bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinical significance of mannose‐binding lectin‐associated serine protease‐2 expression in esophageal squamous cell carcinoma
Authors: Verma Amit , Matta Ajay , Shukla Nootan Kumar , Deo Suryanarayana V.S. , Gupta Siddarth Datta , Ralhan Ranju 
Published: January 2006

AbstractMannan‐binding lectin‐associated serine protease‐2 (MASP‐2) is a serine protease involved in the activation of lectin complement pathway. The differential expression of MASP‐2 in human esophageal squamous cell carcinoma (ESCC) was recently reported from our laboratory using differential display. To determine the expression of MASP‐2 protein, we raised a polyclonal antibody to human MASP‐2 and used it for immunohistochemical analysis of MASP‐2 in ESCCs. The antibody showed a single band of predicted molecular weight by western blotting. In normal human liver tissue, the cytoplasm was distinctly labeled by the antibody. Intriguingly, besides the cytoplasm, the nuclei of esophageal tumor cells were also labeled. To investigate the association of MASP‐2 expression with esophageal tumorigenesis, its expression was analyzed in 51 primary ESCCs, 32 dysplasias, 21 histologically normal esophageal tissues and 6 adenocarcinomas by immunohistochemistry. Increased MASP‐2 expression was observed in ESCCs (p = 0.001, Odd's ratio (OR) = 3.662) and in premalignant condition, dysplasia (p = 0.000, OR = 5.091) in comparison with the normal tissues. MASP‐2 expression in ESCCs was associated with late clinical stage (p = 0.009, O.R. = 3.430) and nodal metastasis (p = 0.001, O.R. = 4.520). In conclusion, our antibody was demonstrated to be useful in recognizing MASP‐2 expression on paraffin embedded tissue sections. To our knowledge, this is the first report showing MASP‐2 expression in a solid tumor. MASP‐2 expression in premalignant stage (dysplasia) as well as in ESCCs and its association with late clinical stage and nodal metastasis suggest that alteration in its expression is maintained during disease progression and is associated with aggressive tumor behavior. © 2006 Wiley‐Liss, Inc.
Cooperative antitumor effects of vitamin D3 derivatives and rosemary preparations in a mouse model of myeloid leukemia
Authors: Sharabani Hagar , Izumchenko Eugene , Wang Qing , Kreinin Rita , Steiner Michael , Barvish Zeev , Kafka Michael , Sharoni Yoav , Levy Joseph , Uskokovic Milan , Studzinski George P. , Danilenko Michael 
Published: January 2006

Abstract1α,25‐dihydroxyvitamin D3 (1,25D3) is a powerful differentiation agent, which has potential for treatment of myeloid leukemias and other types of cancer, but the calcemia produced by pharmacologically active doses precludes the use of this agent in the clinic. We have shown that carnosic acid, the major rosemary polyphenol, enhances the differentiating and antiproliferative effects of low concentrations of 1,25D3 in human myeloid leukemia cell lines (HL60, U937). Here we translated these findings to in vivo conditions using a syngeneic mouse leukemia tumor model. To this end, we first demonstrated that as in HL60 cells, differentiation of WEHI‐3B D− murine myelomonocytic leukemia cells induced by 1 nM 1,25D3 or its low‐calcemic analog, 1,25‐dihydroxy‐16‐ene‐5,6‐trans‐cholecalciferol (Ro25‐4020), can be synergistically potentiated by carnosic acid (10 μM) or the carnosic acid‐rich ethanolic extract of rosemary leaves. This effect was accompanied by cell cycle arrest in G0+G1 phase and a marked inhibition of cell growth. In the in vivo studies, i.p. injections of 2 μg Ro25‐4020 in Balb/c mice bearing WEHI‐3B D− tumors produced a significant delay in tumor appearance and reduction in tumor size, without significant toxicity. Another analog, 1,25‐dihydroxy‐16,23Z‐diene‐20‐epi‐26,27‐hexafluoro‐19‐nor‐cholecalciferol (Ro26‐3884) administered at the same dose was less effective than Ro25‐4020 and profoundly toxic. Importantly, combined treatment with 1% dry rosemary extract (mixed with food) and 1 μg Ro25‐4020 resulted in a strong cooperative antitumor effect, without inducing hypercalcemia. These results indicate for the first time that a plant polyphenolic preparation and a vitamin D derivative can cooperate not only in inducing leukemia cell differentiation in vitro, but also in the antileukemic activity in vivo. These data may suggest novel protocols for chemoprevention or differentiation therapy of myeloid leukemia. © 2006 Wiley‐Liss, Inc.
Loss of RAB25 expression in breast cancer
Authors: Cheng Ji‐Ming , Ding Ming , Aribi Ahmed , Shah Prabodh , Rao Krishna 
Published: January 2006

