management within a National Health Care System (Sweden)
Authors: Eaker Sonja , Halmin Märit , Bellocco Rino , Bergkvist Leif , Ahlgren Johan , Holmberg Lars , Lambe Mats 
Published: October 2008

AbstractEpidemiologic studies have shown that cancer survival is poorer in low compared with high socioeconomic groups. We investigated whether these differences were associated with disparities in tumour characteristics and management. This cohort study was based on 9,908 women aged 20–79 years at diagnosis with primary breast cancer identified in a Swedish population‐based clinical register. Information on socioeconomic standing was obtained from a social database. The 5‐year cause‐specific survival (CSS) and mortality hazard ratios (HR) were estimated by Cox proportional hazard models to assess differences in survival between socioeconomic groups while adjusting for diagnostic intensity, tumour characteristics and treatment. Following adjustment for age, year and stage at diagnosis, the risk of dying of breast cancer was 35% lower among women with high education compared with that of low education (HR = 0.65, 95% CI 0.53–0.80). When compared with women with high education, a lower percentage of women with low education had been investigated for proliferation (84 vs. 76%) or hormone receptor status (89 vs. 81%), had tumours ≤20 mm (68 vs. 64%), were treated at a main hospital (75 vs. 68%) and had received radiation treatment (80 vs. 67%) or chemotherapy (31 vs. 18%). However, these proportional differences could not explain the observed social gradient in survival. To minimize social differences in breast cancer survival, further research should address not only factors leading to inequities in management but also focus on patient factors such as health awareness, comorbidity burden and compliance to adjuvant treatment. © 2008 Wiley‐Liss, Inc.
Breast cancer incidence and mortality in a Caribbean population: Comparisons with African‐Americans
Authors: Hennis Anselm J. , Hambleton Ian R. , Wu Suh‐Yuh , Leske Maria Cristina , Nemesure Barbara ,   on behalf of the Barbados National Cancer Study Group
Published: October 2008

AbstractWe describe breast cancer incidence and mortality in the predominantly African‐origin population of Barbados, which shares an ancestral origin with African‐Americans. Age‐standardized incidence rates were calculated from histologically confirmed breast cancer cases identified during a 45‐month period (July 2002–March 2006). Mortality rates were estimated from death registrations over 10‐years starting January 1995. There were 396 incident cases of breast cancer for an incidence rate of 78.1 (95% confidence interval (CI) 70.5–86.3), standardized to the US population. Breast cancer incidence in African‐Americans between 2000 and 2004 was 143.7 (142.0–145.5) per 100,000. Incidence peaked at 226.6 (174.5–289.4) per 100,000 among Barbadian women aged 50–54 years, and declined thereafter, a pattern in marked contrast to trends in African‐American women, whose rates continued to increase to a peak of 483.5 per 100,000 in those aged 75–79 years. Incidence rate ratios comparing Barbadian and African‐American women showed no statistically significant differences among women aged ≥ 55 years (p ≤ 0.001 at all older ages). The age‐standardized mortality rate in Barbados was 32.9 (29.9–36.0) per 100,000; similar to reported US rates. The pattern of diverging breast cancer incidence between Barbadian and African‐American women may suggest a greater contribution from genetic factors in younger women, and from environmental factors in older women. Studies in intermediate risk populations, such as Barbados, may assist the understanding of racial disparities in breast cancer. © 2008 Wiley‐Liss, Inc.
Nicotine induces cell proliferation, invasion and epithelial‐mesenchymal transition in a variety of human cancer cell lines
Authors: Dasgupta Piyali , Rizwani Wasia , Pillai Smitha , Kinkade Rebecca , Kovacs Michelle , Rastogi Shipra , Banerjee Sarmistha , Carless Melanie , Kim Esther , Coppola Domenico , Haura Eric , Chellappan Srikumar 
Published: October 2008

