bluuebunny/crossref_metadata_2025_split huggingface dataset:
Representing the landslide magnitude–frequency relation: Capilano River basin, British Columbia
Authors: Brardinoni Francesco , Church Michael 
Published: January 2004

AbstractWe use magnitude–frequency analysis as a statistical tool to quantify the erosion caused by landslides and debris ﬂows. Using air‐photo‐ and ground‐derived data we show that the departure from power‐law distribution customarily observed for small magnitude is an artefact of sampling deﬁciencies. Nonetheless, the total distribution is not sensitive to the frequency of small slides and total erosion remains adequately represented in the air‐photo‐derived data. Our data also demonstrate a real departure from simple scaling at much larger magnitudes, the cause of which is not deﬁnitively established. Copyright © 2004 John Wiley & Sons, Ltd.
Enhancement of tumor radioresponse by combined treatment with gefitinib (Iressa, ZD1839), an epidermal growth factor receptor tyrosine kinase inhibitor, is accompanied by inhibition of DNA damage repair and cell growth in oral cancer
Authors: Shintani Satoru , Li Chunnan , Mihara Mariko , Terakado Nagaaki , Yano Junya , Nakashiro Koh‐ichi , Hamakawa Hiroyuki 
Published: January 2004

AbstractMolecular blockade of EGFR with either an EGFR MAb or an EGFR TKI enhances the radiosensitivity of human SCCs. In the present study, we investigated whether treatment with the EGFR TKI gefitinib (Iressa, ZD1839) improves the response to radiotherapy in the OSCC cell lines HSC2 and HSC3. We examined potential mechanisms that may contribute to the enhanced radiation response induced by gefitinib. Growth inhibition was observed in vitro with radiation or gefitinib. A cooperative antiproliferative effect was obtained when cancer cells were treated with radiation followed by gefitinib. Cells treated with a combination of radiation and gefitinib arrested in G1 and G2–M phases, with a decrease in the S‐phase population. While radiation alone did not significantly affect MEK1/2 and p38 MAPK autophosphorylation, the combination of gefitinib and radiation completely inhibited the downstream signaling of EGFR. Results from DNA damage repair analysis in cultured OSCC cells demonstrated that gefitinib had a strong inhibitory effect on DNA‐PKc pathways after radiation. Tumor xenograft studies demonstrated that the combination of gefitinib and radiation caused growth inhibition and tumor regression of well‐established OSCC tumors in athymic mice; tumor volume was reduced from 1,008.2 to 231.4 mm3 in HSC2 cells (p < 0.01) and from 284.2 to 12.4 mm3 in HSC3 cells (p < 0.01). Immunohistochemical analysis of OSCC xenografts revealed that gefitinib caused a striking decrease in tumor cell proliferation when combined with radiotherapy. Overall, we conclude that gefitinib enhances tumor radioresponse by multiple mechanisms that may involve antiproliferative growth inhibition and effects on DNA repair after exposure to radiation. © 2003 Wiley‐Liss, Inc.
Decrease of human pancreatic cancer cell tumorigenicity by α1,3galactosyltransferase gene transfer
Authors: Aubert Muriel , Crotte Christian , Bernard Jean‐Paul , Lombardo Dominique , Sadoulet Marie‐Odile , Mas Eric 
Published: January 2004

AbstractThe enzyme α1,3galactosyltransferase synthesizes the αGal epitope, a carbohydrate structure (Galα1,3Galβ1,4GlcNAc‐R), on glycoconjugates in lower mammals. The enzyme is absent in humans but large amounts of natural antibodies that recognize αGal epitopes are present in human serum. It is likely that these antibodies contribute to the host defense and participate in the hyperacute rejection of xenograft. Previous studies indicated that the glycosyltransferase gene transfer into tumoral cells can modify the structure of glycoconjugates at the cell surface and, as a consequence, modulates the metastatic and tumorigenic behaviors of these cells. The aim of our study was to determine whether the expression of αGal epitope can modify the tumorigenicity of human pancreatic cancer cells. The expression of αGal epitopes in the human pancreatic cancer cell lines BxPC‐3 and Panc‐1 was obtained by selecting stable cell clones transfected with murine α1,3galactosyltransferase gene. The expression of the enzyme activity in BxPC‐3 and Panc‐1 cells resulted in the formation at the cell surface of αGal epitopes that are recognized by human anti‐αGal antibodies. αGal epitope expression at the surface of pancreatic cancer cells was associated with the fixation of complement 1q to human anti‐αGal antibodies. The αGal epitope expression also resulted in a delay in the tumoral development of BxPC‐3 and Panc‐1 cells in vivo after xenograft transplantation of nude mice. In addition to the impairment of the metastatic potential of murine tumor cell lines and the activation of immune response, our study provides evidence that the cell surface expression of αGal epitopes also modulates the tumorigenic behavior of human pancreatic cancer cells. © 2003 Wiley‐Liss, Inc.
Detection of breast cancer cells in the peripheral blood is positively correlated with estrogen‐receptor status and predicts for poor prognosis
Authors: Gaforio José‐Juan , Serrano María‐José , Sanchez‐Rovira Pedro , Sirvent Antonio , Delgado‐Rodriguez Miguel , Campos María , de la Torre Nicolás , Algarra Ignacio , Dueñas Rosario , Lozano Ana 
Published: January 2004

