bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ring Enlargement and Sulfur‐Transfer Processes in SiO2‐Catalyzed Reactions of Thiocarbonyl Compounds with Optically Active Oxiranes
Authors: Malaschichin Sergej , Fu Changchun , Linden Anthony , Heimgartner Heinz 
Published: December 2005

AbstractThe reactions of 1,3‐dioxolane‐2‐thione (3) with (S)‐2‐methyloxirane ((S)‐1) and with (R)‐2‐phenyloxirane ((R)‐2) in the presence of SiO2 in anhydrous dichloroalkanes led to the optically active spirocyclic 1,3‐oxathiolanes 8 with Me at C(7) and 9 with Ph at C(8), respectively (Schemes 2 and 3). The analogous reaction of 1,3‐dimethylimidazolidine‐2‐thione (4a) with (R)‐2 yielded stereoselectively (S)‐2‐phenylthiirane ((S)‐10) in 83% yield and 97% ee together with 1,3‐dimethylimidazolidin‐2‐one (11a). In the cases of 3‐phenyloxazolidine‐2‐thione (4b) and 3‐phenylthiazolidine‐2‐thione (4c), the reaction with (RS)‐2 yielded the racemic thiirane (RS)‐10, and the corresponding carbonyl compounds 11b and 11c (Scheme 4 and Table 1). The analogous reaction of 4a with 1,2‐epoxycyclohexane (= 7‐oxabicyclo[4.1.0]heptane; 7) afforded thiirane 12 and the corresponding carbonyl compound 11a (Scheme 5). On the other hand, the BF3‐catalyzed reaction of imidazolidine‐2‐thione (5) with (RS)‐2 yielded the imidazolidine‐2‐thione derivative 13 almost quantitatively (Scheme 6). In a refluxing xylene solution, 1,3‐diacetylimidazolidine‐2‐thione (6) and (RS)‐2 reacted to give two imidazolidine‐2‐thione derivatives, 13 and 14 (Scheme 7). The structures of 13 and 14 were established by X‐ray crystallography (Fig.).
Synthesis and Stereochemical Aspects of Ethyl 1,1a,2,3,4,5,6,6a‐Octahydro‐4‐octylcyclopropa[f]indene‐1‐carboxylate
Authors: Hussain Zakir , Koley Debasis , Hopf Henning 
Published: December 2005

AbstractA novel approach for the synthesis of carbene adducts 9a/9b and 10/11 is reported. Identification of the geometric and positional isomers of carbene addition was carried out by reversed‐phase HPLC, and the establishment of the structure and configuration of 9a/9b was performed by means of 2D‐NMR.
Cancer incidence in the age range 0–34 years: Historical and actual status in Denmark
Authors: van der Horst Mirjam , Winther Jeanette Falck , Olsen Jørgen H. 
Published: December 2005

AbstractOn the basis of 55 years of continuous cancer registration in Denmark, we present cancer incidence rates, time trends and birth cohort analyses for persons aged 0–34 years. The group of 40,750 cancer patients showed a substantial over‐representation of males aged 1–24 years. The cancer pattern among young (15–34 years) men was dominated by testicular cancer (35%), lymphomas (14%) and tumors of the brain (13%), while the pattern among young women was governed by invasive cervical cancer (19%), malignant melanoma (15%) and cancer of the breast (12%). In this age range, a positive time trend was seen after 1970, equivalent to average annual percentage increases of 1.9% for men and 1.8% for women, due mainly to markedly increasing trends for testicular cancer, malignant melanoma, brain tumors, thyroid cancer, skin carcinomas and skin sarcoma among men, and for brain tumors, non‐Hodgkin lymphoma, malignant melanoma, skin carcinomas and thyroid cancer among women. We saw no clear time trend for breast cancer among women. The cancer pattern among children (0–14 years) was similar to that reported for other white populations. © 2005 Wiley‐Liss, Inc.
Incidence trends and projections for childhood cancer in Ontario
Authors: Agha Mohammed , DiMonte Bruna , Greenberg Mark , Greenberg Corin , Barr Ronald , McLaughlin John R. 
Published: December 2005

