bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tubal sterilization in relation to breast cancer risk
Authors: Eliassen A. Heather , Colditz Graham A. , Rosner Bernard , Hankinson Susan E. 
Published: November 2005

AbstractTubal sterilization methods may damage surrounding tissue, potentially disrupting the ovarian blood supply and hormonal functioning, and may decrease breast cancer risk. We examined this hypothesis, within the Nurses' Health Study, among 77,511 women, aged 30–55 years and free of cancer at the start of follow‐up in 1976. We documented 4,176 cases of invasive breast cancer from 1976 to 2000. Cox proportional hazards models, adjusting for multiple breast cancer risk factors, provided rate ratios (RR) and 95% confidence intervals (CI). Overall, tubal sterilization was not associated with breast cancer risk (RR = 0.95, 95% CI = 0.88–1.03). However, tubal sterilizations performed from 1970 to 1974 were inversely associated with risk (RR = 0.84, 95% CI = 0.73–0.97), while procedures performed in other years were not associated with risk. Among women with procedures performed in 1970–1974, those who were ≥35 years old at the time of sterilization were at the lowest risk (RR = 0.81, 95% CI = 0.66–0.98), while younger women had a suggested decreased risk (RR = 0.87, 95% CI = 0.72–1.06). Overall, tubal sterilization was not associated with breast cancer risk. However, a modest inverse association was observed at a time when the potentially destructive unipolar electrocautery method was commonly used, providing some support for an association between lower lifetime exposure to hormones and a decreased risk of breast cancer. © 2005 Wiley‐Liss, Inc.
Rearrangement of the COL12A1 and COL4A5 genes in subungual exostosis: molecular cytogenetic delineation of the tumor‐specific translocationt(X;6)(q13‐14;q22)
Authors: Storlazzi Clelia Tiziana , Wozniak Agnieszka , Panagopoulos Ioannis , Sciot Raf , Mandahl Nils , Mertens Fredrik , Debiec‐Rychter Maria 
Published: November 2005

AbstractSubungual exostosis is a benign bone‐ and cartilage‐producing tumor occurring in the hands and feet of children and young adults. The recent identification of a recurrent chromosomal translocation t(X;6)(q24‐q26;q15‐21) in short‐term‐cultured tumor cells strongly suggests that subungual exostosis is a neoplastic lesion caused by rearrangement of genes in the two breakpoints. To identify the genes that are critical for neoplastic transformation, we have studied five subungual exostoses by interphase or metaphase FISH. The results of these analyses demonstrated a clustering of the breakpoints to the regions harboring the collagen genes COL12A1 and COL4A5 in chromosome bands 6q13‐14 and Xq22, respectively. Furthermore, in all but one case, these two genes were shown to colocalize on the derivative chromosomes X and 6, strongly suggesting that at least one of them is consistently involved in the formation of a chimeric fusion gene or in the exchange of regulatory sequences. Because collagen molecules are important for tissue remodeling during physiologic growth and differentiation, both COL12A1 and COL4A5 constitute good candidate target genes in the pathogenesis of subungual exostosis. Further investigations on the transcript level are required to elucidate the functional outcome of the t(X;6) translocation in subungual exostoses. © 2005 Wiley‐Liss, Inc.
Total and specific fluid consumption as determinants of bladder cancer risk
Authors: Villanueva Cristina M. , Cantor Kenneth P. , King Will D. , Jaakkola Jouni J.K. , Cordier Sylvaine , Lynch Charles F. , Porru Stefano , Kogevinas Manolis 
Published: November 2005

