bluuebunny/crossref_metadata_2025_split huggingface dataset:
Deficiency of tenascin C attenuates allergen‐induced bronchial asthma in the mouse
Authors: Nakahara Hiroki , Gabazza Esteban C. , Fujimoto Hajime , Nishii Yoichi , D'Alessandro‐Gabazza Corina N. , Bruno Nelson E. , Takagi Takehiro , Hayashi Tatsuya , Maruyama Junko , Maruyama Kazuo , Imanaka‐Yoshida Kyoko , Suzuki Koji , Yoshida Toshimichi , Adachi Yukihiko , Taguchi Osamu 
Published: November 2006

AbstractTenascin C (TN‐C) is an extracellular matrix glycoprotein whose expression is increased in several inflammatory diseases of the lung, including bronchial asthma. However, the exact function of TN‐C in the pathogenesis of lung inflammation remains unclear. In the present study, we compared the degree of bronchial asthma in wild‐type and TN‐C‐deficient (–/–) BALB/c mice. Bronchial asthma was induced by sensitization and challenge with ovalbumin. Littermates treated with saline were used as controls. Cytokines in bronchoalveolar lavage fluid and plasma were measured by enzyme immunoassays. The number of eosinophils in the lung was significantly increased in wild‐type mice compared with TN‐C‐knockout mice. Airway hyperreactivity, NF‐κB activation and concentrations of monocyte chemoattractant protein‐1, IL‐5, IL‐13, metalloproteinase‐9 and immunoglobulin‐E in the bronchoalveolar lavage fluid were significantly decreased in ovalbumin‐sensitized/challenged TN‐C‐knockout mice compared with their wild‐type counterparts. In vitro experiments disclosed that TN‐C significantly stimulates the secretion of IL‐5, IL‐13, IFN‐γ and immunoglobulin‐E from spleen lymphocytes. These observations suggest that TN‐C is involved in the pathogenesis of bronchial asthma.
Functional and structural requirements for the internalization of distinct BCR‐ligand complexes
Authors: Caballero Adriana , Katkere Bhuvana , Wen Xiao‐Yun , Drake Lisa , Nashar Toufic O. , Drake James R. 
Published: November 2006

AbstractAntigen (Ag) binding to the BCR rapidly initiates two important events: a phosphorylation cascade that results in the production of secondary signaling intermediaries and the internalization of Ag‐BCR complexes. Previous studies using anti‐BCR antibodies (Ab) have suggested that BCR signaling is an essential requirement for BCR endocytosis and have further implicated lipid rafts as essential platforms for both BCR functions. However, published data from our laboratory indicate that lipid rafts and consequently raft‐mediated signaling are dispensable for BCR‐mediated internalization of Ag‐specific BCR. Therefore, we investigated the relationship between BCR signaling and endocytosis by defining the role of early kinase signaling in the BCR‐mediated internalization of a model Ag (haptenated protein). The results demonstrate that Src kinases and Syk‐mediated BCR signaling are not essential for BCR‐mediated Ag internalization. Moreover, by comparing Ag and Ab, it was determined that while both localize to clathrin‐coated pits, the internalization of Ab‐BCR complexes is more susceptible to inhibition of signaling and highly sensitive to disruption of lipid rafts and the actin cytoskeleton compared to Ag‐BCR complexes. Thus, these results demonstrate that the nature of the ligand ultimately determines the functional requirements and relative contribution of lipid rafts and other membrane structures to the internalization of BCR‐ligand complexes.
Involvement of leptin signaling in the survival and maturation of bone marrow‐derived dendritic cells
Authors: Lam Queenie Lai Kwan , Liu Shuxun , Cao Xuetao , Lu Liwei 
Published: November 2006

AbstractPrevious studies demonstrated that lymphocyte development is impaired in leptin receptor (Ob‐R)‐deficient db/db mice. However, it remains unclear whether or not leptin signaling plays a physiological role in dendritic cell (DC) development and function. In this study, we first detected Ob‐R expression in murine DC. Using db/db mice at a pre‐diabetic stage, we demonstrate that the total number of DC generated from bone marrow (BM) cultures is significantly lower than in WT controls. Similarly, selective blockade of leptin with a soluble mouse Ob‐R chimera (Ob‐R:Fc) inhibited DC generation in wild‐type BM cultures. The reduced DC yield in db/db BM culture was attributed to significantly increased apoptosis, which was associated with dysregulated expression of Bcl‐2 family genes. Moreover, db/db DC displayed markedly reduced expression of co‐stimulatory molecules and a Th2‐type cytokine profile, with a poor capacity to stimulate allogeneic T cell proliferation. Consistent with their impaired DC phenotype and function, db/db DC showed significantly down‐regulated activities of the PI3K/Akt pathway as well as STAT‐3 and IκB‐α. In conclusion, our findings demonstrate the involvement of leptin signaling in DC survival and maturation.See accompanying commentary: http://dx.doi.org/10.1002/eji.200636770
Risk‐based selection from the general population in a screening trial: Selection criteria, recruitment and power for the Dutch‐Belgian randomised lung cancer multi‐slice CT screening trial (NELSON)
Authors: van Iersel Carola A. , de Koning Harry J. , Draisma Gerrit , Mali Willem P.T.M. , Scholten Ernst Th. , Nackaerts Kristiaan , Prokop Mathias , Habbema J. Dik. F. , Oudkerk Mathijs , van Klaveren Rob J. 
Published: November 2006