AbstractWe investigated whether detection of cytokeratin‐positive (CK+) cells in the peripheral blood (PB) of breast cancer patients before chemotherapy could be a prognostic factor. Blood from a total of 92 breast cancer patients was evaluated for the presence of CK+ cells. Blood samples were collected before chemotherapy. Patients entered in the study included: neoadjuvant (n = 25), adjuvant (n = 42) and metastatic (n = 25). Blood samples (10 ml) were centrifuged using a double density‐gradient to recovering the mononuclear cell (MNC) and granulocyte cell (GC) fractions. Subsequently, positive immunomagnetic cell separation was carried out to isolating CK+ cells. The enriched cell fraction was cytocentrifuged and then immunocytochemically labeled using an anti‐cytokeratin antibody. Our results indicated that breast tumor cells sediment with both MNC and GC fractions. We therefore recommend examination of both fractions in all enrichment protocols. CK+ cells in PB were identified in 57 of 92 (62%) patients when MNC and GC fractions were assessed (range = 1–61 cells, median = 8). No CK+ cells were detected in blood samples of 16 healthy donors. There were significant differences in the presence of CK+ cells according to estrogen receptor expression (p = 0.049), and lymph node status (p = 0.033), but not to the age, menopausal status, type of patient (neoadjuvant, adjuvant or metastatic), TNM stage, histological type, progesterone receptor expression, c‐erbB2 expression, p53 expression or Ki67 expression. Regarding the relationship between tumor size (T) and the presence of CK+ cells, a borderline significant trend was observed (p = 0.07). The median follow‐up of the patients was 21 months and statistical analysis (Kaplan‐Meier analysis) showed that using the method we present, the detection of CK+ cells in PB before starting the chemotherapy in breast cancer patients was significantly correlated with both progression‐free survival (p = 0.058) and overall survival (p = 0.003). In conclusion, the present study suggests that detection of CK+ cells in PB before chemotherapy might identify breast cancer patients with poor prognosis. © 2003 Wiley‐Liss, Inc.
Birth weight and risk of breast cancer in a cohort of 106,504 women
Authors: Ahlgren Martin , Sørensen Thorkild , Wohlfahrt Jan , Haflidadóttir Ágústa , Holst Claus , Melbye Mads 
Published: January 2004

AbstractThe possible association between prenatal factors and breast cancer has been discussed for more than a decade. Birth weight has been used commonly as a proxy measure for intrauterine growth. Whereas some previous studies have found support for an association between birth weight and breast cancer, others have been inconclusive or found no association. We investigated the relationship between birth weight and risk of female breast cancer in a cohort of 106,504 Danish women. Birth weights were obtained from school health records on girls born between 1930–1975. Information on breast cancer came from linking the cohort with the Danish Cancer Registry and the Danish Breast Cancer Cooperative Groups Registry. A total of 2,334 cases of primary breast cancer were diagnosed in the cohort during 3,255,549 person‐years of follow‐up among women with birth weight between 500–6,000 g. Of these, 922 (40%) were diagnosed with primary breast cancer at the age of 50 years or older. A significant association between birth weight and breast cancer was found equivalent to an increase in risk of 9% per 1,000 g increase in birth weight (95% CI 2–17). The increase was observed for all age groups, representing both pre‐ and post‐menopausal women, and irrespective of tumor characteristics. Adjustment for age at first birth and parity did not influence the results. Birth weight is positively associated with risk of breast cancer, indicating that prenatal factors are important in the etiology of breast cancer. © 2003 Wiley‐Liss, Inc.
Inhibition of tumor cell growth by antibodies induced after vaccination with peptides derived from the extracellular domain of Her‐2/neu
Authors: Jasinska Joanna , Wagner Stefan , Radauer Christian , Sedivy Roland , Brodowicz Thomas , Wiltschke Christoph , Breiteneder Heimo , Pehamberger Hubert , Scheiner Otto , Wiedermann Ursula , Zielinski Christoph C. 
Published: January 2004