AbstractA novel breast cancer cell line (RAO‐3) was established by transduction of the Q61L mutant RAS into human mammary epithelial cells that were immortalized with catalytic subunit of telomerase (hTERT). The cells displayed anchorage‐independent growth and proliferation, and formed human mammary spindle cell carcinoma when injected into nude mice. Chromosome locus 1q22‐23 was partially duplicated and inverted on one of the 3 chromosomes present in the cell line. We report here that mutations of chromosome 1q22‐23 locus have resulted in the loss of RAB25 expression in the breast cancer cell line. Transduction of RAB25 into the breast cancer cell line arrests anchorage‐independent growth. We have also demonstrated loss of RAB25 in human breast tumor tissue. These data suggest that loss of RAB25 might contribute to tumorigenesis of breast cancer, and RAB25 is likely to be an important factor in the development of breast cancer. RAB25 could be used as biological marker of breast cancer and provides a target for gene replacement therapy. © 2006 Wiley‐Liss, Inc.
Use of hormone therapy and risk of breast cancer detected at screening and between mammographic screens
Authors: Hofvind Solveig , Møller Bjørn , Thoresen Steinar , Ursin Giske 
Published: January 2006

AbstractPostmenopausal hormone therapy (HT) is associated with increased risk of breast cancer, but in women undergoing breast cancer screening it is not clear whether use of HT is associated with increased risk of breast cancer detected at screening or between screens (interval cancer). Further, it is unclear whether the use of the HTs that have been common in Scandinavia is associated with higher risk of breast cancer than the HTs used in other countries. Our study was based on data from 296,651 women aged 50–69 years, who participated in the Norwegian Breast Cancer Screening Program during 1995–2004. After a mean enrollment time of 3.8 years, 1,512 women were diagnosed with invasive screen detected breast cancer, and 814 with invasive interval breast cancer. Cox regression models were used to estimate hazard ratios (HRs) of breast cancer associated with HT use, after adjusting for confounders. Ever users of HT had a 58% increased risk of breast cancer, compared to never users. The HRs associated with HT use were 1.45 (95% confidence interval (CI) = 1.29–1.63) for screen detected and 1.89 (95% CI = 1.61–2.23) for interval cancer. The difference between screen detected and interval cancer was statistically significant (p = 0.011). The HR of breast cancer increased with duration of HT use, but significantly more so for interval than for screen detected cancer (use of HT for 5 or more years compared to never use; HR = 2.91, 95% CI = 2.10–4.04 and HR = 1.94, 95% CI = 1.51–2.50, respectively; p = 0.002). The population attributable fraction of breast cancer due to HT use was 19.8% overall. Ever users of HT tended to develop a cancer of lower grade. No other differences in histological tumor characteristics were observed between ever and never users of HT among screen detected or interval cancers. The estimated risks of either breast cancer overall with HT use are higher in Norway than reported in similar studies from the U.S. HT‐use is a stronger risk factor for interval cancer than for screen detected cancer. The increased risk of interval cancer, which may partly be due to decreased sensitivity of mammograms in HT users, remains a challenge in breast cancer screening programs. © 2006 Wiley‐Liss, Inc.
Tea drinking and the risk of biliary tract cancers and biliary stones: A population‐based case–control study in Shanghai, China
Authors: Zhang Xue‐Hong , Andreotti Gabriella , Gao Yu‐Tang , Deng Jie , Liu Enju , Rashid Asif , Wu Kai , Sun Lu , Sakoda Lori C. , Cheng Jia‐Rong , Shen Ming‐Chang , Wang Bing‐Sheng , Han Tian‐Quan , Zhang Bai‐He , Gridley Gloria , Fraumeni Joseph F. , Hsing Ann W. 
Published: January 2006

