bluuebunny/crossref_metadata_2025_split huggingface dataset:
Case‐control study of anthropometric measures and breast cancer risk
Authors: Friedenreich Christine M. , Courneya Kerry S. , Bryant Heather E. 
Published: August 2002

AbstractA population‐based case‐control study of 1,233 incident breast cancer cases and 1,241 controls was conducted in Alberta between 1995 and 1997 to examine the influence of anthropometric factors on the risk of breast cancer using several newly derived variables. Data on current height, weight and waist and hip circumference were collected by interviewers using standardized methods. Respondents recalled their body weight at each decade from age 20 to the referent year. Several variables were estimated, and unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). No statistically significant associations for any of the estimated variables with breast cancer risk for premenopausal women (462 cases, 475 controls) were found. The results for postmenopausal women (771 cases, 762 controls) in the highest vs. lowest quartiles were, for waist circumference, OR = 1.30 (95% CI 0.97–1.73); waist–hip ratio, OR = 1.43 (95% CI 1.07–1.93); weight gain since age 20, OR = 1.35 (05% CI 1.01–1.81); difference between maximum and minimum weights over adult lifetime, OR = 1.56 (95% CI 1.16–2.08); and the reference weight minus the minimum weight since age 20, OR = 1.47 (95% CI 1.10–1.97). Statistically significant trends in risk were observed for these variables. Effect modification with hormone replacement therapy use was found for most variables assessed for postmenopausal women, with much stronger associations found among never‐users compared to ever‐users. We found strong evidence that waist–hip ratio and weight gained over lifetime, as assessed by different variables, are postmenopausal breast cancer risk factors. These effects were independent of dietary intake and lifetime total physical activity. © 2002 Wiley‐Liss, Inc.
Common and differential chemokine expression patterns in rs cells of NLP, EBV positive and negative classical hodgkin lymphomas
Authors: Maggio Ewerton M. , Van den Berg Anke , Visser Lydia , Diepstra Arjan , Kluiver Joust , Emmens Roelke , Poppema Sibrand 
Published: August 2002

AbstractHodgkin lymphoma (HL) is characterized by a minority of neoplastic cells, the so‐called Reed‐Sternberg (RS) cells and a vast majority of reactive cells. RS cells produce chemokines that can attract subsets of peripheral blood cells into HL tissues. To gain insight in the chemokines involved in HL, 16 chemokines were selected based on their ability to recruit different subsets of cells. Five HL, 5 non‐HL‐derived cell lines, 22 HL, 5 non‐HL and 3 control tissues were analyzed by reverse transcriptase‐polymerase chain reaction (RT‐PCR). Products for 13 of these 16 chemokines were detected in 1 or more of the cell lines tested. No or only very faint signals were obtained in HL for CXCL12, CCL7 and CCL8, but CXCL10, CCL5, CCL13, CCL17 and CCL22 were highly or differentially expressed in HL cell lines and tissues. Immunohistochemistry was performed with antibodies reactive with the latter 5 chemokines on paraffin sections of 21 cases of HL. CCL17 and CCL22 had the highest signals in RS cells at gene expression and at protein levels. CCL17 was specific for the classic HL subtypes, whereas CCL22 also had low signals in NLP samples, as well as in some non‐HL. CXCL10 was expressed in a large proportion of HL cases with a predominant expression in EBV‐positive cases. The results indicate that RS cells produce a complex pattern of chemokines that are involved in the recruitment of reactive cells and contribute to the paradox of an extensive but ineffective host immune response. © 2002 Wiley‐Liss, Inc.
Radiation‐induced leukemia risk among those aged 0–20 at the time of the Chernobyl accident: A case‐control study in the Ukraine
Authors: Noshchenko Andriy G. , Zamostyan Pavlo V. , Bondar Oleksandra Yu. , Drozdova Vira D. 
Published: August 2002

