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Träfflista för sökning "hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Cancer och onkologi) srt2:(2000-2004);srt2:(2002)"

Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Cancer och onkologi) > (2000-2004) > (2002)

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  • Brakebusch, Cord, et al. (författare)
  • Integrins in invasive growth.
  • 2002
  • Ingår i: Journal of Clinical Investigation. - Am Soc Clin Investig. - 0021-9738. ; 109:8, s. 999-1006
  • Tidskriftsartikel (refereegranskat)
  • Brandau, Oliver, et al. (författare)
  • Chondromodulin I Is Dispensable during Enchondral Ossification and Eye Development.
  • 2002
  • Ingår i: Molecular and Cellular Biology. - American Society for Microbiology. - 0270-7306. ; 22:18, s. 6627-6635
  • Tidskriftsartikel (refereegranskat)abstract
    • Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during enchondral ossification. In vitro and in vivo assays with the purified protein have shown chondrocyte-modulating and angiogenesis-inhibiting functions. To investigate chm-I function in vivo, we generated transgenic mice lacking chm-I mRNA and protein. Null mice are viable and fertile and show no morphological changes. No abnormalities in vascular invasion and cartilage development were detectable. No evidence was found for a compensating function of tendin, a recently published homologue highly expressed in tendons and also, at low levels, in cartilage. Furthermore, no differences in the expression of other angiogenic or antiangiogenic factors such as transforming growth factor beta1 (TGF-beta1), TGF-beta2, TGF-beta3, fibroblast growth factor 2, and vascular endothelial growth factor were found. The surprising lack of phenotype in the chm-I-deficient mice suggests either a different function for chm-I in vivo than has been proposed or compensatory changes in uninvestigated angiogenic or angiogenesis-inhibiting factors. Further analysis using double-knockout technology will be necessary to analyze the function of chm-I in the complex process of enchondral ossification.
  • Braun, Attila, et al. (författare)
  • Genomic organization of profilin-III and evidence for a transcript expressed exclusively in testis.
  • 2002
  • Ingår i: Gene. - Elsevier. - 1879-0038. ; 283:1-2, s. 219-225
  • Tidskriftsartikel (refereegranskat)abstract
    • Profilins are small, widely expressed actin binding proteins, thought to be key regulators of actin dynamics in living cells. So far, three profilin-genes have been described: profilin-I (PFN1), profilin-II (PFN2) with two splice variants and the recently identified profilin-III (PFN3). Here we describe the genomic organization of the genes encoding human and mouse profilin-III. Both are single exon genes and lie in close vicinity to the renal sodium-phosphate transport gene 2 (SLC34A1, NPT2) which is highly expressed in kidney. Northern hybridization to rat tissues has previously demonstrated expression of an approximately 4.5 kb long profilin-III mRNA transcript in kidney and a mRNA transcript of approximately 1 kb in length in testis. Here we show that mouse profilin-III expression is restricted to testis and that the 4.2 kb profilin-III mRNA in kidney is the result of a slc34a1 transcript which includes the antisense profilin-III open reading frame in its 3prime prime or minute-untranslated region. Finally, we demonstrate by in situ hybridization that profilin-III mRNA is localized to cells in the late stage of spermatogenesis.
  • Broberg Palmgren, Karin, et al. (författare)
  • Fusion of RDC1 with HMGA2 in lipomas as the result of chromosome aberrations involving 2q35-37 and 12q13-15.
  • 2002
  • Ingår i: International Journal of Oncology. - D.A. Spandidos. - 1019-6439. ; 21:2, s. 321-326
  • Tidskriftsartikel (refereegranskat)abstract
    • Rearrangements of chromosome bands 12q13-15 are frequent in various benign mesenchymal and epithelial tumors, and the gene HMGA2 seems to be the most common target within this chromosome region. In the majority of cases, the rearrangements result in a fusion of the first three exons of HMGA2 with different translocation partners. Despite the large number of HMGA2 mutations that have been reported, very little is known about the fusion partners. In this study, we have characterized a recurrent fusion of the first three exons of HMGA2 5' to the G protein-coupled receptor gene (RDC1) in lipomas with rearrangements involving chromosome bands 2q35-37 and 12q13-15, one of several recurrent chromosomal rearrangements in lipomas. The functional impact of the fusion is truncation of HMGA2, because the RDC1 part contributes with a stop codon one amino acid downstream of the breakpoint. The breakpoint within RDC1 was localized in a previously uncharacterized exon of the gene, and our data suggest that RDC1 is subject to alternative splicing.