AbstractWe pooled the data from 6 case‐control studies of bladder cancer with detailed information on fluid intake and water pollutants, particularly trihalomethanes (THM), and evaluated the bladder cancer risk associated with total and specific fluid consumption. The analysis included 2,729 cases and 5,150 controls. Odds ratios (OR) and 95% confidence intervals (CI) for fluid consumption were adjusted for age, gender, study, smoking status, occupation and education. Total fluid intake was associated with an increased risk of bladder cancer in men. The adjusted OR for 1 l/day increase in intake was 1.08, (95% CI 1.03–1.14, p‐value for linear trend <0.001), while no trend was observed in women (OR = 1.04, 0.94–1.15; p‐value = 0.7). OR was 1.33 (1.12–1.58) for men in the highest category of intake (>3.5 l/day) as compared to those in the lowest (≤2 l/day). An increased risk was associated with intake of tap water. OR for >2 l/day vs. ≤0.5 l/day was 1.46 (1.20–1.78), with a higher risk among men (OR = 1.50, 1.21–1.88). No increased risk was observed for the same intake groups of nontap water in men (OR = 0.97, 0.77–1.22) or in women (OR = 0.85, 0.50–1.42). Increased bladder cancer risks were observed for an intake of >5 cups of coffee daily vs. <5 and for THM exposure, but neither exposure confounded or modified the OR for tap water intake. The association of bladder cancer with tap water consumption, but not with nontap water fluids, suggests that carcinogenic chemicals in tap water may explain the increased risk. © 2005 Wiley‐Liss, Inc.
A prospective study of breast size and premenopausal breast cancer incidence
Authors: Kusano Aaron S. , Trichopoulos Dimitrios , Terry Kathryn L. , Chen Wendy Y. , Willett Walter C. , Michels Karin B. 
Published: November 2005

AbstractStudies of the association between breast size, as a proxy for mammary gland mass, and breast cancer risk have given equivocal results. Most have been case‐control studies with limited statistical power. We conducted a prospective analysis of the relation between breast size as measured by self‐reported bra cup size and breast cancer risk among premenopausal women enrolled in the Nurses' Health Study II. Bra cup size at age 20 was assessed among 89,268 premenopausal women aged 29–47 in 1993. Subsequent incident cases of invasive breast cancer were assessed until 2001. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated with a Cox proportional hazards model adjusting for potential confounders and risk factors for breast cancer. During 622,732 person‐years of follow‐up, 803 premenopausal women were newly diagnosed with invasive breast cancer. For women with a BMI below 25 kg/m2, those with a bra cup size of “D or larger” had a significantly higher incidence of breast cancer than women who reported “A or smaller” (covariate adjusted HR = 1.80; 95% CI 1.13–2.88; ptrend = 0.01). There was no significant association among women with a BMI of 25 kg/m2 or higher. Stratifying by BMI at age 18 at a cutoff point of 21 kg/m2 gave similar results. Larger bra cup size at a young age is associated with a higher incidence of premenopausal breast cancer, though this association is limited to leaner women. © 2005 Wiley‐Liss, Inc.
Retracted: Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells
Authors: Wang Zhiwei , Zhang Yuxiang , Banerjee Sanjeev , Li Yiwei , Sarkar Fazlul H. 
Published: November 2005

AbstractThis article has been retracted at the request of: Editor‐in‐Chief and Author‘Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells’, by Wang, Z., Zhang, Y., Banerjee, S., Li, Y. and Sarkar, F. H.The above article and associated erratum, published online on 11 November 2005 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. In addition to what was corrected in the erratum, a university investigation involving the first and the corresponding author determined that several figures in this paper 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.ReferenceWang, Z., Zhang, Y., Banerjee, S., Li, Y. and Sarkar, F. H. (2006), Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells. Int. J. Cancer, 118:1930–1936. doi:10.1002/ijc.21589; corrected by Erratum: Inhibition of nuclear factor κb activity by genistein is mediated via Notch‐1 signaling pathway in pancreatic cancer cells. Int. J. Cancer, 134: E3. doi: 10.1002/ijc.28709.
Inactivation of Id‐1 in prostate cancer cells: A potential therapeutic target in inducing chemosensitization to taxol through activation of JNK pathway
Authors: Zhang Xiaomeng , Ling Ming‐Tat , Wang Xianghong , Wong Y.C. 
Published: November 2005