AbstractA case‐control study was conducted to estimate the radiation‐induced acute leukemia risk for the period 1987–1997 among residents aged 0–20 at the time of the Chernobyl accident in the most radioactively contaminated territories of the Ukraine (Rivno and Zhytomir regions). Data were collected on 272 leukemia cases diagnosed between 1 January 1987 and 31 December 1997. Of these, 98 cases were verified and interviewed. Verified cases were compared to 151 randomly selected controls matched by age, gender and type of settlement. The mean value of the estimated accumulated equivalent dose to the bone marrow was 4.5 mSv, and the maximum value was 101 mSv. A statistically significant increased risk of leukemia was found among males whose estimated radiation exposure was higher than 10 mSv. This association was statistically significant for acute leukemia cases that occurred in the period 1993–1997, particularly for acute lymphoblastic leukemia. A similar association was found for acute myeloid leukemia, diagnosed in the period 1987–1992. © 2002 Wiley‐Liss, Inc.
Epidermal growth factor receptor mutation type iii transfected into a small cell lung cancer cell line is predominantly localized at the cell surface and enhances the malignant phenotype
Authors: Damstrup Lars , Wandahl Pedersen Mikkel , Bastholm Lone , Elling Folmer , Skovgaard Poulsen Hans 
Published: August 2002

AbstractIn the present study we transfected the epidermal growth factor receptor (EGFR)‐negative small cell lung cancer cell line, GLC3, with the type III EGFR mutation (EGFRvIII). The EGFRvIII protein could be detected by Western blot analysis as a 145‐kDa protein, which by immunohistochemistry appeared to be localized at the cell surface. Ultrastructurally EGFRvIII was expressed mainly at the cell surface with clusters at cell–cell contacts. In the in vitro invasion assay, GLC3‐EGFRvIII cells had a ≈5‐fold increased invasion compared with uninduced GLC3‐EGFRvIII, GLC3‐Tet‐On and the parental cell line. GLC3‐Tet‐On appeared uniform in size with adherence junctions at cell–cell contacts. In uninduced GLC3‐EGFRvIII cells adherence junctions were also present but less distinct. In doxycycline‐pretreated GLC3‐EGFRvIII cells, adherence junctions were absent. We conclude that the expression of EGFRvIII results in a more malignant phenotype. This effect appears to involve the disruption of adherence junctions. © 2002 Wiley‐Liss, Inc.
Induction of immune tolerance toward tumor‐associated‐antigens enables growth of human hepatoma in mice
Authors: Gotsman Israel , Israeli David , Alper Ruslana , Rabbani Elazar , Engelhardt Dean , Ilan Yaron 
Published: August 2002

AbstractAdoptive transfer of immunity against hepatitis B surface antigen (HBsAg) was previously shown to facilitate suppression of experimental human hepatocellular carcinoma (HCC) expressing HBsAg in athymic mice. We have shown that oral tolerance induces antigen‐specific immune suppression of HBsAg by feeding hepatitis B virus (HBV) antigens. In the present study we evaluated the effect of oral tolerance induction toward HBV or HCC antigens on the growth of experimental HCC‐expressing HBsAg in mice. Tolerance induction was induced in mice by 5 oral feedings of 1 μg HBV antigens or HCC‐extracted proteins (50 μg protein) before vaccination with recombinant HBsAg. Splenocytes (2 × 106) from these mice were transferred to sublethally irradiated athymic BALB/c mice previously transplanted subcutaneously with 107 human hepatoma Hep3B cells. Adoptive transfer of splenocytes immunized toward HBsAg prevented tumor growth. At 4 weeks after splenocyte transplantation, tumor volume and serum alpha‐fetoprotein (AFP) levels in athymic mice transplanted with splenocytes immunized to HBsAg were undetectable as compared with 1,048 ± 738 mm3 and 2,500 ± 1,431 ng/ml in recipients of naïve splenocytes (p < 0.0001). Mice receiving splenocytes tolerized toward Hep3B cells, as manifested by reduced serum HBs antibody levels, reduced HBV‐specific stimulation index and reduced HBV‐specific‐IFNγ spot‐forming cells, had early tumor growth evident by elevated AFP serum levels, weight loss and mortality, which were suppressed at 6 weeks. Mice transplanted with splenocytes tolerized toward HBV antigens did not have direct evidence of tumor growth. Induction of oral tolerance toward HCC‐extracted proteins enabled transient tumor growth in this model. This effect was mediated through downregulation of the anti‐HBV immune response. © 2002 Wiley‐Liss, Inc.
A very early induction of major vault protein accompanied by increased drug resistance in U‐937 cells
Authors: Hu Yi , Stephen Andrew G. , Cao Jin , Tanzer Lee R. , Slapak Christopher A. , Harrison Steadman D. , Devanarayan Viswanath , Dantzig Anne H. , Starling James J. , Rome Leonard H. , Moore Robert E. 
Published: August 2002