AbstractA method to obtain the optimal selection criteria, taking into account available resources and capacity and the impact on power, is presented for the Dutch‐Belgian randomised lung cancer screening trial (NELSON). NELSON investigates whether 16‐detector multi‐slice computed tomography screening will decrease lung cancer mortality compared to no screening. A questionnaire was sent to 335,441 (mainly) men, aged 50–75. Smoking exposure (years smoked, cigarettes/day, years quit) was determined, and expected lung cancer mortality was estimated for different selection scenarios for the 106,931 respondents, using lung cancer mortality data by level of smoking exposure (US Cancer Prevention Study I and II). Selection criteria were chosen so that the required response among eligible subjects to reach sufficient sample size was minimised and the required sample size was within our capacity. Inviting current and former smokers (quit ≤ 10 years ago) who smoked >15 cigarettes/day during >25 years or >10 cigarettes/day during >30 years was most optimal. With a power of 80%, 17,300–27,900 participants are needed to show a 20–25% lung cancer mortality reduction 10 years after randomisation. Until October 18, 2005 11,103 (first recruitment round) and 4,325 (second recruitment round) (total = 15,428) participants have been randomised. Selecting participants for lung cancer screening trials based on risk estimates is feasible and helpful to minimize sample size and costs. When pooling with Danish trial data (n = ±4,000) NELSON is the only trial without screening in controls that is expected to have 80% power to show a lung cancer mortality reduction of at least 25% 10 years after randomisation. © 2006 Wiley‐Liss, Inc.
Human papillomavirus seropositivity and risks of head and neck cancer
Authors: Smith Elaine M. , Ritchie Justine M. , Pawlita Michael , Rubenstein Linda M. , Haugen Thomas H. , Turek Lubomir P. , Hamsikova Eva 
Published: November 2006

AbstractWe examined antibody response to VLP HPV‐16, HPV‐16 E6 and E7 antibodies as potential seromarkers of HPV‐related head and neck cancer (HNC). The study included 204 HNC cases and 326 controls evaluated for HPV presence in sera using ELISAs for anti‐HPV VLP antibodies and HPV‐16 E6 and/or E7 antibodies, and in tumor tissue using PCR and DNA sequencing. Anti‐HPV‐16 VLP was detected in 33.8% of cases and 22.4% of controls, anti‐E6 in 20.6% of cases and 0.9% of controls and anti‐E7 in 18.6% of cases and 0.6% of controls. HPV‐16 DNA was detected in 26.1% of tumors. The adjusted risk of HNC was elevated among those seropositive for HPV‐16 VLP (odds ratio (OR) = 1.7, 1.1–2.5), E6 (OR = 32.8, 9.7–110.8) or E7 (OR = 37.5, 8.7–161.2). Compared to HPV DNA‐negative/seronegative cases, tumor HPV‐16 cases had increased risk of detection with anti‐VLP antibodies (OR = 6.8, 3.1–14.9). The odds were more pronounced among cases seropositive for E6 (OR = 69.0, 19.3–247) or E7 (OR = 50.1, 14.7–171). Antibodies against E6 or E7 were associated with risk of cancer in the oral cavity (OR = 5.1, 1.2–22.4) and oropharynx (OR = 72.8, 16.0–330), and with disease characteristics: stage, grade and nodal status. Anti‐E6 and/or E7 antibodies were found in 74% of tumor HPV‐16 positive cases but in only 5% of tumor HPV‐negative cases (K =0.7, 0.6–0.8) suggesting good correlation between the serologic marker and HPV tumor status. Antibodies to HPV‐16 E6 and/or E7 represent a more specific biomarker than anti‐HPV‐16 VLP of an HPV‐related HNC. Because of the survival advantage of HPV‐related HNC, HPV‐16 E6/E7 detection may be useful in therapy targeted for HPV‐related tumors. © 2006 Wiley‐Liss, Inc.
Retracted: In vitro and in vivo molecular evidence of genistein action in augmenting the efficacy of cisplatin in pancreatic cancer
Authors: Banerjee Sanjeev , Zhang Yuxiang , Wang Zhiwei , Che Mingxin , Chiao Paul J , Abbruzzese James L , Sarkar Fazlul H. 
Published: November 2006