AbstractResistance to anticancer drugs is the major problem in the treatment of many advanced cancers, including androgen‐independent prostate cancer. Recently, increased expression of Id‐1, a basic helix‐loop‐helix protein, is reported in several types of advanced cancer. It is suggested that high expression of Id‐1 may provide an advantage for cancer cell survival and inactivation of Id‐1 may be able to increase cancer cells' susceptibility to apoptosis. To test this hypothesis, in this study, by using RNA interfering technology, we inactivated the Id‐1 gene in 2 androgen‐independent prostate cancer cell lines, DU145 and PC3, and investigated whether downregulation of Id‐1 could lead to increased sensitivity to a commonly used anticancer drug, taxol. By using colony forming assay and MTT assay, we found that inactivation of Id‐1 resulted in both decreased colony forming ability and cell viability in prostate cancer cells, after taxol treatment. In addition, the si‐Id‐1‐induced sensitization to taxol was associated with activation of apoptosis pathway, which is demonstrated by increased apoptotic index, DNA laddering, sub‐G1 phase of the cell cycle, as well as cleaved‐PARP and Caspase 3. Furthermore, c‐Jun N‐terminal kinase (JNK), one of the common pathways responsible for taxol‐induced apoptosis, was also activated in the si‐Id‐1 transfected cells. Inhibition of JNK activity by a specific inhibitor, SP600125, blocked the si‐Id‐1‐induced sensitivity to taxol. These results indicate that increased Id‐1 expression in prostate cancer cells may play a protective role against apoptosis, and downregulation of Id‐1 may be a potential target to increase sensitivity of taxol‐induced apoptosis in prostate cancer cells. © 2005 Wiley‐Liss, Inc.
The leukocyte protein L‐plastin induces proliferation, invasion and loss of E‐cadherin expression in colon cancer cells
Authors: Foran Eilis , McWilliam Peter , Kelleher Dermot , Croke David T. , Long Aideen 
Published: November 2005

AbstractL‐plastin, a gene that codes for an actin‐bundling protein, is upregulated in the metastatic colon cancer cell line SW620, when compared to its premetastatic counterpart SW480. The aim of our study was to characterise the effect of L‐plastin overexpression on SW480 cells in the context of the acquisition of a metastatic phenotype. SW480 cell lines overexpressing L‐plastin were established (SW480‐LPL). Analysis of these cell lines revealed significantly higher rates of proliferation and invasion than the control cell line (SW480‐Ctrl). In addition, the expression of E‐cadherin was lost from SW480‐LPL cells. Treatment of SW480‐LPL cells with cytochalasin B, an inhibitor of endocytosis, attenuated the loss of E‐cadherin expression in these cells. The association of L‐plastin overexpression with an increased rate of proliferation and invasion, and loss of E‐cadherin expression in the SW480 colon cancer cell line indicates that L‐plastin plays an important mechanistic role in colorectal cancer metastasis (supplementary material for this article can be found on the International Journal of Cancer website at http://www.interscience.wiley.com/jpages/0020‐7136/suppmat/index.html). © 2005 Wiley‐Liss, Inc.
High frequency of latent membrane protein‐1 30‐bp deletion variant with specific single mutations in Epstein‐Barr virus‐associated nasopharyngeal carcinoma in Moroccan patients
Authors: Dardari Rkia , Khyatti Meriem , Cordeiro Paulo , Odda Mohieddine , ElGueddari Brahim , Hassar Mohammad , Menezes José 
Published: November 2005

AbstractLatent membrane protein 1 (LMP‐1) is an Epstein‐Barr virus‐encoded oncoprotein expressed in ∼50–70% of nasopharyngeal carcinoma (NPC). Previous studies have shown that NPC‐derived LMP‐1 variants carrying 30 bp deletion and specific mutations in the 3′C‐terminal region confer high oncogenic potential and a weak immunogenicity. Although numerous polymorphism studies of LMP‐1 have been carried out so far in the Asian population with NPC, very little is known in this regard on NPC patients from Northern Africa where there is a significantly high occurrence of this tumor. In our study, we examined the frequency of different LMP‐1 sequence variants derived from Moroccan NPC patients. As compared to healthy donors, NPC patients showed a high prevalence of the 30bp deletion variant of LMP‐1 (i.e. 84% vs. 36%; p < 0.0005). Moreover, the del‐LMP‐1 variant derived from NPC tumors shared identical amino acid substitutions at positions 322, 334, 338, 352 and 366 with the Mediterranean (Med) variant, whereas those derived from peripheral blood mononuclear cells (PBMC) had similar mutation pattern as China1 variant. Additional mutations within the 342–352 regions (identified in LMP‐1 variants without deletion derived from NPC tumors) were not found in healthy donors' PBMC. Our results support the assumption that the distribution of LMP‐1 variants in NPC tumors co‐segregate with geographic regions. Indeed, Med variant is found more frequently in tumors from NPC Moroccan patients, whereas China1 variant is more prevalent in tumors from NPC patients in endemic regions for NPC. © 2005 Wiley‐Liss, Inc.
Essential contribution of a chemokine, CCL3, and its receptor, CCR1, to hepatocellular carcinoma progression
Authors: Yang Xiaoqin , Lu Peirong , Fujii Chifumi , Nakamoto Yasunari , Gao Ji‐Liang , Kaneko Shuichi , Murphy Philip M. , Mukaida Naofumi 
Published: November 2005