AbstractCigarette smoking is strongly correlated with the onset of nonsmall cell lung cancer (NSCLC). Nicotine, an active component of cigarettes, has been found to induce proliferation of lung cancer cell lines. In addition, nicotine can induce angiogenesis and confer resistance to apoptosis. All these events are mediated through the nicotinic acetylcholine receptors (nAChRs) on lung cancer cells. In this study, we demonstrate that nicotine can promote anchorage‐independent growth in NSCLCs. In addition, nicotine also induces morphological changes characteristic of a migratory, invasive phenotype in NSCLCs on collagen gel. These morphological changes were similar to those induced by the promigratory growth factor VEGF. The proinvasive effects of nicotine were mediated by α7‐nAChRs on NSCLCs. RT‐PCR analysis showed that the α7‐nAChRs were also expressed on human breast cancer and pancreatic cancer cell lines. Nicotine was found to promote proliferation and invasion in human breast cancer. The proinvasive effects of nicotine were mediated via a nAChR, Src and calcium‐dependent signaling pathway in breast cancer cells. In a similar fashion, nicotine could also induce proliferation and invasion of Aspc1 pancreatic cancer cells. Most importantly, nicotine could induce changes in gene expression consistent with epithelial to mesenchymal transition (EMT), characterized by reduction of epithelial markers like E‐cadherin expression, ZO‐1 staining and concomitant increase in levels of mesenchymal proteins like vimentin and fibronectin in human breast and lung cancer cells. Therefore, it is probable that the ability of nicotine to induce invasion and EMT may contribute to the progression of breast and lung cancers. © 2008 Wiley‐Liss, Inc.
Transcriptional upregulation of HSP70‐2 by HIF‐1 in cancer cells in response to hypoxia
Authors: Huang Wen‐Jie , Xia Li‐Min , Zhu Fan , Huang Bo , Zhou Chun , Zhu Hui‐Fen , Wang Bo , Chen Bin , Lei Ping , Shen Guan‐Xin , De‐AnTian  
Published: October 2008

AbstractHeat shock protein 70‐2 (HSP70‐2) can be expressed by cancer cells and act as an important regulator of cancer cell growth and survival. Here, we show the molecular mechanisms by which hypoxia regulate HSP70‐2 expression in cancer cells. When cells were subjected to hypoxia (1% O2), the expression of HSP70‐2 had a significant increase in cancer cells. Such increase was due to the direct binding of hypoxia‐inducible factor to hypoxia‐responsive elements (HREs) in the HSP70‐2 promoter. By luciferase assays, we demonstrated that the HRE1 at position −446 was essential for transcriptional activation of HSP70‐2 promoter under hypoxic conditions. We also demonstrated that HIF‐1α binds to the HSP70‐2 promoter and the binding is specific, as revealed by HIF binding/competition and chromatin immunoprecipitation assays. Consequently, the upregulation of HSP70‐2 enhanced the resistance of tumor cells to hypoxia‐induced apoptosis. These findings provide a new insight into how tumor cells overcome hypoxic stress and survive, and also disclose a new regulatory mechanism of HSP70‐2 expression in tumor cells. © 2008 Wiley‐Liss, Inc.
A Joinpoint regression analysis of long‐term trends in cancer mortality in Japan (1958–2004)
Authors: Qiu Dongmei , Katanoda Kota , Marugame Tomomi , Sobue Tomotaka 
Published: October 2008

AbstractCancer is one of the major targets of disease control programs in Japan. A Joinpoint regression model was used to analyze the long‐term trends of mortality related to overall cancer and the 15 most common cancers based on published data from the National Vital Statistics of Japan between 1958 and 2004. Since 1996, a decline has been seen in overall cancer for both sexes in Japan. Most of the common sites, including cancers of the stomach, colon, liver, gallbladder and lung and leukemia in both sexes, cancer of esophagus in men and rectal and ovarian cancers in women showed a decreasing trend, and cancers of the rectum, pancreas, prostate and urinary bladder and malignant lymphoma in men and cancers of the esophagus and uterus in women leveled off during the most recent period. However, an increasing trend was confirmed for cancers of the pancreas, breast and urinary bladder and malignant lymphoma in women. An effective cancer control program including prevention, early detection and treatment should be implemented to further reduce the cancer mortality, particularly for cancer sites that show higher mortality rates or increasing trends. © 2008 Wiley‐Liss, Inc.
Somatic mutations of adenomatous polyposis coli gene and nuclear b‐catenin accumulation have prognostic significance in invasive urothelial carcinomas: Evidence for Wnt pathway implication
Authors: Kastritis Efstathios , Murray Samuel , Kyriakou Fani , Horti Maria , Tamvakis Nicolaos , Kavantzas Nicolaos , Patsouris Efstratios S. , Noni Aphrodite , Legaki Sofia , Dimopoulos Meletios A. , Bamias Aristotle 
Published: October 2008