AbstractStudies of cancer incidence patterns and trends can provide useful measures of health burden and possible disease etiology, which can aid the planning of cancer care services. This report aims to characterize trends in incidence of childhood cancer, and to assess the implications of these trends by generating incidence projections to 2015. Cancer incidence data were obtained from the database of the Pediatric Oncology Group of Ontario (POGO), which has registered all cancer cases in Ontario since 1985. Annual incidence rates were calculated with census‐based population estimates for the 1986–2001 period. Poisson regression models were used to analyze trends, and to calculate projected numbers of cases up to the year 2015. From 1986 to 2001, 5,163 cancer cases occurred among children aged 0–14. Leukemia, CNS tumors and lymphomas were the most common cancers. The number of incident cases increased by 14%, from 296 in 1986 to 336 in 2001. For all cancers, average annual age‐standardized rates increased from 147 per million in 1991 to 157 per million in 2001. Over the next 15 years, the 0–14 year population is expected to decrease from 2.28 million in 2000 to 2.13 million in 2015. A marginally statistically significant trend in incidence was projected for all cancers combined (0.5% increase per year p < 0.10) and a statistically significant increase for lymphomas, (1.2% per year 95% CI = 0.0–3.9%). During this period, the number of cases of leukemia and CNS tumors is expected to remain relatively stable. The number of cases of all cancers is expected to increase by 8%, from the average of 320 in 1995 to ∼347 in 2015. Understanding of these projections will facilitate health care resource planning. © 2005 Wiley‐Liss, Inc.
Calcitonin stimulates the secretion of urokinase‐type plasminogen activator from prostate cancer cells: Its possible implications on tumor cell invasion
Authors: Sabbisetti Venkata , Chigurupati Srinivasulu , Thomas Shibu , Shah Girish 
Published: December 2005

AbstractCalcitonin (CT) is synthesized and secreted in prostate epithelium, and its secretion from malignant prostates is several folds higher than that in benign prostates. CT receptor (CTR) is expressed in malignant prostate epithelium, and its activation increases invasiveness of prostate cancer (PC) cells via activation of protein kinase A. Since the role of urokinase‐type plasminogen activator (uPA) in invasion of PC has been established, we tested the hypothesis that CT increases invasion of PC cells by stimulating uPA secretion from PC cells. Exogenously added CT stimulated the secretion of uPA from PC‐3M cells in a dose‐dependent manner, which was blocked by Rp.cAMP, a competitive inhibitor of protein kinase A. CT stimulated the secretion of MMP‐2 and MMP‐9 from PC‐3M cells, and also increased their invasiveness. Both these actions of CT were blocked by uPA‐neutralizing antibodies. Immunofluorescence studies with PC‐3M cells suggest that CT stimulated redistribution of cellular uPA to focal adhesion sites, which was further confirmed by co‐immunoprecipitation of uPA with focal adhesion kinase (FAK) in response to CT. These results suggest that CT increases invasiveness of PC cells by stimulating PKA‐mediated uPA secretion and by redirecting the secreted uPA to focal adhesion sites. The results also suggest that uPA may, at least in part, mediate proinvasive actions of CT on PC cells by stimulating the secretion of gelatinases and degradation of focal adhesion sites. © 2005 Wiley‐Liss, Inc.
Inhibition of human prostate cancer growth, osteolysis and angiogenesis in a bone metastasis model by a novel mechanism‐based selective gelatinase inhibitor
Authors: Bonfil R. Daniel , Sabbota Aaron , Nabha Sanaa , Bernardo M. Margarida , Dong Zhong , Meng Hong , Yamamoto Hamilto , Chinni Sreenivasa R. , Lim Int Taek , Chang Mayland , Filetti Lusia C. , Mobashery Shahriar , Cher Michael L. , Fridman Rafael 
Published: December 2005