AbstractBiliary tract cancers, encompassing tumors of the gallbladder, extrahepatic bile ducts and ampulla of Vater, are rare but highly fatal malignancies. Apart from gallstones, etiologic factors for biliary tract cancer are not clearly defined. Several epidemiologic studies have suggested that consumption of tea, especially green tea, is protective against a variety of cancers, including gastrointestinal malignancies. As part of a large population‐based case–control study of biliary tract disease in Shanghai, China, we evaluated the effects of tea consumption on the risk of biliary tract cancers and biliary stones. The study included 627 incident cases with biliary tract cancer, 1,037 cases with biliary stones and 959 randomly selected controls. Study subjects were interviewed to ascertain data on demographic, medical and dietary factors, including tea consumption. Forty‐one percent of the controls were ever tea drinkers, defined as those who consumed at least 1 cup of tea per day for at least 6 months. After adjustment for age, education and body mass index, among women, ever tea drinkers had significantly reduced risks of biliary stones (OR = 0.73, 95% CI = 0.54–0.98) and gallbladder cancer (OR = 0.56, 95% CI = 0.38–0.83). The inverse relationship between tea consumption and gallbladder cancer risk was independent of gallstone disease. Among men, tea drinkers were more likely to be cigarette smokers, and the risk estimates were generally below 1.0, but were not statistically significant. Further studies are needed to confirm these results in other populations and clarify the hormonal and other mechanisms that may be involved. © 2006 Wiley‐Liss, Inc.
An overview of the association between allergy and cancer
Authors: Turner Michelle C. , Chen Yue , Krewski Daniel , Ghadirian Parviz 
Published: January 2006

AbstractNumerous epidemiological studies have evaluated some aspect of the association between a history of allergy and cancer occurrence. In this article, an overview of the epidemiological evidence is presented with a discussion of a number of methodological issues important in this area of study. Literature searches were conducted using the MEDLINE database from 1966 through to August 2005 to identify articles that explored a personal history of allergic disorders as a risk factor for cancer. Although it is difficult to draw conclusions between allergy and cancer at many sites because of insufficient evidence or a lack of consistency both within and among studies completed to date, strong inverse associations have been reported for pancreatic cancer and glioma, whereas lung cancer was positively associated with asthma. Additional studies are needed to confirm these finding and to address the limitations of previous studies, including the validity and reliability of exposure measures and control for confounding. Further, large prospective studies using cancer incidence would be particularly useful, including studies using biological markers of allergic status to reduce potential misclassification and to confirm the results of previous studies based on self‐report. There is also a need for further basic research to clarify a potential mechanism, should an association exist. © 2006 Wiley‐Liss, Inc.
Asthma history, occupational exposure to pesticides and the risk of non‐Hodgkin's lymphoma
Authors: Lee Won Jin , Purdue Mark P. , Stewart Patricia , Schenk Maryjean , De Roos Anneclaire J. , Cerhan James R. , Severson Richard K. , Cozen Wendy , Hartge Patricia , Blair Aaron 
Published: January 2006