  • Brodin, Greger, 1968- (författare)
  • Smad7 in TGF-β Signalling
  • 2002
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • <p>Members of the transforming growth factor-β (TGF-β) superfamily of growth and differentiation factors regulate a vast array of biological functions in the adult, and are of great importance in governing cell fate determination and patterning in the developing embryo. The TGF-β signal is propagated intracellularly by Smad proteins resulting in transcriptional responses. Smad6 and Smad7 are inhibitory Smads known to downregulate the TGF-β signal and thereby possibly modulating the biological response. This thesis describes a functional analysis of the inhibitory Smad7 from an <i>in vitro </i>and <i>in vivo </i>perspective<i>.</i></p><p>The prostate gland is dependent on androgens for its growth and differentiation. Androgen withdrawal can cause regression and apoptosis in normal and malignant prostate. Previous studies suggest a role for TGF-β in the apoptotic mechanism. We investigated the expression levels of Smad proteins in the rat ventral prostate as well as in an androgen sensitive prostate tumor model (Dunning R3327 PAP) by immunohistochemistry. We observed an increased immunoreactivity for Smad3, Smad4 and phosphorylated Smad2 in the rat ventral prostate epithelial cells after castration, as well as in the prostate tumor cells. Expression of inhibitory Smad6 and Smad7 were also increased in both normal and malignant prostate in response to castration. </p><p>Several studies have shown that Smad7 is upregulated in response to TGF-β stimuli, suggesting a role in a negative feedback loop attenuating the TGF-β response. We investigated the molecular mechanism behind that response by studying the transcriptional regulation of the Smad7 gene. We identified a palindromic Smad binding element (SBE) in the promoter. Point mutations introduced into the SBE abolished transcriptional activation via TGF-β. We also observed that mutating or deleting binding motifs for Sp1 and AP-1, led to an attenuation of the TGF-β mediated transcriptional induction as well as the basal promoter activity.</p><p>Gene ablation of Smad proteins has revealed specific physiological and developmental roles. We analysed mice targeted on the Smad7 locus. The mice appeared viable and fertile with a slight reduction in litter size, suggesting a perinatal loss. Biochemical analysis of mouse embryonic fibroblasts (MEFs) showed no major difference between wild type and mutant MEFs. </p>
  • Capocaccia, R, et al. (författare)
  • Measuring cancer prevalence in Europe: the EUROPREVAL project
  • 2002
  • Ingår i: Annals of Oncology. - Oxford University Press. - 1569-8041. ; 13:6, s. 831-839
  • Tidskriftsartikel (refereegranskat)abstract
    • Cancer prevalence is the proportion of individuals in a population who at some stage during their lifetime have been diagnosed with cancer, irrespective of the date of diagnosis. Cancer prevalence statistics have generally been provided by a limited number of well established cancer registries that have been in existence for several decades. The advent of systematic follow-up of life status of incident cases and the availability of new statistical methodologies, now makes it possible for registries established during the 1970s or 1980s to provide prevalence data. The main problems encountered in the estimation of prevalence are the inclusion of: (i) cases lost to follow-up; (ii) cases known only from their death certificate; (iii) cases diagnosed before the start of registration; and (iv) the treatment of multiple tumours and migrations. The main aim of this paper was to review these problems and discuss, through the experience gained with EUROPREVAL, how they can be overcome. A method is presented for the calculation of prevalence of all cancers combined in the populations covered by the 45 cancer registries participating in EUROPREVAL. Prevalence of cancer is estimated to be 2% on average, with the highest values (3%) in Sweden and the lowest in Eastern Europe, with a minimum of approximately 1% in Poland.