AbstractMetastasis to the bone is a major clinical complication in patients with prostate cancer (PC). However, therapeutic options for treatment of PC bone metastasis are limited. Gelatinases are members of the matrix metalloproteinase (MMP) family and have been shown to play a key role in PC metastasis. Herein, we investigated the effect of SB‐3CT, a covalent mechanism‐based MMP inhibitor with high selectivity for gelatinases, in an experimental model of PC bone metastases. Intraperitoneal (i.p.) treatment with SB‐3CT (50 mg/kg) inhibited intraosseous growth of human PC3 cells within the marrow of human fetal femur fragments previously implanted in SCID mice, as demonstrated by histomorphometry and Ki‐67 immunohistochemistry. The anti‐osteolytic effect of SB‐3CT was confirmed by radiographic images. Treatment with SB‐3CT also reduced intratumoral vascular density and bone degradation in the PC3 bone tumors. A direct inhibition of bone marrow endothelial cell invasion and tubule formation in Matrigel by SB‐3CT in vitro was also demonstrated. The use of the highly selective gelatinase inhibitors holds the promise of effective intervention of metastases of PC to the bone. © 2005 Wiley‐Liss, Inc.
LIM kinase 1 increases tumor metastasis of human breast cancer cells via regulation of the urokinase‐type plasminogen activator system
Authors: Bagheri‐Yarmand Rozita , Mazumdar Abhijit , Sahin Aysegul A. , Kumar Rakesh 
Published: December 2005

AbstractMammalian LIM kinase 1 (LIMK1) phosphorylates and inactivates the actin‐binding and ‐depolymerizing factor cofilin and induces actin cytoskeletal changes. LIMK1 is reported to play an important role in cell motility, but the mechanism of induction of cell motility and the role of LIMK1 in tumor growth, angiogenesis and invasion are poorly understood. Here we show that expression of LIMK1 in MDA‐MB‐435 human breast cancer cells enhanced cell proliferation and cell invasiveness and promoted in vitro angiogenesis. Since tumor metastasis requires degradation of the extracellular matrix by the serine protease urokinase type plasminogen activator (uPA), we examined the role of LIMK1 in the regulation of uPA/uPAR system. LIMK1 overexpression in breast cancer cells upregulated the uPA system, increased uPA promoter activity, induced uPA and uPAR mRNA and protein expression and induced uPA secretion. In contrast, cells transfected with the catalytically inactive LIMK mutant D460N‐LIMK1 did not exhibit these phenotypic changes. Blocking antibodies against uPA and uPAR suppressed LIMK1‐induced cell invasiveness. In addition, LIMK1 overexpression increased tumor growth in female athymic nude mice, promoted tumor angiogenesis and induced metastasis to livers and lungs, possibly by increasing uPA expression in the tumors. Finally, LIMK1 and uPAR were coordinately overexpressed in human breast tumors. These results suggested an important role for LIMK1 signaling in breast cancer tumor growth, angiogenesis and invasion and a regulatory connection between LIMK1 and the uPA system. © 2005 Wiley‐Liss, Inc.
Ectopic expression of neutrophil gelatinase‐associated lipocalin suppresses the invasion and liver metastasis of colon cancer cells
Authors: Lee Ho‐Jeong , Lee Eun‐Kyoung , Lee Kong‐Ju , Hong Soon‐Won , Yoon Yeup , Kim Jang‐Seong 
Published: December 2005