AbstractWnt pathway signaling is crucial in many cancers and data indicate crosstalk with other key cancer pathways, however in urothelial carcinogenesis it has not been extensively studied. We searched for mutations in adenomatous polyposis coli (APC), a key regulator of the pathway, and studied b‐catenin expression and interactions with the expression of other markers of apoptosis, angiogenesis, and proliferation in patients with invasive urothelial cancer. The mutation cluster region of APC was directly sequenced in 70 patients with muscle invasive disease who were treated with surgery and adjuvant chemotherapy. COX‐2, p53, Ki67, and b‐catenin were studied immunohistochemically and micro vessel density was quantified by CD105 expression. Single somatic amino‐acid substitutions (missense) were found in 9 (13%) and frameshift deletions in 2 (3%) tumors, all located in regions adjacent to b‐catenin binding sites. Patients having either APC missense mutations or b‐catenin nuclear accumulation had less frequent COX‐2 overexpression (24% vs. 76%, p = 0.043) and more frequent lymph node involvement (75% vs. 38%, p = 0.023). Patients with either APC mutations or b‐catenin accumulation had shorter disease‐free interval (13.4 vs. 28 months, p = 0.07), whereas in multivariate analysis they had shorter disease‐specific survival (60.5 vs. 20.6 months, p = 0.048). Somatic APC missense mutations are not rare in advanced urothelial neoplasms. Either APC mutations and/or aberrant expression of b‐catenin are associated with worse outcome. Further study of the role of the Wnt pathway, potential crosstalk with other pathways and potential candidate therapeutic targets in urothelial cancer is needed. © 2008 Wiley‐Liss, Inc.
Serum pepsinogens and risk of esophageal squamous dysplasia
Authors: Kamangar Farin , Diaw Lena , Wei Wen‐Qiang , Abnet Christian C. , Wang Guo‐Qing , Roth Mark J. , Liu Bing , Lu Ning , Giffen Carol , Qiao You‐Lin , Dawsey Sanford M. 
Published: October 2008

AbstractPepsinogens are a class of endopeptidases that are secreted by the gastric epithelium and released into the circulation. Low serum pepsinogen I (PGI) and low serum pepsinogen I/pepsinogen II ratio (PGI/II ratio) are markers of gastric fundic atrophy, and have recently been shown to be associated with increased risk of esophageal squamous cell carcinoma (ESCC). We conducted the current study to test whether these markers are also associated with esophageal squamous dysplasia (ESD), the precursor lesion of ESCC. We measured serum PGI and PGII, using enzyme‐linked immunosorbent assays, in 125 case subjects (patients with moderate or severe ESD) and 250 sex‐matched control subjects (no ESD) selected from an endoscopic screening study in Linxian, China. We used conditional logistic regression models adjusted for age, smoking and place of residence to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs). Serum PGI showed no statistically significant association with ESD, whether analyzed as a dichotomous, ordinal (quartiles) or continuous variable. Lower serum PGI/II ratio, however, showed a dose‐response association with increased risk of ESD, with an adjusted OR (95% CI) of 2.12 (1.08–4.18), comparing the lowest versus the highest quartile. The association between the lower serum PGI/II ratio and log OR of ESD was nearly linear, and the p‐value for the continuous association was 0.03. Lower serum PGI/II ratio was linearly associated with higher risk of ESD. This result is consistent with recent findings that gastric atrophy may increase the risk of ESCC. Published 2008 Wiley‐Liss, Inc.
EGF and HGF levels are increased during active HBV infection and enhance survival signaling through extracellular matrix interactions in primary human hepatocytes
Authors: Barreiros Ana Paula , Sprinzl Martin , Rosset Sylvia , Höhler Thomas , Otto Gerd , Theobald Matthias , Galle Peter R. , Strand Dennis , Strand Susanne 
Published: October 2008