AbstractThe anti Her‐2/neu monoclonal antibody Trastuzumab has strong inhibiting effects on tumor growth in vitro and in vivo and is therefore used for immunotherapy in breast cancer patients. Due to necessity of frequent applications, however, cost intensiveness of Trastuzumab treatment and its limited duration of affectivity, an active immunization inducing a perhaps preventive and long‐term immunity to Her‐2/neu remains a desirable goal. We attempted to induce anti Her‐2/neu antibodies by peptide vaccination and to test their efficacy in inhibiting tumor cell growth in vitro. By computer aided analyses, 7 putative B cell epitopes of Her‐2/neu were defined and synthesized. These peptide epitopes were coupled to tetanus toxoid and used for immunization in BALB/c mice. Among these peptides, immunizations with 2 single peptides or a combination of 2 peptides induced anti‐peptide antibody levels, primarily of the IgG1 isotype. These antibodies were also directed against the native Her‐2/neu antigen, as shown in precipitation assays and ELISA with cell lysates of the Her‐2/neu overexpressing breast cancer cell line SK‐BR‐3. Isolated IgG fractions from immune sera incubated with SK‐BR‐3 cells led to a moderate inhibition of the tumor cell growth in vitro, as well as to complement dependent cell lyses comparable to that achieved by incubation with Trastuzumab. Moreover, peptide immunization in rabbits generated anti‐Her 2‐neu IgG that, in contrast to mouse sera, were able to mediate a 31–46% lysis of SK‐BR‐3 cells in ADCC experiments. We conclude from our data that immunization with Her‐2/neu peptides successfully induced humoral immune response with anti‐tumor activity in an animal model. © 2003 Wiley‐Liss, Inc.
The IGF‐1 receptor in cancer biology
Authors: Baserga Renato , Peruzzi Francesca , Reiss Krysztof 
Published: January 2004

AbstractThe type 1 insulin‐like growth factor receptor (IGF‐1R) plays an important role in the establishment and maintenance of the transformed phenotype. It also has a strong antiapoptotic activity and has a significant influence on the control of cell and body size. Downregulation of the IGF‐1R leads to massive apoptosis of cancer cells. These characteristics make it an attractive target for anticancer therapy. © 2003 Wiley‐Liss, Inc.
Comparative evaluation of urokinase‐type plasminogen activator receptor expression in primary breast carcinomas and on metastatic tumor cells
Authors: Hemsen Alice , Riethdorf Lutz , Brünner Nils , Berger Jürgen , Ebel Sebastian , Thomssen Christoph , Jänicke Fritz , Pantel Klaus 
Published: January 2004

AbstractThe urokinase‐type plasminogen activator receptor (uPAR, CD87) plays a central role in the plasminogen activation cascade, which participates in extracellular matrix degradation, cell migration and invasion. Here we performed a comprehensive immmunohistochemical evaluation of uPAR expression in primary tumor cells, tumor‐surrounding fibroblasts, lymph node metastases and micrometastatic cells in bone marrow of patients with breast carcinomas at the time of primary diagnosis. Variable degrees of uPAR staining of tumor cells were observed in 84 of 93 (90%) carcinomas, whereas intratumoral fibroblasts were uPAR‐positive in 70 (75%) carcinomas. The fraction of uPAR‐positive primary tumor cells but not fibroblasts was positively correlated with the presence of tumor cells in bone marrow (p = 0.037), whereas no correlation with lymph node metastasis was found. Immunophenotyping of bone marrow and lymph node specimens revealed expression of uPAR on metastatic tumor cells in 10 of 13 and 22 of 23 cases, respectively. Direct comparison to the autologous primary tumor cells showed different uPAR staining scores in most patients with evidence for both up‐ and downregulation of uPAR on metastatic cells. Our results indicate that uPAR plays an active role in breast cancer metastasis and may therefore be a promising target for new biologic therapies. © 2003 Wiley‐Liss, Inc.
Novel retinoic acid derivative ABPN has potent inhibitory activity on cell growth and apoptosis in cancer cells
Authors: Um Soo‐Jong , Han Hye‐Sook , Kwon Youn‐Ja , Park Si‐Ho , Rho Young‐Soy , Sin Hong‐Sig , Park Jong‐Sup 
Published: January 2004

