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  • 1
    Electronic Resource
    Electronic Resource
    On telomere shortening in soft-tissue tumors (1998)
    Springer
    Journal of cancer research and clinical oncology 124 (1998), S. 165-171 
    Details
    ISSN: 1432-1335
    Keywords: Key words Telomeres ; Soft-tissue tumors ; Telomerase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: Specific simple DNA repeats occur at the telomeric ends of mammalian chromosomes. Loss of (G+C)-rich repeats can result in genetic instability, associated with tumorigenesis. So far, data on telomere shortening have not been available for different types of soft-tissue tumors. Methods: Using tumor material and the blood of the corresponding patient, high-molecular-mass DNA was prepared by digestion with proteinase K and extraction with phenol/chloroform. A 10-μg sample of DNA was digested with the restriction enzyme HinfI. DNA fragments were separated in a 0.7% agarose gel, and in-gel hybridization was performed with the telomere-specific repeat probe (TTAGGG)3. Results: Shortening of the telomere repeat was observed in 14/30 soft-tissue tumors; 5 tumors showed elongated telomere repeats, whereas the telomeres appeared unchanged in 11 tumors. Decreased telomere repeat length correlated with advanced age, DNA ploidy, and a higher proliferation index. There was no association between telomere repeat length and tumor grade. Interestingly, in contrast to other entities, all malignant schwannomas and leiomyosarcomas showed significantly reduced telomere lengths. An explanation for the telomere heterogeneity in liposarcomas may include differential telomerase reactivation in well and poorly differentiated tumors. Conclusions: Telomere shortening is frequent but not a uniform phenomenon in different types of soft-tissue tumor. Studies on telomerase activity should be performed in the same cohort of sarcomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050150
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  • 2
    Electronic Resource
    Electronic Resource
    p53 gene mutations in soft-tissue sarcomas-correlations with p53 immunohistochemistry and DNA ploidy (1997)
    Springer
    Journal of cancer research and clinical oncology 123 (1997), S. 211-218 
    Details
    ISSN: 1432-1335
    Keywords: Soft-tissue tumors ; p53 gene mutation ; p53 immunohistochemistry ; PCR SSCP analysis ; DNA ploidy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The significance ofp53 mutations in a group of 67 soft-tissue tumors was examined using single-strand conformation polymorphism and direct sequencing analysis. Molecular findings were correlated with immunohistochemical detection of thep53 protein and DNA ploidy status. Mutations of thep53 gene were detected in 13 (19.5%) out of 67 cases of soft-tissue tumors. Only there were localized outside the conservative regions of thep53 gene. Six mutations were described for the first time in these tumors. Most of the mutations were point mutations in exons 5–8 and, in one case, a deletion at the 3′-splice site of exon 5 could be demonstrated. There was no significant correlation between the occurrence ofp53 mutations and the histological grade, although a high number of mutations were defined in poorly differentiated tumors (grade 3). Molecular finding of ap53 gene mutation and immunohistochemical detection ofp53 expression did not correlate, which may be due to the high percentage of nonsense mutations in our study (50%). We confirm that only DNA sequencing allows a unique identification and differentiation of mutations in thep53 gene. Other factors may be responsible for the detection ofp53 protein in many cases. Histological grade correlated with aneuploidy. The frequency of mutations observed was in accordance with values quoted in the literature. Generally,p53 mutations andp53 overexpression are more likely to represent a late event in the oncogenesis of soft-tissue tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01240317
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  • 3
    Electronic Resource
    Electronic Resource
    Overexpression of Platelet-Derived Growth Factor (PDGF) B Chain and Type β PDGF Receptor in Human Chronic Pancreatitis (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 567-574 
    Details
    ISSN: 1573-2568
    Keywords: PLATELET-DERIVED GROWTH FACTOR ; CHRONIC PANCREATITIS ; EXPRESSION
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Platelet-derived growth factors (PDGF) aremitogenic polypeptides that are involved in cellularproliferation and tissue repair. The expression of PDGFsand type β PDGF receptor was examined in the normal human pancreas and in chronic pancreatitis, afibrotic disease associated with fibroblasticproliferation, atrophy, and acinar celldedifferentiation. In the normal human pancreas, PDGF Achain mRNA levels were relatively abundant, whereas PDGF B chainmRNA levels were not detected, and type β PDGFreceptor mRNA transcripts were present at low levels. Inthe normal pancreas, PDGF immunoreactivity was present in islet cells, whereas type β PDGFreceptor immunoreactivity was present in acinar cells.In chronic pancreatitis, PDGF A chain mRNA transcriptswere also abundant, and 11 of 19 samples exhibited the PDGF B chain mRNA transcript. In addition,there was a significant increase in the mRNA levels oftype β PDGF receptor in the pancreatitis samples bycomparison with the normal pancreas (P 〈 0.001). In chronic pancreatitis tissues, PDGF and typeβ PDGF receptor immunoreactivity were present inacinar, ductal, islet, and endothelial cells,fibroblasts, and leukocytes. The concomitantoverexpression of PDGFs and of the type β PDGF receptorpoints to the existence of autocrine and paracrinePDGFdependent loops in human chronicpancreatitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018867209170
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    Paper (German National Licenses)
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