AbstractNeutrophil gelatinase‐associated lipocalin (NGAL), also known as lipocalin 2, is a 25‐kDa lipocalin initially purified from neutrophil granules. It is thought to play a role in regulating cellular growth since its expression is highly upregulated in a variety of proliferative cells such as cancer cells. However, experimental evidence showing a clear causal relationship between NGAL expression and the proliferation of tumor cells is lacking. Here, we found NGAL expression in highly and poorly metastatic colon cancer cell lines of the same genetic origin correlated inversely with the metastatic potential of these cells, which suggests NGAL participates in the metastatic process. To explore the role NGAL plays in tumor growth and metastasis, the KM12SM human colon cancer cell line, which is highly metastatic while showing decreased NGAL expression, was genetically manipulated to overexpress NGAL. The effects of this on tumor growth and liver metastasis were then analyzed using experimental animal models established by injecting BALB/c nude mice with tumor cells subcutaneously or intrasplenically. Ectopic expression of NGAL in the colon cancer cells had little effect on the growth and viability of the tumor cells both in vitro and in vivo. However, NGAL expression not only suppressed the ability of the colon carcinoma cells to invade Matrigel in vitro, it also substantially inhibited liver metastasis in an experimental animal model. Collectively, these results indicate that NGAL may be a candidate metastasis suppressor in colon cancer cells. © 2005 Wiley‐Liss, Inc.
Lifetime occupational and recreational physical activity and risk of benign prostatic hyperplasia
Authors: Maso Luigino Dal , Zucchetto Antonella , Tavani Alessandra , Montella Maurizio , Ramazzotti Valerio , Polesel Jerry , Bravi Francesca , Talamini Renato , La Vecchia Carlo , Franceschi Silvia 
Published: December 2005

AbstractTo investigate the relation between occupational and recreational physical activity (PA) in different periods of life and the risk of benign prostatic hyperplasia (BPH), we conducted a hospital‐based, case‐control study in Italy. The study included 1,369 histologically confirmed BPH and 1,451 controls, admitted to the same hospitals for acute, nonneoplastic diseases. Odds ratios (ORs) and 95% confidence intervals (CIs) of BPH, according to lifetime PA, were obtained by unconditional multiple logistic regression models, including terms for age, study center and education. Compared to the lowest level of occupational PA, the multivariate ORs for BPH for the heavy/strenuous level were 0.6 (95% CI, 0.4–0.8) at age 15–19, 0.6 (95% CI, 0.4–0.8) at age 30–39 and 0.7 (95% CI, 0.5–0.9) at age 50–59. Moreover, compared to <2 hr/week of recreational PA, the ORs for BPH for the highest level (≥≥5 hr/week) were 0.5 (95% CI, 0.4–0.7) at age 15–19, 0.6 (95% CI, 0.5–0.8) at age 30–39, and 0.7 (95% CI, 0.5–0.8) at age 50–59. All inverse trends in risk were significant, and no heterogeneity was found by reason of BPH‐diagnosis, age at diagnosis, and body mass index (BMI). The inverse association between PA and BPH risk may be due to favorable hormonal correlates of PA, but residual confounding by socioeconomic covariates cannot be excluded. A moderate PA at any ages may help reducing a sizeable number of BPH. © 2005 Wiley‐Liss, Inc.
Selenium binding protein 1 in ovarian cancer
Authors: Huang Kuan‐Chun , Park Dong Choon , Ng Shu‐Kay , Lee Ji Young , Ni Xiaoyan , Ng Wing‐Chung , Bandera Christina A. , Welch William R. , Berkowitz Ross S. , Mok Samuel C. , Ng Shu‐Wing 
Published: December 2005