AbstractWe previously reported that, although asthma did not increase the risk of non‐Hodgkin's lymphoma (NHL), the risk from pesticide exposures was higher among asthmatics than that among nonasthmatics. To further evaluate this finding, we analyzed data from a population‐based case–control study of NHL conducted in Iowa, Detroit, Los Angeles and Seattle. Cases (n = 668) diagnosed with NHL from 1998 to 2000 and controls (n = 543) randomly selected from the same geographical areas as that of the cases were included in this analysis. Odds ratios (OR) for the risk of NHL from potential occupational exposure to pesticides tended to be higher among asthmatics (OR = 1.7; 95% CI 0.3–9.1) when compared with that among nonasthmatics (OR = 0.9; 95% CI 0.6–1.5). The risks of NHL associated with pesticide exposure were also higher among asthmatics who had history of hospitalization (OR = 2.1; 95% CI 0.2–29.0) or daily medication for asthma (OR = infinite) than those among asthmatics who did not have such histories. Our results support the previous finding that the risk of NHL from pesticide exposure may be greater among asthmatics. © 2006 Wiley‐Liss, Inc.
Role of Rac1 and Cdc42 in hypoxia induced p53 and von Hippel‐Lindau suppression and HIF1α activation
Authors: Xue Yan , Bi Feng , Zhang Xueyong , Zhang Siyuan , Pan Yanglin , Liu Na , Shi Yongquan , Yao Xuebiao , Zheng Yi , Fan Daiming 
Published: January 2006

AbstractLow oxygen tension can influence tumor progression by enhancing angiogenesis, a process that may involve Rho GTPases whose activities have been implicated in tumorigenesis and metastasis. In the present study, we show that hypoxia can increase the mRNA levels and intracellular activities of Rac1 and Cdc42 in a time‐dependent manner. The hypoxia‐stimulated activities of Rac1 and Cdc42 could be blocked by the phosphatidylinositol 3′‐kinase (PI3K) inhibitor LY294002 and the protein tyrosine kinase (PTK) inhibitor genistein but were not affected by the p38MAPK inhibitor SB203580 or the MEK‐1 inhibitor PD98059, suggesting that the hypoxia‐mediated signals were through PI3K and PTK. Correlating with the increased activities of Rac1 and Cdc42, the expression of the pro‐angiogenesis factors HIF‐1α and vascular endothelial growth factor (VEGF) was upregulated by hypoxia, whereas the expression of the tumor suppressors von Hippel‐Lindau and p53 was down‐regulated. Dominant negative N17Rac1 and N17Cdc42 could upregulate the expression of p53 and pVHL but downregulate that of HIF‐1α and VEGF under hypoxia. Furthermore, the preconditioned medium from N17Rac1 or N17Cdc42‐expressing gastric cancer cells was able to inhibit the proliferation of HUVECs. Our results indicate that PI3K and PTK‐mediated activations of Rac1 and Cdc42 are involved in the hypoxia‐induced production of angiogenesis‐promoting factors and tumor suppressors, and suggest that the Rho family GTPases Rac1 and Cdc42 may contribute to the hypoxia‐mediated angiogenesis. © 2006 Wiley‐Liss, Inc.
Inhibition of antitumor immunity by invariant natural killer T cells in a T‐cell lymphoma model in vivo
Authors: Renukaradhya Gourapura J. , Sriram Venkataraman , Du Wenjun , Gervay‐Hague Jacquelyn , Van Kaer Luc , Brutkiewicz Randy R. 
Published: January 2006

AbstractWe have investigated the role of the host's CD1d‐dependent innate antitumor immune response in a murine T‐cell lymphoma model in vivo. We found that C57BL/6 wildtype (WT) mice inoculated with RMA/S cells transfected with murine CD1d1 died at the same rate as mice inoculated with vector‐transfected cells. In contrast, natural killer T (NKT) cell‐deficient CD1d or Jα18 knockout mice inoculated with CD1d‐transfected RMA/S cells survived significantly longer than mice inoculated with vector‐transfected RMA/S cells, implicating the involvement of invariant NKT (iNKT) cells in inhibiting antitumor activity in vivo. In contrast to the mutant mice, which produced more of the proinflammatory cytokines IFN‐γ and GM‐CSF, WT mice produced significantly elevated amounts of IL‐13. Antitumor activity in the knockout mice was not due to the development of CD1d‐specific cytotoxic T lymphocytes or circulating antibodies. However, iNKT cell numbers were elevated in tumor‐bearing mice. Thus, iNKT cells may be playing a negative role in the host's antitumor immune response against T‐cell lymphomas in a CD1d‐dependent manner. © 2006 Wiley‐Liss, Inc.
p38 MAPK turns hepatocyte growth factor to a death signal that commits ovarian cancer cells to chemotherapy‐induced apoptosis
Authors: Coltella Nadia , Rasola Andrea , Nano Elisa , Bardella Chiara , Fassetta Michela , Filigheddu Nicoletta , Graziani Andrea , Comoglio Paolo M. , Di Renzo Maria Flavia 
Published: January 2006