AbstractThe hepatitis B virus (HBV) is a major causative agent of chronic liver disease and subsequent liver cirrhosis worldwide. The reduced sensitivity of virus‐infected liver cells to apoptosis may play a role in the failure to remove virus‐infected cells and eventually promote viral chronicity. The purpose of our study was to investigate whether survival factors induced during compensatory liver regeneration may protect hepatocytes against apoptosis. We evaluated the serum levels of hepatocyte growth factor (HGF) and epidermal growth factor (EGF) in HBV‐infected patients and found significant increases in HGF and EGF in patients with active virus infection. In primary human hepatocytes we show that HGF and EGF have a protective effect against CD95‐mediated apoptosis and cytotoxic T‐cell killing. Simultaneous treatment with both regeneration factors enhanced the cytoprotective effect. The PI 3‐K/Akt kinase inhibitor, wortmannin, and the STAT3 pathway inhibitor, Tyrphostin AG490, both effectively attenuated the cytoprotective effect of HGF and EGF. Furthermore, we show an EGF/HGF‐dependent upregulation of β1‐integrin chains, increased adhesion to extracellular matrix and an increase in focal adhesions, suggesting outside‐in signaling from the extracellular matrix as an additional cytoprotective mechanism. Our study demonstrates that HGF and EGF can interfere with CD95‐mediated apoptosis and the action of cytotoxic T‐cells through multiple mechanisms in human hepatocytes. Together our results argue that a survival mileau generated by activation of liver regeneration factors may be a risk factor for establishing viral persistence. © 2008 Wiley‐Liss, Inc.
Diagnostic value of FDG‐PET in recurrent colorectal carcinoma: A meta‐analysis
Authors: Zhang Chenpeng , Chen Yumei , Xue Huiping , Zheng Ping , Tong Jinlu , Liu Jianjun , Sun Xiaoguang , Huang Gang 
Published: October 2008

AbstractAccurate detection of recurrent colorectal carcinoma remains a diagnostic challenge. The purposes of this study were to evaluate the diagnostic value of Positron emission tomography (PET) using fluor‐18‐deoxyglucose (FDG) in recurrent colorectal carcinoma with a meta‐analysis. All the published studies in English relating the diagnostic value of FDG‐PET in the detection of recurrent colorectal carcinoma were collected. Methodological quality of the included studies was evaluated. Pooled sensitivity, specificity and diagnostic odds ratio and SROC (summary receiver operating characteristic curves) were obtained by the statistical software. Twenty‐seven studies were included in the meta‐analysis. The pooled sensitivity and specificity for FDG‐PET detecting distant metastasis or whole body involvement in recurrent colorectal carcinoma were 0.91 (95% CI 0.88–0.92) and 0.83 (95% CI 0.79–0.87), respectively. The pooled sensitivity and specificity for FDG‐PET detecting hepatic metastasis were 0.97 (95% CI 0.95–0.98) and 0.98 (95% CI 0.97–0.99). The pooled sensitivity and specificity for pelvic metastasis or local regional recurrence were 0.94 (95% CI 0.91–0.97) and 0.94 (95% CI 0.92–0.96). FDG‐PET is valuable for the assessment of recurrent colorectal carcinoma. © 2008 Wiley‐Liss, Inc.
Space‐time clustering of childhood cancer around the residence at birth
Authors: McNally Richard J.Q. , Bithell John F. , Vincent Tim J. , Murphy Michael F.G. 
Published: October 2008

AbstractPreviously, we identified space‐time clustering in certain childhood cancers around diagnosis residence. These findings provided support for the involvement of environmental agents in etiological processes occurring close to diagnosis. We have reanalyzed the same British population‐based dataset. The aim of the study was to determine whether there was space‐time clustering around the residence at birth in relation to time of birth and separately from time of diagnosis. A total of 29,553 cases, diagnosed during the period 1969–1993, were examined by a second‐order procedure based on K‐functions. Locations were birth addresses, but separately, both dates of birth and diagnosis were analyzed. There was statistically significant space‐time clustering for Hodgkin lymphoma (HL) and central nervous system (CNS) tumors (p = 0.047 and 0.01, respectively, based on birth date) and for total leukemia at ages 1–4 years only, Non‐Hodgkin lymphoma (NHL) and Wilms tumor (p = 0.01, 0.02 and 0.006, respectively, based on diagnosis date). These results, interpreted together with other epidemiological evidence, suggest an etiological role for environmental factors focused around birth address for certain childhood cancers. For HL and CNS tumors, findings suggest that etiological exposures occurred at similar ages or in utero. For leukemia, NHL and Wilms tumor there is support for exposures occurring at similar times before diagnosis. For leukemia, HL, NHL and CNS tumors, but not Wilms tumor, the findings are consistent with infectious hypotheses. © 2008 Wiley‐Liss, Inc.
Inhibition of migration and invasion of carcinoma cells by urokinase‐derived antagonists of αvβ5 integrin activation
Authors: Vocca Immacolata , Franco Paola , Alfano Daniela , Votta Giuseppina , Carriero Maria Vincenza , Estrada Yeriel , Caputi Mario , Netti Paolo A. , Ossowski Liliana , Stoppelli Maria Patrizia 
Published: October 2008