AbstractSelenium binding protein 1 (SELENBP1) was identified to be the most significantly down‐regulated protein in ovarian cancer cells by a membrane proteome profiling analysis. SELENBP1 expression levels in 4 normal ovaries, 8 benign ovarian tumors, 12 borderline ovarian tumors and 141 invasive ovarian cancers were analyzed with immunohistochemical assay. SELENBP1 expression was reduced in 87% cases of invasive ovarian cancer (122/141) and was significantly reduced in borderline tumors and invasive cancers (p < 0.001). Cox multivariate analysis within the 141 invasive cancer tissues showed that SELENBP1 expression score was a potential prognostic indicator for unfavorable prognosis of ovarian cancer (hazard ratio [HR], 2.18; 95% CI = 1.22–3.90; p = 0.009). Selenium can disrupt the androgen pathway, which has been implicated in modulating SELENBP1 expression. We investigated the effects of selenium and androgen on normal human ovarian surface epithelial (HOSE) cells and cancer cells. Interestingly, SELENBP1 mRNA and protein levels were reduced by androgen and elevated by selenium treatment in the normal HOSE cells, whereas reversed responses were observed in the ovarian cancer cell lines. These results suggest that changes of SELENBP1 expression in malignant ovarian cancer are an indicator of aberration of selenium/androgen pathways and may reveal prognostic information of ovarian cancer. © 2005 Wiley‐Liss, Inc.
Tumor shedding of laminin binding protein modulates angiostatin production in vitro and interferes with plasmin‐derived inhibition of angiogenesis in aortic ring cultures
Authors: Moss Britney L. , Taubner Lara , Sample Yekaterina K. , Kazmin Dmitri A. , Copié Valérie , Starkey Jean R. 
Published: December 2005

AbstractThe growth of solid tumors is largely controlled by the process of angiogenesis. A 67 kDa protein, the laminin binding protein (LBP), is shed from malignant cells in significant amounts and binds to laminin‐1 (Starkey et al., Cytometry 1999;35:37–47; Karpatová et al., J Cell Biochem 1996;60:226–34). However, the functions of shed LBP are not fully understood. We hypothesize that matrix‐bound LBP could modulate local tumor angiogenesis. In support of this hypothesis, we demonstrate that shed LBP exhibits sulfhydryl oxidase‐like activities, and modifies the production of angiostatins from plasmin in vitro. The molecular weights of the autocatalytic products of lys‐plasmin incubated with LBP in vitro suggest that PMDs (plasmin A chains attached to degraded B chains) (Ohyama et al., Eur J Biochem 2004;271:809–20) are preferentially generated. Using rat aortic ring assays, we also show that shed LBP reverses plasmin‐dependent inhibition of vascular outgrowth. To elucidate which LBP region(s) are active in modulating angiogenesis, limited proteolysis experiments were conducted to determine stable rLBP domains likely to fold correctly, and these were cloned, expressed and purified. The stable LBP fragments were tested for binding to laminin‐1 and for competition with shed LBP activity in the aortic ring assay. Results of these studies suggest that the active LBP domains lie within the 137–230 amino acid sequence, a region known to contain 2 bioactive sequences. Since this fragment binds to laminin‐1 and modulates angiogenesis, it appears likely that binding of shed LBP to matrix laminin‐1 is related to its functions in tumor angiogenesis. The findings presented in this manuscript suggest that LBP shedding could provide a useful therapeutic target. © 2005 Wiley‐Liss, Inc.
Hypoxia inducible factor‐1α is a prognostic marker in premenopausal patients with intermediate to highly differentiated breast cancer but not a predictive marker for tamoxifen response
Authors: Kronblad Åsa , Jirström Karin , Rydén Lisa , Nordenskjöld Bo , Landberg Göran 
Published: December 2005