AbstractThis article has been retracted at the request of: Editor‐in‐Chief and Author‘In vitro and in vivo molecular evidence of genistein action in augmenting the efficacy of cisplatin in pancreatic cancer’ by Banerjee, S., Zhang, Y., Wang, Z., Che, M., Chiao, P. J., Abbruzzese, J. L. and Sarkar, F. H.The above article and associated erratum, published online on 27 November 2006 and 6 February 2014, respectively, in Wiley Online Library (wileyonlinelibrary.com), have been retracted by agreement between the authors, the journal Editor‐in‐Chief, Professor Peter Lichter, and Wiley Periodicals, Inc. A university investigation involving the first and the corresponding author determined that several figures in this paper, including the b‐actin bands in Fig. 1C in the erratum, were re‐used, mislabeled, manipulated, or duplicated while processing/compiling the final figures assembled from the original data sources. Therefore, the authors are retracting the paper in its entirety although they maintain that these issues did not affect the major conclusions. They apologize for any inconvenience this may have caused.ReferenceBanerjee, S., Zhang, Y., Wang, Z., Che, M., Chiao, P. J., Abbruzzese, J. L. and Sarkar, F. H. (2007), In vitro and in vivo molecular evidence of genistein action in augmenting the efficacy of cisplatin in pancreatic cancer. Int. J. Cancer, 120: 906–917. doi: 10.1002/ijc.22332; corrected by Erratum: In vitro and in vivo molecular evidence of genistein action in augmenting the efficacy of cisplatin in pancreatic cancer. Int. J. Cancer, 134: E4. doi: 10.1002/ijc.28710.
Combining high selectivity of replication via CXCR4 promoter with fiber chimerism for effective adenoviral oncolysis in breast cancer
Authors: Stoff‐Khalili Mariam A. , Rivera Angel A. , Stoff Alexander , Michael Mathis J. , Rocconi Rodney P. , Matthews Qiana L. , Numnum Michael T. , Herrmann Isabell , Dall Peter , Eckhoff Devin E. , Douglas Joanne T. , Siegal Gene P. , Zhu Zeng B. , Curiel David T. 
Published: November 2006

AbstractConditionally replicative adenoviruses (CRAds) represent novel therapeutic agents that have been recently applied in the context of breast cancer therapy. However, deficiencies in the ability of the adenovirus to infect target tumor cells and to specifically replicate within the tumor target represent key deficiencies preventing the realization of the full potential of this therapeutic approach. Minimal expression of the adenovirus serotype 5 (Ad5) receptor CAR (coxsackie and adenovirus receptor) on breast cancer cells represents a major limitation for Ad5‐based virotherapy. Genetic fiber chimerism is a method to alter the tropism of Ad5‐based CRAds to achieve CAR‐independent infectivity of tumor cells. Here, we describe the use of a CRAd with cancer specific transcriptional control of the essential Ad5 E1A gene using the human CXCR4 gene promoter. We further modified the fiber protein of this agent by switching the knob domain with that of the adenovirus serotype 3. The oncolytic activity of this 5/3 fiber‐modified CRAd was studied in breast cancer cell lines, primary breast cancer and human liver tissue slices from patients, and in a xenograft breast cancer mouse model. This infectivity enhanced CRAd agent showed improved replication and killing in breast cancer cells in vitro and in vivo with a remarkable specificity profile that was strongly attenuated in nonbreast cancer cells, as well as in normal human breast and liver tissues. In conclusion, utilization of a CRAd that combined infectivity enhancement strategies and transcriptional targeting improved the CRAd‐based antineoplastic effects for breast cancer therapy. © 2006 Wiley‐Liss, Inc.
Up‐regulation of Mac‐2 binding protein by hTERT in gastric cancer
Authors: Park Yuk Pheel , Choi Seung‐Chul , Kim Joo Heon , Song Eun Young , Kim Jae Wha , Yoon Do‐Young , Yeom Young Il , Lim Jong‐Seok , Kim Jong Wan , Paik Sang‐Gi , Lee Hee Gu 
Published: November 2006