AbstractWe previously observed that a chemokine, macrophage inflammatory protein‐1 α/CCL3, and its receptor, CCR1, were aberrantly expressed in human hepatocellular carcinoma (HCC) tissues. Here, we show that CCL3 and CCR1 are also expressed in 2 different models of this cancer; N‐nitrosodiethylamine (DEN)‐induced HCC and HCC induced by hepatitis B virus surface (HBs) antigen‐primed splenocyte transfer to myelo‐ablated syngeneic HBs antigen transgenic mice. At 10 months after DEN treatment, foci number and sizes were remarkably reduced in CCR1‐ and CCL3‐deficient mice, compared with those of wild‐type (WT) mice, although tumor incidence were marginally, but significantly, higher in CCR1‐ and CCL3‐deficient mice than in WT mice. Of note is that tumor angiogenesis was also markedly diminished in CCL3‐ and CCR1‐deficient mice, with a concomitant reduction in the number of intratumoral Kupffer cells, a rich source of growth factors and matrix metalloproteinases (MMPs). Among growth factors and MMPs that we examined, only MMP9 and MMP13 gene expression was augmented progressively in liver of WT mice after DEN treatment. Moreover, MMP9, but not MMP13, gene expression was attenuated in CCR1‐ and CCL3‐deficient mice, compared with that of WT mice. Furthermore, MMP9 was expressed mainly by mononuclear cells but not hepatoma cells, and MMP9‐expressing cell numbers were decreased in CCR1‐ or CCL3‐deficient mice, compared with WT mice. These observations suggest the contribution of the CCR1‐CCL3 axis to HCC progression. © 2005 Wiley‐Liss, Inc.
Interleukin‐10 expression significantly correlates with minor CD8+ T‐cell infiltration and high microvessel density in patients with gastric cancer
Authors: Sakamoto Teruhisa , Saito Hiroaki , Tatebe Shigeru , Tsujitani Shunichi , Ozaki Mitsuhiko , Ito Hisao , Ikeguchi Masahide 
Published: November 2005

AbstractWe aimed to investigate the relationships between interleukin‐10 (IL‐10) expression and both the clinicopathological findings and prognoses in patients with gastric cancer and to compare IL‐10 expression with microvessel (MV) density and CD8+ T lymphocyte infiltration to evaluate its effects on angiogenesis and immune responses in gastric cancer. IL‐10 expression was determined in gastric cancer patients by reverse transcription‐polymerase chain reaction (RT‐PCR) or immunohistochemical procedures. Two of 7 normal gastric tissues showed IL‐10 mRNA expression, while its expressions were confirmed in all advanced gastric carcinoma tissues examined (n = 11) by RT‐PCR. Immunohistochemical staining demonstrated that IL‐10 expression was detected in 52 (47.7%) of 109 cases. There was a close correlation between IL‐10 expression and MV density. IL‐10 expression inversely correlated with CD8+ T‐lymphocyte infiltration. The prognoses of patients whose tumors expressed IL‐10 were significantly worse than those of patients whose tumors did not express IL‐10. Multivariate analysis indicated IL‐10 expression was an independent prognostic factor. IL‐10 might be associated with tumor progression by stimulating angiogenesis and suppressing immune responses in gastric cancer. © 2005 Wiley‐Liss, Inc.
Oxidation and inactivation of low molecular weight protein tyrosine phosphatase by the anticancer drug Aplidin
Authors: Taddei Maria Letizia , Chiarugi Paola , Cuevas Carmen , Ramponi Giampietro , Raugei Giovanni 
Published: November 2005