AbstractHypoxia is common in many solid tumours, including breast cancer. Hypoxia triggers the expression of hypoxia inducible factor‐1α (HIF‐1α), and HIF‐1α has been associated with an impaired prognosis in breast cancer and down‐regulation of the oestrogen receptor (ER), potentially affecting the treatment efficiency of antioestrogens. The role of HIF‐1α regarding prognostic and treatment predictive information in breast cancer has not been established and we therefore analyzed HIF‐1α using immunohistochemistry in a cohort of 377 premenopausal stage II breast cancers arranged in a tissue microarray. The patients were included in a randomized trial with either 2 years of tamoxifen or no adjuvant treatment. The tamoxifen treatment effect could be studied in subgroups of breast cancer and pure prognostic information could be scrutinized for untreated control patients. HIF‐1α was scored as positive in 24% of the tumours and correlated positively to tumour size, Nottingham histological grade (NHG), Ki‐67, Her2 and cyclin E expression and negatively to lymph node status, cyclin D1, ER and PR (progesterone receptor) expression. Surprisingly, there was no difference in tamoxifen response for patients with high or low HIF‐1α expressing tumours. In lymph node‐positive patients as well as NHG 1/2 tumours, high HIF‐1α protein expression was significantly associated with an impaired recurrence‐free survival (p = 0.014, 0.018). When analyzing the subgroup of NHG 1/2 tumours, a high HIF‐1α expression was the only independent significant prognostic marker in multivariate analysis, including standard prognostic markers, suggesting that HIF‐1α might be a useful prognostic marker in this subgroup of breast cancer, with a rather good but diverse prognosis. © 2005 Wiley‐Liss, Inc.
Fruit and vegetable intake and the risk of stomach and oesophagus adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC–EURGAST)
Authors: González Carlos A. , Pera Guillem , Agudo Antonio , Bueno‐de‐Mesquita H. Bas , Ceroti Marco , Boeing Heiner , Schulz Mandy , Del Giudice Giuseppe , Plebani Mario , Carneiro Fátima , Berrino Franco , Sacerdote Carlotta , Tumino Rosario , Panico Salvatore , Berglund Göran , Simán Henrik , Hallmans Göran , Stenling Roger , Martinez Carmen , Dorronsoro Miren , Barricarte Aurelio , Navarro Carmen , Quiros José R. , Allen Naomi , Key Timothy J. , Bingham Sheila , Day Nicholas E. , Linseisen Jakob , Nagel Gabriele , Overvad Kim , Jensen Majken K. , Olsen Anja , Tjønneland Anne , Büchner Frederike L. , Peeters Petra HM. , Numans Mattijs E. , Clavel‐Chapelon Françoise , Boutron‐Ruault Marie‐Christine , Roukos Dimitrios , Trichopoulou Antonia , Psaltopoulou Theodora , Lund Eiliv , Casagrande Corinne , Slimani Nadia , Jenab Mazda , Riboli Elio 
Published: December 2005

AbstractIt is considered that fruit and vegetable (F&V) protect against oesophagus and gastric cancer (GC). However, 2 recent meta‐analyses suggest that the strength of association on GC seems to be weaker for vegetables than for fruit and weaker in cohort than in case‐control studies. No evidence exists from cohort studies about adenocarcinoma of oesophagus (ACO). In 521,457 men and women participating in the EPIC cohort in 10 European countries, information of diet and lifestyle was collected at baseline. After an average of 6.5 years of follow‐up, a total of 330 GC and 65 ACO, confirmed and classified by a panel of pathologists, was used for the analysis. We examined the relation between F&V intake and GC and ACO. A calibration study in a sub‐sample was used to control diet measurement errors. In a sub‐sample of cases and a random sample of controls, antibodies against Helicobacter pylori (Hp) were measured and interactions with F&V were examined in a nested case‐control study. We observed no association with total vegetable intake or specific groups of vegetables and GC risk, except for the intestinal type, where a negative association is possible regarding total vegetable (calibrated HR 0.66; 95% CI 0.35–1.22 per 100 g increase) and onion and garlic intake (calibrated HR 0.70; 95% CI 0.38–1.29 per 10 g increase). No evidence of association between fresh fruit intake and GC risk was observed. We found a negative but non significant association between citrus fruit intake and the cardia site (calibrated HR 0.77; 95% CI 0.47–1.22 per 100 g increase) while no association was observed with the non‐cardia site. Regarding ACO, we found a non significant negative association for vegetable intake and for citrus intake (calibrated HRs 0.72; 95% CI 0.32–1.64 and 0.77; 95% CI 0.46–1.28 per 100 and 50 g increase, respectively). It seems that Hp infection does not modify the effect of F&V intake. Our study supports a possible protective role of vegetable intake in the intestinal type of GC and the ACO. Citrus fruit consumption may have a role in the protection against cardia GC and ACO. © 2005 Wiley‐Liss, Inc.