AbstractWe recently showed that Hepatocyte Growth Factor (HGF), known as a survival factor, unexpectedly enhances apoptosis in human ovarian cancer cells treated with the front‐line chemotherapeutics cisplatin (CDDP) and paclitaxel (PTX). Here we demonstrate that this effect depends on the p38 mitogen‐activated kinase (MAPK). In fact, p38 MAPK activity is stimulated by HGF and further increased by the combined treatment with HGF and either CDDP or PTX. The expression of a dominant negative form of p38 MAPK abrogates apoptosis elicited by drugs, alone or in combination with HGF. HGF and drugs also activate the ERK1/2 MAPKs, the PI3K/AKT and the AKT substrate mTOR. However, activation of these survival pathways does not hinder the ability of HGF to enhance drug‐dependent apoptosis. Altogether data show that p38 MAPK is necessary for HGF sensitization of ovarian cancer cells to low‐doses of CDDP and PTX and might be sufficient to overcome activation of survival pathways. Therefore, the p38 MAPK pathway might be a suitable target to improve response to conventional chemotherapy in human ovarian cancer. © 2006 Wiley‐Liss, Inc.
Frequency permutation arrays
Authors: Huczynska Sophie , Mullen Gary L. 
Published: January 2006

AbstractMotivated by recent interest in permutation arrays, we introduce and investigate the more general concept of frequency permutation arrays (FPAs). An FPA of lengthn = mλ and distancedis a setTof multipermutations on a multiset ofmsymbols, each repeated with frequency λ, such that the Hamming distance between any distinctx,y∈Tis at leastd. Such arrays have potential applications in powerline communication. In this article, we establish basic properties of FPAs, and provide direct constructions for FPAs using a range of combinatorial objects, including polynomials over finite fields, combinatorial designs, and codes. We also provide recursive constructions, and give bounds for the maximum size of such arrays. © 2006 Wiley Periodicals, Inc. J Combin Designs 14: 463–478, 2006
Skin responses to fractional photothermolysis
Authors: Laubach Hans‐Joachim , Tannous Zeina , Anderson R. Rox , Manstein Dieter 
Published: January 2006