AbstractMac‐2 binding protein (Mac‐2BP) is a secreted tumor antigen that is elevated in many cancers and implicated in tumor metastasis, as well as cell adhesion and immune functions. We focused on the human telomerase reverse transcriptase (hTERT) induced Mac‐2BP expression and the relationship between Mac‐2BP expression and the progression of gastric cancer. A cDNA expression array analysis was performed on the telomerase‐negative cell line, SW13, which was engineered to overexpress hTERT when compared with the parental SW13 cell. hTERT‐induced Mac‐2BP expression was confirmed via RT‐PCR and Northern blotting. ELISA and flow cytometric analyses revealed that Mac‐2BP protein was increased by 2‐ to 4‐fold in hTERT‐overexpressing cells compared with the mock control. Mac‐2BP expression was significantly reduced when the overexpressed hTERT was neutralized by the introduction of hTERT‐specific siRNA. These results suggest that Mac‐2BP expression is modulated by hTERT. Mac‐2BP levels in both gastric cancer cells and tumor tissues were determined via Northern blot analysis and immunohistochemistry. Mac‐2BP protein was highly expressed in most gastric cancer cell lines, and gastric tumor tissues were stained more densely than normal tissues. The intracellular and secreted Mac‐2BP levels were also evaluated via ELISA, indicating that Mac‐2BP was expressed and secreted more abundantly in gastric cancer patients than in healthy donors. The elevated serum Mac‐2BP level in gastric tumor patients was also significantly associated with distant metastasis (p = 0.05) and higher tumor stage (p = 0.04). Our findings suggest that Mac‐2BP is induced by hTERT, and that it may prove to be a useful prognostic marker for the detection of malignant progression of metastatic stomach cancers. © 2006 Wiley‐Liss, Inc.
Micronutrients and the risk of renal cell cancer: A case‐control study from Italy
Authors: Bosetti Cristina , Scotti Lorenza , Maso Luigino Dal , Talamini Renato , Montella Maurizio , Negri Eva , Ramazzotti Valerio , Franceschi Silvia , Vecchia Carlo La 
Published: November 2006

AbstractThe role of various micronutrients on the risk of renal cell cancer (RCC) was examined in a multicentric case‐control study from Italy, in which information on dietary habits were collected using a validated food‐frequency questionnaire. Cases were 767 patients (494 men and 273 women) with incident, histologically confirmed RCC; controls were 1,534 subjects (988 men and 546 women) admitted to the same hospitals as cases for a wide spectrum of acute, nonneoplastic conditions. After allowing for energy and other major covariates, a significant inverse association was found for vitamin E (odds ratio, OR, for the highest quintile of intake versus the lowest one 0.56, 95% confidence interval, CI 0.41–0.75), and vitamin C (OR = 0.72, 95% CI = 0.54–0.96), although the trend in risk for vitamin C was of borderline significance. No significant trend of decreasing risk was found for other micronutrients analyzed, although for most of them the risk estimates were below unity for intakes above the lowest. The ORs for the upper quintile of intake when compared with the lowest one were 0.80 (95% confidence interval, CI = 0.59–1.08) for retinol, 0.82 (95% CI = 0.61–1.10) for α‐carotene, 0.90 (95% CI = 0.68–1.20) for β‐carotene, 0.94 (95% CI = 0.73–1.21) for β‐criptoxanthin, 0.85 (95% CI = 0.63–1.14) for lutein/zeaxanthin, 0.76 (95% CI = 0.57–1.01) for vitamin D, 0.75 (95% CI = 0.55–1.01) for thiamine, 0.88 (95% CI = 0.66–1.19) for riboflavin, 0.85 for vitamin B6 (95% CI = 0.64–1.13), 0.85 (95% CI = 0.64–1.12) for folate and 0.80 (95% CI = 0.60–1.07) for niacin. No meaningful associations emerged for lycopene (OR = 1.11). The present findings support a possible beneficial effect of vitamin E and C on RCC. © 2006 Wiley‐Liss, Inc.
Time trends of esophageal cancer in Hong Kong: Age, period and birth cohort analyses
Authors: Tse Lap‐ah , Yu Ignatius Tak‐sun , Mang Oscar Wai‐Kong 
Published: November 2006