AbstractWe previously showed that, while binding to urokinase receptor (uPAR) through its growth factor domain (GFD, residues 1–49), urokinase (uPA) can engage αvβ5 integrin through an internal domain (CP, residues 132–158). This novel uPA/αvβ5 interaction promotes cytoskeletal rearrangements and directional cell migration (Franco et al., J Cell Sci 2006;119:3424–34). We now show that treatment of cells with phosphomimic uPA (uPA138E/303E, serine 138 and 303 substituted with glutamic acid) strongly inhibits matrix‐induced cell migration. Unlike uPA, binding of uPA138E/303E to cell surface did not induce F‐actin enriched protruding structures and caused a 5‐fold reduction in cell translocation speed, as determined by video tracking of living cells. Inhibition of migration was found to be independent of uPAR, since uPA variants lacking the GFD domain, but carrying the relevant Ser to Glu substitutions were as effective inhibitor as uPA138E/303E. Through several independent approaches, we established that the phosphomimics specifically bind to αvβ5 integrin through the CP region carrying the S138E mutation. This interaction blocks integrin activation, as determined by a decreased affinity of αvβ5 to vitronectin and a reduced association of the β5 cytoplasmic tail with talin. Finally, stable expression of uPA138E/303E in human squamous carcinoma cells prevented tumor cell invasion in vivo. Thus, when expressed in cancer cells, the inhibitory phosphomimic effect was dominant over the effect of endogenously produced uPA. These results shed light on the regulation of cell migration by uPA phosphorylation and provide a realistic opportunity for a novel antiinvasive/metastatic therapeutic intervention. © 2008 Wiley‐Liss, Inc.
NDRG2 suppresses cell proliferation through down‐regulation of AP‐1 activity in human colon carcinoma cells
Authors: Kim Young Jun , Yoon Sun Young , Kim Jong‐Tae , Choi Seung Cheol , Lim Jong‐Seok , Kim Joo Heon , Song Eun Young , Lee Hee Gu , Choi Inpyoi , Kim Jae Wha 
Published: October 2008

AbstractRecently, the anti‐tumor activity of N‐myc downstream‐regulated gene 2 (NDRG2) was elucidated, but the molecular mechanism of how NDRG2 works as a tumor suppressor is not well known. To determine the function of NDRG2 as a tumor suppressor, we established stable cell lines expressing NDRG2 protein or its mutant forms, and studied their effects on tumor cell growth. Interestingly, constitutive expression of wild‐type NDRG2 induced the growth retardation of SW620 colon carcinoma cells. Introduction of NDRG2 into SW620 cells induced the decrease of c‐Jun phosphorylation at Ser63, followed by the attenuation of activator protein‐1 (AP‐1) function as a transcriptional activator. Subsequently, the down‐regulation of cyclin D1, which is known as a major target for AP‐1 transcription activator, resulted in cell cycle arrest at G1/S phase. Additionally, treatment of NDRG2‐siRNA on NDRG2‐expressing cells has induced the recovery of c‐Jun phosphorylation and cyclin D1 expression. Cell proliferation of those cells was also increased compared with untreated cells. NDRG2 mutants of which the phosphorylation sites at C‐terminal region were removed by deletion or site‐directed mutagenesis have shown no effect on cyclin D1 expression and could not induce cell growth retardation. In conclusion, NDRG2 modulates intracellular signals to control cell cycle through the regulation of cyclin D1 expression via phosphorylation pathway. © 2008 Wiley‐Liss, Inc.