AbstractBackground and ObjectiveFractional photothermolysis (FP) is a new concept using arrays of microscopic thermal damage patterns to stimulate a therapeutic response. We analyzed epidermal and dermal response to FP with the aim of correlating histological and clinical response.Study Design/Materials and MethodsTwelve subjects received a single treatment with a prototype diode laser emitting at a wavelength of 1,500 nm, delivering 5 mJ per microscopic treatment zone (MTZ), and a density of 1,600 MTZs/cm2 on the forearm. Biopsies were procured over a period of 3 months. The biopsies were analyzed by two blinded dermatopathologists using hematoxylin and eosin (Hematoxylin and Eosin Stain), Elastica von Gieson, nitro‐blue‐tetrazolium‐chloride (NBTC) viability, and immunohistochemistry stains. Furthermore, the treatment sites were evaluated in vivo by confocal microscopy.Results and DiscussionTwenty‐four hours after fractional photothermolysis, the continuity of the epidermal basal cell layer is restored. Complete epidermal regeneration is obtained 7 days after the treatment. Microscopic epidermal necrotic debris (MENDs) are seen as early as 1 day after FP. MENDs contain melanin pigment, and are shed from the epidermis within 7 days. Evidence of increased collagen III production is shown with immunohistochemistry (IHC) staining 7 days after FP. IHC for heat shock protein 70 (HSP 70) shows the expression of HSP 1 day after FP, and IHC for alpha smooth muscle actin shows the presence of myofibroblasts 7 days after FP. These findings are concordant with the induction of a wound healing response by FP. There is no evidence of residual dermal fibrosis 3 months after treatment.ConclusionA single treatment with fractional photothermolysis induces a wound healing response in the dermis. A mechanism for the precise removal of epidermal melanin is described, in which MENDs act as a melanin shuttle. Lasers Surg. Med. 38:142–149, 2006. © 2006 Wiley‐Liss, Inc.
Photodynamic therapy using meso tetra hydroxy phenyl chlorin (mTHPC) in early prostate cancer
Authors: Moore C.M. , Nathan T.R. , Lees W.R. , Mosse C.A. , Freeman A. , Emberton M. , Bown S.G. 
Published: January 2006

AbstractBackground and ObjectivesProstate cancer is increasing in incidence, but current treatments including surgery and radiotherapy have significant side effects. This pilot study was designed to assess the potential of photodynamic therapy (PDT) using meso tetra hydroxy phenyl chlorin (mTHPC) for organ confined prostate cancer.Study Design/Patients and MethodsSix men with organ confined prostate cancer were photosensitised with mTHPC (0.15 mg/kg). Between 2 and 5 days later, red light (652 nm) was delivered to areas of biopsy proven cancer via fibres inserted through transperineal needles (50–100 J per site).ResultsAfter 8 of 10 PDT sessions, the prostate specific antigen (PSA) fell by up to 67%. Early MRI scans showed oedema and patchy necrosis, which resolved over 2 months. Biopsies of treated areas revealed necrosis and fibrosis at 1–2 months.ConclusionsPDT for primary prostate cancer appears safe and can reduce PSA levels. As this was a phase I study, no attempt was made to treat the whole prostate; this or targeted tumour ablation could be attempted in a phase II study with an increased number of fibres. This technique merits further investigation in early prostate cancer. Lasers Surg. Med. © 2005 Wiley‐Liss, Inc.
The effect of admission to a geriatric ward on medication use: 2002 versus 1985
Authors: Frankfort Suzanne V. , Tulner Linda R. , van Campen Jos. P. C. M. , Koks Cornelis H. W. , Beijnen Jos H. 
Published: January 2006

AbstractPurposeTo investigate the changes in pharmacotherapy of patients during and after admission to a geriatric ward in 2002 and to investigate if this goes along with reduction of drugs. To describe the differences of the admitted patients and their medication in 2002 compared to 1985.MethodsIncluded patients were admitted to the geriatric ward of a general hospital in the Netherlands during 2002 (n = 258, mean age 84.2 years). Medication at admission, during admission and at discharge were described after retrospective reviewing of medical charts. A comparable study was performed at the same ward in 1985.ResultsIn 2002, most frequently used medication at admission was acetylsalicylic acid (30.2%). Pantoprazole was during admission used in 38.8% of patients and at discharge in 31.8%. Folic acid that was at admission used by 11.6% of patients was at discharge increased to 23.4%. At discharge, vitamin D was used in 21.5% of patients, whereas lisinopril was used in 17.8% of patients. Both in 1985 and 2002 vitamins were added and use of antibiotics was increased during admission. A mean addition of 1.0 drug in 1985 and of 0.7 drugs in 2002 was observed.ConclusionsGeriatric hospital admission resulted both in 1985 and 2002 in addition of medication. In both periods reductions in medication were nullified by addition of medication for reason of therapy optimisation. Compared to 1985 admitted patients receive more medication resulting from new insights into pharmacotherapy and more use of preventive medicine. Copyright © 2006 John Wiley & Sons, Ltd.