AbstractThe marine plitidepsin Aplidin derived from the Mediterranean tunicate Aplidium albicans is a strong apoptotic inducer with promising antitumor activity. However, little is known about the mechanism of action of the molecule. In this article, we report that Aplidin is cytotoxic for NIH3T3 cells and that its action is exerted through the production of reactive oxygen species (ROS). Rotenone, but not other selective inhibitors of ROS production, blocks the induction of ROS, suggesting the involvement of the mitochondrial respiratory chain in Aplidin action. The intracellular rise of redox potential caused by Aplidin inactivates several molecular targets. Among these targets, we focused our attention on protein tyrosine phosphatases (PTPs). In agreement with the well‐characterized effect of ROS‐mediated PTP oxidation, due to the presence of a cysteine residue in their catalytic site, we found that Aplidin induces a strong decrease in PTP activity. In particular, since the expression of low molecular weight‐PTP (LMW‐PTP) is strongly associated with tumor onset and progression, we investigated the effect of Aplidin on this enzyme. Our data show that LMW‐PTP is oxidized and inactivated during Aplidin treatment, thus causing a hyper‐phosphorylation of its substrate β‐catenin. These findings demonstrate that, at least in part, the antitumoral activity of Aplidin could be due to the direct inhibition of LMW‐PTP and its related oncogenic potential. © 2005 Wiley‐Liss, Inc.
Osteoprotegerin (OPG)—a potential new role in the regulation of endothelialcell phenotype and tumour angiogenesis?
Authors: Cross Simon S. , Yang Zhiyong , Brown Nicola J. , Balasubramanian Sabapathy P. , Evans Clair A. , Woodward Julia K. , Neville‐Webbe Helen L. , Lippitt Jenny M. , Reed Malcolm W.R. , Coleman Robert E. , Holen Ingunn 
Published: November 2005

AbstractThe progression of cancer depends on the establishment of a tumour blood supply, and therefore tumour angiogenesis has been identified as a major target for new anticancer agents. Recent reports have suggested that osteoprotegerin (OPG) is involved in the control of endothelial cell survival through the inhibition of the activity of tumour necrosis factor‐ (TNF) related apoptosis‐inducing ligand (TRAIL). The role of OPG in human tumour development and angiogenesis is currently unknown. In the present study we demonstrate the ability of OPG to support endothelial cell survival, as well as the formation of cord‐like structures in vitro using a matrigel tubule formation assay. Investigation of various human cancers demonstrated endothelial OPG expression in 59% of malignant tumours (n = 512), but in contrast, OPG was absent in endothelial cells associated with benign tumours and normal tissues (n = 178). In a series of 400 breast tumours, endothelial OPG expression was associated with high tumour grade and certain histological types. Our data show a clear separation in endothelial OPG expression between malignant tumours and nonmalignant tissues, supporting a potential biological role for this molecule in the development and/or maintenance of the tumour vasculature. This is the first study to report the proangiogenic effects of OPG in vitro, as well as correlating expression of OPG by tumour endothelial cells with clinicopathological data in human tumours. © 2005 Wiley‐Liss, Inc.
Antioxidant inhibition of poly(carbonate urethane) in vivo biodegradation
Authors: Christenson Elizabeth M. , Anderson James M. , Hiltner Anne 
Published: November 2005

AbstractThis study compared the effect of an antioxidant on the in vivo biodegradation of a poly(carbonate urethane) (PCU) and a poly(ether urethane) (PEU). Unstrained PEU and PCU films with and without Santowhite® were implanted subcutaneously into 3‐month‐old Sprague‐Dawley rats for 3, 6, and 12 months. Characterization of unstabilized PEU and PCU with ATR‐FTIR and SEM showed soft‐segment and hard‐segment degradation consistent with previous studies. In particular, evidence of chain scission and crosslinking of the surface was present in the ATR‐FTIR spectra of explanted specimens. Addition of 2.2 wt % antioxidant inhibited the in vivo degradation of both PCU and PEU. Although the antioxidant probably improved polyurethane biostability by decreasing the susceptibility of the polymer to degradation, modulation of the cellular response to prevent the release of degradative agents was also possible. To differentiate the effects, the foreign‐body response was investigated with the use of a standard cage implant protocol. Polyurethane films were implanted in wire mesh cages subcutaneously in rats for 4, 7, and 21 days. There were no statistical differences among materials in the inflammatory exudate cell counts, adherent cell densities, or percent fusion of macrophages into foreign‐body giant cells (FBGCs). Therefore, it was concluded that the antioxidant inhibited degradation by capturing oxygen radicals that would otherwise cause polyurethane chain scission and crosslinking. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res, 2006