  • Carlsson, J, et al. (författare)
  • Therapy with radiopharmaceuticals
  • 2002
  • Ingår i: Acta Oncologica. - Taylor & Francis. - 1651-226X. ; 41:7-8, s. 623-628
  • Tidskriftsartikel (refereegranskat)abstract
    • In an investigation by the Swedish Cancer Society, an expert group described the present status, critical issues and future aspects and potentials for each of nine major areas of radiation therapy research. The present report deals with therapy with radiopharmaceuticals.
  • Crnalic, S, et al. (författare)
  • Establishment and characterisation of a human clear cell sarcoma model in nude mice
  • 2002
  • Ingår i: International Journal of Cancer. - John Wiley and Sons Inc.. - 0020-7136. ; 101:6, s. 505-511
  • Tidskriftsartikel (refereegranskat)abstract
    • We have established a new experimental model of human clear cell sarcoma, UM-CCSI, using serial subcutaneous transplantation of intact tumour tissue in nude mice. The heterotransplanted nude mouse tumours retained characteristic morphological features of the primary clear cell sarcoma. Immunohistochemical analysis showed the retained expression patterns of S-100 protein, melanoma-associated antigen HMB-45 and vimentin in the xenografts as compared to the primary tumour. DNA index showed low variations both between the xenografts in the same passage and between the serial passages. Cytogenetic analysis of the primary tumour and the xenografts showed the unbalanced translocation der(6)t(6; I 2)(p23;q13). Based on the combined genetic data a reasonable interpretation of our findings is that there was a complex chromosomal rearrangement resulting in a cytogenetically cryptic EWS-ATFI fusion gene. Analysis of cell kinetics using in vivo incorporation of iododeoxyuridine and flow cytometry showed generally short potential doubling time (T-pot) of the xenografts. Volume doubling time showed low variations without correlation with T-pot. The retained phenotypic and genotypic characteristics of the primary tumour and the morphological and structural stability over time makes the model suitable for studies on the tumour biology and treatment of clear cell sarcoma. (C) 2002 Wiley-Liss, Inc.
  • Danen, EHJ, et al. (författare)
  • The fibronectin-binding integrins alpha 5 beta 1 and alpha v beta 3 differentially modulate RhoA-GTP loading, organization of cell matrix adhesions, and fibronectin fibrillogenesis
  • 2002
  • Ingår i: Journal of Cell Biology. - Rockefeller University Press. - 0021-9525. ; 159:6, s. 1071-1086
  • Tidskriftsartikel (refereegranskat)abstract
    • We have studied the formation of different types of cell matrix adhesions in cells that bind to fibronectin via either alpha5beta1 or alphavbeta3. In both cases, cell adhesion to fibronectin leads to a rapid decrease in RhoA activity. However, alpha5beta1 but not alphavbeta3 supports high levels of RhoA activity at later stages of cell spreading, which are associated with a translocation of focal contacts to peripheral cell protrusions, recruitment of tensin into fibrillar adhesions, and fibronectin fibrillogenesis. Expression of an activated mutant of RhoA stimulates alphavbeta3-mediated fibrillogenesis. Despite the fact that alpha5beta1-mediated adhesion to the central cell-binding domain of fibronectin supports activation of RhoA, other regions of fibronectin are required for the development of alpha5beta1-mediated but not alphavbeta3-mediatecl focal contacts. Using chimeras of beta1 and beta3 subunits, we find that the extracellular domain of beta1 controls RhoA activity. By expressing both beta1 and beta3 at high levels, we show that beta1-mediated control of the levels of beta3 is important for the distribution of focal contacts. Our findings demonstrate that the pattern of fibronectin receptors expressed on a cell dictates the ability of fibronectin to stimulate RhoA-mediated organization of cell matrix adhesions.
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