AbstractU‐937 human leukemia cells were selected for resistance to doxorubicin in the presence or absence of a specific drug modulator that inhibits the activity of P‐glycoprotein (Pgp), encoded by the multidrug‐resistance gene (MDR1). Parental cells expressed low basal levels of the multidrug‐resistance‐associated gene (MRP1) and major vault protein (MVP) mRNAs and no MDR1 mRNA. Two doxorubicin‐resistant cell lines were selected. Both drug‐resistant cell lines upregulated the MVP mRNA level 1.5‐fold within 1 cell passage. The MVP mRNA level continued to increase over time as the doxorubicin selection pressure was increased. MVP protein levels generally paralleled the mRNA levels. The 2 high molecular weight vault protein mRNAs were always expressed at constitutive levels. Fully formed vault particles consisting of the MVP, the 2 high molecular weight proteins and the vault RNA assembled and accumulated to increased levels in drug‐selected cells. MVP induction is therefore the rate‐limiting step for vault particle formation in U‐937 cells. By passage 25 and thereafter, the selected cells were resistant to doxorubicin, etoposide, mitoxantrone and 5‐fluorouracil by a pathway that was independent of MDR1, MRP1, MRP2 and breast cancer resistance protein. In summary, U‐937 doxorubicin‐selected cells are programmed to rapidly upregulate MVP mRNA levels, to accumulate vault particles and to become multidrug resistant. © 2002 Wiley‐Liss, Inc.
CD151 enhances cell motility and metastasis of cancer cells in the presence of focal adhesion kinase
Authors: Kohno Masashi , Hasegawa Hitoshi , Miyake Masayuki , Yamamoto Tadashi , Fujita Shigeru 
Published: August 2002

AbstractWe have examined the role of the protein CD151 in cell motility, invasion and metastasis of cancer cells by using CD151‐overexpressing cells prepared by transfection of CD151 cDNA into three cancer cell lines established from different origins; a human colon cancer RPMI4788, a human glioblastoma A172 and a human fibrosarcoma HT1080. Invasion into Matrigel and cell motility of all 3 CD151‐overexpressing cancer cells were enhanced significantly when compared to control parental cells. Pulmonary metastasis of 2 metastatic CD151‐overexpressing cancer cell lines, RPMI4788/CD151 and HT1080/CD151, was higher than that of control parental cells and was markedly inhibited by anti‐CD151 monoclonal antibody (MAb), SFA1.2B4. To examine whether focal adhesion kinase (FAK) is associated with promotion of cell motility and invasion of cancer cells through CD151, we transfected human CD151 cDNA into FAK (+/+) or FAK (−/−) fibroblasts that were isolated from embryos in FAK‐deficient mice and compared invasion into Matrigel and cell motility between each CD151‐transfected cells and controls. The invasion into Matrigel and cell motility of CD151‐transfected FAK (+/+) fibroblasts increased significantly above those of parental cells and were inhibited by anti‐CD151 MAb, whereas those of CD151‐transfected FAK (−/−) fibroblasts were not enhanced at all and were not blocked by anti‐CD151 MAb. These findings indicate that the CD151 molecule enhances cell motility, invasion and metastasis of cancer cells and that FAK is needed for these events through CD151. © 2001 Wiley‐Liss, Inc.
Human chondrosarcoma secretes vascular endothelial growth factor to induce tumor angiogenesis and stores basic fibroblast growth factor for regulation of its own growth
Authors: Furumatsu Takayuki , Nishida Keiichiro , Kawai Akira , Namba Masayoshi , Inoue Hajime , Ninomiya Yoshifumi 
Published: August 2002

AbstractVascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) are well‐known factors that induce neovascularization in many tumors. The molecular mechanisms that regulate tumor angiogenesis in human chondrosarcoma are not clear. We assessed in this work the angiogenic activities of a human chondrosarcoma cell line (OUMS‐27) in vivo and determined the efficacies of angiogenic factors derived from OUMS‐27 cells on human umbilical vein endothelial cells (HUVECs) in vitro. Tumor xenografts induced an increase in the formation of neovessels, but the distributions of Ki‐67 antigen, VEGF and bFGF were unaffected. We also demonstrated that OUMS‐27 cells secreted VEGF165 into the culture medium and that it was the maximal angiogenic factor to stimulate endothelial proliferation and migration in chondrosarcoma. Anti‐VEGF antibodies induced an approximately 70% inhibition of these responses of HUVECs, but did not have any effect on OUMS‐27 cells. Anti‐bFGF antibodies suppressed not only the activities of HUVECs but also the growth of tumor cells in vitro. We indicate that angiogenesis is principally elicited by VEGF165 and that tumorigenesis is mainly regulated by bFGF stored in the extracellular matrix of OUMS‐27 cells. The present study may offer the availability of combination therapies for inhibition of VEGF and bFGF action on vascular endothelial cells and chondrosarcoma cells, respectively. © 2001 Wiley‐Liss, Inc.
Inverse scattering of a buried imperfect conductor by the genetic algorithm
Authors: Chiu Chien‐Ching , Chen Wei‐Ting 
Published: August 2002