AbstractRetinoids are natural and synthetic derivatives of vitamin A that have great promise for cancer therapy and chemoprevention. Of the retinoids developed so far, 4‐(N‐hydroxyphenyl)retinamide (4‐HPR or fenretinide) appears to have the best therapeutic potential in vitro and in vivo and is currently being tested in clinical trials for cancer prevention and therapy. To develop other potentially potent antitumor agents, we synthesized 85 retinoid derivatives. In an initial screening of these synthetic retinoids using the HCT116 colon cancer cell line, we found that 4‐amino‐2‐(butyrylamino)phenyl(2E,4E,6E,8E)‐3,7‐dimethyl‐9‐(2,6,6‐trimethyl‐1‐cyclohexenyl)‐2,4,6,8‐nonatetraenoate (ABPN or CBG41) induced the greatest growth inhibition, with an IC50 value of 0.6 μM. Subsequent studies in other cancer cell lines indicated that ABPN was much more growth‐inhibitory than all‐trans retinoic acid or 4‐HPR. Compared to 4‐HPR, ABPN induced 5.5‐ to 70.0‐fold more growth inhibition in most cancer cells, with the exception of gynecologic cancer cells. In these cells, the antiproliferative effect was only 1.5‐ to 2.8‐fold more than 4‐HPR. We examined the molecular mechanism underlying the difference in growth inhibition between 4‐HPR and ABPN. DAPI staining, DNA fragmentation, FACS and Western blotting analyses suggest that ABPN induced apoptosis by activating caspase‐3 and ‐8, which may result in increased PARP cleavage. Unlike 4‐HPR, ABPN activated all 3 RAR isotypes to an extent similar to AtRA. In addition, ABPN significantly inhibited AP‐1 transcriptional activity and thus greatly suppressed the expression of the matrix metalloproteinase ‐1, ‐2 and ‐3 genes, which are involved in tumor invasion. These results suggest that ABPN may be a promising retinoid derivative offering not only enhanced cytotoxicity, but also increased inhibition of tumor invasiveness. © 2003 Wiley‐Liss, Inc.
Fruits, vegetables and lung cancer: A pooled analysis of cohort studies
Authors: Smith‐Warner Stephanie A. , Spiegelman Donna , Yaun Shiaw‐Shyuan , Albanes Demetrius , Beeson W. Lawrence , van den Brandt Piet A. , Feskanich Diane , Folsom Aaron R. , Fraser Gary E. , Freudenheim Jo L. , Giovannucci Edward , Goldbohm R. Alexandra , Graham Saxon , Kushi Lawrence H. , Miller Anthony B. , Pietinen Pirjo , Rohan Thomas E. , Speizer Frank E. , Willett Walter C. , Hunter David J. 
Published: January 2004

AbstractInverse associations between fruit and vegetable consumption and lung cancer risk have been consistently reported. However, identifying the specific fruits and vegetables associated with lung cancer is difficult because the food groups and foods evaluated have varied across studies. We analyzed fruit and vegetable groups using standardized exposure and covariate definitions in 8 prospective studies. We combined study‐specific relative risks (RRs) using a random effects model. In the pooled database, 3,206 incident lung cancer cases occurred among 430,281 women and men followed for up to 6–16 years across studies. Controlling for smoking habits and other lung cancer risk factors, a 16–23% reduction in lung cancer risk was observed for quintiles 2 through 5 vs. the lowest quintile of consumption for total fruits (RR = 0.77; 95% CI = 0.67–0.87 for quintile 5; p‐value, test for trend < 0.001) and for total fruits and vegetables (RR = 0.79; 95% CI = 0.69–0.90; p‐value, test for trend = 0.001). For the same comparison, the association was weaker for total vegetable consumption (RR = 0.88; 95% CI = 0.78–1.00; p‐value, test for trend = 0.12). Associations were similar between never, past, and current smokers. These results suggest that elevated fruit and vegetable consumption is associated with a modest reduction in lung cancer risk, which is mostly attributable to fruit, not vegetable, intake. However, we cannot rule out the possibility that our results are due to residual confounding by smoking. The primary focus for reducing lung cancer incidence should continue to be smoking prevention and cessation. © 2003 Wiley‐Liss, Inc.
Expression of TGF‐β type II receptor antisense RNA impairs TGF‐β signaling in vitro and promotes mammary gland differentiation in vivo
Authors: Lenferink Anne E.G. , Magoon Joanne , Pepin Marie‐Claude , Guimond Alain , O'Connor‐McCourt Maureen D. 
Published: January 2004