AbstractThis study was to examine the time trend of the incidence rates of esophageal cancer during the period 1979–2003 in Hong Kong and to identify the effects of year of diagnosis (period) and year of birth (cohort) on the observed time trends using regression models. Cancer incidence data were obtained from Hong Kong Cancer Registry and population data were from the Census and Statistics Department. Age‐standardized incidence rates were computed by the direct method using the World population of 1966. Annual percentage change (APC) in incidence rate was calculated using nonlinear regression. Period and cohort effects were assessed using 2 separate Poisson regression models after adjusting for age. During the period 1979–2003, a steady decrease in the age‐standardized incidence rate was observed for both males (APC = −3.38%, 95% confidence interval [CI]: −2.89%, −3.86%) and females (APC = −3.92%, 95% CI: −3.15%, −4.69%). The incidence rates were consistently higher among males than females. After the adjustment for age and with the period 1989–1993 or birth cohort of 1934–1938 as reference, the relative risk of more recent periods or birth cohorts significantly decreased. The age‐cohort model provided a better description of the data than the age‐period model. Given reasonable latency between exposures and esophageal cancer incidence, the declining birth cohort effects in the recent generations were in line with the increased intakes of fresh vegetables and decreased consumptions of alcohol drinking, tobacco smoking, and preserved foods observed in population, thus supported their importance in influencing the burden of esophageal cancer. © 2006 Wiley‐Liss, Inc.
A novel copper complex of 3‐benzoyl‐α methyl benzene acetic acid with antitumor activity mediated via cyclooxygenase pathway
Authors: Ahmed Fakhara , Adsule Shreelekha , Ali Ashhar S. , Banerjee Sanjeev , Ali Shadan , Kulkarni Sudhir , Padhye Subhash , Sarkar Fazlul H 
Published: November 2006

AbstractPancreatic cancer (PC) is characterized as one of the deadliest malignancies and its treatment is a great challenge to clinical oncologists. Expression of COX‐2 is detectable in 75% of PCs among which 50% showed overexpression, suggesting the importance of COX‐2 enzyme and its metabolic product prostaglandin E2 (PGE2) in PC. Here the authors report the synthesis and biological activity of a novel COX‐2 inhibitor, FPA‐306, and its effects on PC cells with different levels of COX‐2 expression. Using MTT assay, the authors found a significant growth inhibition of BxPC‐3 cells treated by FPA‐306 with an IC50 of 10 μmol/L, which was lower than that of ketoprofen (IC50 = 35.4 μmol/L) and celecoxib (IC50 > 100 μmol/L). There was no such effect found in MIAPaCa cell line, which does not express COX‐2. The authors also found dose dependent reduction in cell survival and induction of apoptosis by FPA‐306 treatment in BxPC‐3 cells but not in MIAPaCa cells. These results were correlated with apoptosis data and secreted PGE2 levels. The molecular modeling of FPA‐306 in the COX‐2 active site showed that FPA‐306 is potentially able to inhibit the activity of enzyme by blocking the active site, thereby resulting in decreased PGE2 production. The authors also found a significant reduction of COX‐2 at the mRNA and protein levels together with downregulation of NF‐κB DNA binding activity and its downstream genes, Bcl‐2 and survivin. These results suggest that FPA‐306 is an effective and potent agent in inhibiting the growth of PC cells. © 2006 Wiley‐Liss, Inc.
Mitofilin and titin as target antigens in melanoma‐associated retinopathy
Authors: Pföhler Claudia , Preuss Klaus‐Dieter , Tilgen Wolfgang , Stark Alexandra , Regitz Evi , Fadle Natalie , Pfreundschuh Michael 
Published: November 2006

AbstractMelanoma‐associated retinopathy (MAR) is a rare paraneoplastic syndrome in patients with melanoma. Since the onset of MAR symptoms is often associated with tumor progression or recrudescence of metastases, MAR‐related symptoms are prognostic relevant. The pathomechanism underlying MAR is supposed to result from antibody production against yet unknown melanoma‐associated antigens that are also expressed in retinal tissue, leading to the destruction of retinal cells and resulting in defective signal transduction. Only a 35 kDa protein in Müller glial cells, a 22 kDa neuronal antigen and retinal transducin have been identified as MAR‐associated antigens to date. To identify additional antigens potentially involved in the pathogenesis of MAR, we screened a retina cDNA phage library for reactivity with antibodies in the sera from 9 patients with MAR or subclinical MAR using the serological analysis of recombinantly expressed clones (SEREX) approach. Six sera from melanoma patients without evidence of MAR and 10 sera from healthy donors served as controls. Mitofilin and titin were identified as antigens against which antibodies were found exclusively in sera of MAR patients, but not in the sera of MM patients without MAR or healthy donors. This is the first study to demonstrate that titin is highly expressed from retinal tissue and melanoma. The fact that none of the MAR‐associated antigens detected to date by their capacity to elicit a humoral immune response is located on the cell surface questions a major pathogenetic role of the respective antibodies and suggests that cellular, rather than humoral mechanisms are operative in the primary immune attack against the retina in MAR. © 2006 Wiley‐Liss, Inc.