AbstractInverse scattering of an imperfectly conducting cylinder buried in a half‐space is presented. A conducting cylinder of unknown shape and conductivity is buried in one half‐space and scatters the incident field from another half‐space. Based on the measured scattered field and the boundary condition, a set of nonlinear integral equations is derived and the inverse problem is reformulated into an optimization problem. The genetic algorithm is then employed to find the global extreme solution of the object function. As a result, the shape and the conductivity of the scatterer can be reconstructed. Even when the initial guess is far away from the exact one, the genetic algorithm can avoid the local extreme and converge to a global extreme solution. In such a case, the gradient‐based method often gets stuck in a local extreme. Numerical results are given to show the effectiveness of the genetic algorithm. Multiple incident directions permit good reconstruction of shape and, to a lesser extent, conductivity in the presence of noise in measured data. © 2001 John Wiley & Sons, Inc. Int J Imaging Syst Technol 11, 355–360, 2000
Transverse process fusion with bovine anorganic bone
Authors: Frank Edmund H. , Gong Xi , Sipe Richard V. , Buck Dave C. , Hollinger Jeffrey O. 
Published: August 2002

AbstractA biodegradable collagen membrane and bovine anorganic bone were studied in a rabbit spine fusion model. The bovine, anorganic bone is a nonantigenic, acellular clinical product used as a bone substitute for dento‐alveolar applications. We reasoned this product with a collagen membrane could be useful for spine fusions. Our hypothesis was that bovine, anorganic bone, and a collagen membrane would promote spine fusion equivalent to an autogenous bone graft. To test the hypothesis, the transverse processes of the fourth and fifth lumbar vertebrae were decorticated in 30 rabbits divided equally among five groups. In one group, following decortication, no treatment was administered, whereas in the remaining four groups, treatments consisted of either autograft, collagen membrane, anorganic bone, or anorganic bone plus collagen membrane. Rabbits were euthanized 6 weeks after surgery, and the lumbar vertebrae were removed, radiographed, and processed for histology. The radiographs and histological sections were subjected to quantitative morphometric analyses and post hoc statistical testing (p ≤ 0.05). We determined anorganic bone without a collagen membrane migrated into the soft tissues contiguous to the transverse processes. However, with a collagen membrane, the anorganic bone remained at the implant site, causing an osseous fusion of the transverse processes. Although the autograft promoted the greatest amount of new bone formation, significant transverse process fusion was accomplished with the anorganic bone and collagen membrane. Additional longer term studies are contemplated to validate feasibility of this clinical option, including a biomechanical component. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 60: 118–125, 2002
The subpopulation of CF‐1 mice deficient in P‐glycoprotein contains a murine retroviral insertion in the mdr1a gene
Authors: Pippert Todd R. , Umbenhauer Diane R. 
Published: August 2002

AbstractA subpopulation of the CF‐1 mouse strain is sensitive to neurotoxicity following exposure to avermectins, a family of structurally related antiparasitic agents. This unusual sensitivity is the result of a deficiency in the mdr1a P‐glycoprotein that normally contributes to a functional blood‐brain barrier. Previous studies demonstrated a correlation between P‐glycoprotein levels in the brain, intestine, testis, and placenta with an restriction fragment length polymorphism (RFLP) pattern from DNA isolated from the animals. We have demonstrated that only P‐glycoprotein derived from the mdr1a gene is deficient in these mice. In this article, we describe the genetic defect in the subpopulation of CF‐1 mice resulting in an absence of P‐glycoprotein. The data presented describes a reverse transcription–polymerase chain reaction (RT‐PCR) protocol that specifically amplifies mdr1a mRNA from tissue and confirms that the P‐glycoprotein defect results from a truncated mRNA with a deleted exon 23. Genomic amplification and sequencing of the intron between exon 22 and 23 in Pgp‐deficient animals reveals an insertion of approximately 8.35 kb of DNA at the exon 23 intron–exon junction corresponding to a murine leukemia virus. This insertion results in the aberrant splicing of the mRNA and the loss of exon 23 during RNA processing. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:83–89, 2001
Serum hyperviscosity syndrome responding to therapeutic plasmapheresis in a patient with primary Sjögren's syndrome
Authors: Simón J. Abraham , Lazo‐Langner Alejandro , Duarte‐Rojo Andrés , Velázquez‐González Antonio , Sánchez‐Guerrero Sergio A. , Sánchez‐Guerrero Jorge 
Published: August 2002