AbstractIn order to clarify the role of TGF‐β in mammary development and tumorigenesis, we investigated the efficacy of full‐ or partial‐length TβRII antisense RNA specifically to reduce TβRII levels in both in vitro and in vivo model systems. Here we show that the expression of TβRII antisense RNA in vitro reduced TβRII cell surface expression and inhibited the antiproliferative and transcriptional responses to exogenous TGF‐β. Expression of full‐length TβRII antisense RNA in a transgenic mouse model under control of the mouse mammary tumor virus promotor resulted in precocious lobuloalveolar development of the mammary gland, a phenotype that resembles that of early pregnancy. These data demonstrate that TβRII plays a critical role in maintaining the nondifferentiated character of virgin mammary gland epithelium. © 2003 Wiley‐Liss, Inc.
Near‐infrared Raman spectroscopy for optical diagnosis of lung cancer
Authors: Huang Zhiwei , McWilliams Annette , Lui Harvey , McLean David I. , Lam Stephen , Zeng Haishan 
Published: January 2004

AbstractRaman spectroscopy is a vibrational spectroscopic technique that can be used to optically probe the molecular changes associated with diseased tissues. The objective of our study was to explore near‐infrared (NIR) Raman spectroscopy for distinguishing tumor from normal bronchial tissue. Bronchial tissue specimens (12 normal, 10 squamous cell carcinoma (SCC) and 6 adenocarcinoma) were obtained from 10 patients with known or suspected malignancies of the lung. A rapid‐acquisition dispersive‐type NIR Raman spectroscopy system was used for tissue Raman studies at 785 nm excitation. High‐quality Raman spectra in the 700–1,800 cm–1 range from human bronchial tissues in vitro could be obtained within 5 sec. Raman spectra differed significantly between normal and malignant tumor tissue, with tumors showing higher percentage signals for nucleic acid, tryptophan and phenylalanine and lower percentage signals for phospholipids, proline and valine, compared to normal tissue. Raman spectral shape differences between normal and tumor tissue were also observed particularly in the spectral ranges of 1,000–1,100, 1,200–1,400 and 1,500–1,700 cm–1, which contain signals related to protein and lipid conformations and nucleic acid's CH stretching modes. The ratio of Raman intensities at 1,445 to 1,655 cm–1 provided good differentiation between normal and malignant bronchial tissue (p < 0.0001). The results of this exploratory study indicate that NIR Raman spectroscopy provides significant potential for the noninvasive diagnosis of lung cancers in vivo based on the optic evaluation of biomolecules. © 2003 Wiley‐Liss, Inc.
Induced antitumor immunity against DMBA‐4 metastatic mammary tumors in rats using laser immunotherapy
Authors: Chen Wei R. , Jeong Sang Won , Lucroy Michael D. , Wolf Roman F. , Howard Eric W. , Liu Hong , Nordquist Robert E. 
Published: January 2004

AbstractInduced antitumor immunity is a highly effective and long‐term cure for cancer, particularly for metastatic tumors. Laser immunotherapy was developed to induce such an immunologic response. It involves intratumoral administration of a light‐absorbing dye and a specially formulated immunoadjuvant, followed by noninvasive irradiation of a near‐infrared laser. Treatment of DMBA‐4 metastatic mammary tumors in rats with this approach has resulted in local control of primary tumors and eradication of untreated distant metastases. After laser immunotherapy, rats were resistant to tumor rechallenge and developed immunity, which could be adoptively transferred. To better understand the immunity induced in this tumor model, immunization using freeze–thaw DMBA‐4 cell lysates was performed, followed by tumor challenge 21 days later. Tumor cell lysate immunization delayed the emergence of metastases but did not provide immunity against the tumor challenge. Also performed was surgical resection of primary tumors before the observation of metastatic tumors. Removal of primary tumors was unsuccessful at changing the course of tumor progression. Tumors re‐emerged at the primary sites, and metastases developed at multiple remote sites. In contrast, tumor‐bearing rats successfully treated by laser immunotherapy experienced tumor regression and eradication and developed strong resistance to repeated challenges by tumor cells of the same type. Our results show that laser immunotherapy could have potential for the treatment of metastatic tumors by inducing tumor‐specific, long‐lasting immunity. © 2003 Wiley‐Liss, Inc.