AbstractHyperviscosity syndrome is a disorder first described in patients with Waldenström's macroglobulinemia and is not commonly seen in rheumatic diseases. Its association with Sjögren's syndrome is very rare and it has been reported in very few patients. We report the case of a patient with primary Sjögren's syndrome presenting as hyperviscosity syndrome who was successfully treated with therapeutic plasma exchange. J. Clin. Apheresis 17:44–46, 2002.
Mechanical regulation of IGF‐I and IGF‐binding protein gene transcription in bladder smooth muscle cells
Authors: Chaqour Brahim , Han Ji‐Soo , Tamura Isao , Macarak Edward 
Published: August 2002

AbstractMechanical forces are well known to modulate smooth muscle cell growth and synthetic phenotype. The signals controlling this process are complex and potentially involve changes in the expression of peptide growth factor genes such as those of the insulin‐like growth factor (IGF) system. This study was designed to investigate the mechanical regulation of IGF‐I and the binding proteins for IGF (IGFBPs) in smooth muscle cells cultured on a deformable surface and subjected to cyclic stretch. Using the RNase protection assay, we found that the application of a cyclic biaxial strain to cells induced a 2.5‐ to 4‐fold increase in IGF‐I mRNA levels after 8 h and an even greater increase after 16–24 h of stretch. This change was not affected by variations in the magnitude of the applied strain but was attenuated (∼40%) when cells were treated with antagonists for angiotensin II receptors. Furthermore, the transcript levels of the three major IGF binding proteins produced in smooth muscle cells, e.g., IGFBP‐2, IGFBP‐4, and IGFBP‐5, varied between stretched and control cells. Both IGFBP‐2 and IGFBP‐4 mRNA levels were consistently reduced in stretched cells but remained comparable to those of the control cells when the angiotensin II transducing pathway was blocked by inhibitors prior to the application of mechanical strain. Conversely, the gene expression of IGFBP‐5 was upregulated in stretched cells, and neutralizing antibodies to IGF‐I blocked this activation. Similarly, pharmacologic inhibition of the phosphatidylinositol 3‐kinase, an important component of the IGF receptor transduction pathway, inhibited IGFBP‐5 gene expression in stretched cells. These results suggest that the downstream effects of mechanical strain on IGF‐I and IGFBP transcript levels are mediated, to greater or lesser extent, either through an angiotensin II tranducing pathway or via a feedback loop involving the autocrine secretion of IGF‐I itself. J. Cell. Biochem. 84: 264–277, 2002. © 2001 Wiley‐Liss, Inc.
Genomic cloning and promoter analysis of the GAHSP40 gene
Authors: Hamajima Fumiyasu , Hasegawa Tadao , Nakashima Izumi , Isobe Ken‐ichi 
Published: August 2002

AbstractThe new heat shock protein (GAHSP40), which binds to Gadd34, is a member of the Hsp40 family gene and has a J domain, which is similar to bacterial DNAJ. We have isolated and sequenced the mouse GAHSP40 gene including 1.6 kb of the 5′‐flanking region. Primer extension analysis revealed that the transcription initiation site was located 36‐bp upstream of the ATG translation initiation codon. In order to identify the heat‐responsive regions in the GAHSP40, NIH3T3 cells were transiently transfected with a series of 5′ terminus‐truncated mutants of the GAHSP40 promoter linked to the luciferase reporter gene. We found that the region of −284 to −184 bp from initiation start site responded to heat shock treatment. By the gel shift analysis, we found the heat shock elements (HSEs) located in this region from −257 to −225. This HSEs has five 5 bp motifs. The transfection studies using HSEs mutant vectors revealed that those 3′ two 5 bp motifs are essential for heat responsive transcription. J. Cell. Biochem. 84: 401–407, 2002. © 2001 Wiley‐Liss, Inc.