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  • 1
    Electronic Resource
    Electronic Resource
    Expression of S100A2 and S100B proteins in epithelial tumors of the skin (2003)
    Oxford, UK : Munksgaard International Publishers
    Journal of cutaneous pathology 30 (2003), S. 0 
    Details
    ISSN: 1600-0560
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  The purpose of this study was to evaluate the expression of Ca2+-binding S100 proteins, S100A2 and S100B, in normal skin. These immunohistochemical stain patterns were compared with those in a variety of epithelial tumors.Methods:  Paraffin-embedded tissues of 38 skin tumors were evaluated immunohistochemically with S100A2 and S100B antibodies.Results:  Epidermal basal cells, epithelial cells of sebaceous glands, hair follicle epithelia, and eccrine ducts reacted strongly with S100A2 antibody. Langerhans' cells and melanocytes were labeled by S100B. Varying types of skin appendage tumors and most peripheral cells in tumor nests of basal cell carcinoma and squamous cell carcinoma showed positive S100A2 immunoreactivity in neoplastic cells. Basophilic cells of calcifying epithelioma were occasionally stained with S100A2 antibody. Chondroid syringoma containing neoplastic myoepithelial cells stained strongly for both S100A2 and S100B.Conclusions:  We conclude that S100A2 can be a specific marker of epithelial cells in the different skin tumors. However, these antibodies are not of much help in classifying skin appendage tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0560.2003.00081.x
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  • 2
    Electronic Resource
    Electronic Resource
    Expression profiles of p63, p53, survivin, and hTERT in skin tumors (2004)
    Oxford, UK; Malden, USA : Munksgaard International Publishers
    Journal of cutaneous pathology 31 (2004), S. 0 
    Details
    ISSN: 1600-0560
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  p63 is a p53 homolog and a marker expressed in replicating keratinocytes. Survivin is a recently characterized inhibitor of apoptosis protein that is abundantly expressed in most solid and hematologic malignancies. Telomerase reverse transcriptase (TERT) is the major determinant of human telomerase activity, and its expression is indicative of unlimited replication. We herein evaluated the expression profiles of p63, p53, survivin, and hTERT in usual skin cancers, including squamous cell carcinoma (SCC) and basal cell carcinoma (BCC) and putative preneoplastic epidermal lesions, including actinic keratosis (AK), Bowen's diasease, and porokeratosis.Methods:  Immunohistochemistry using antibodies against p63, p53, survivin, and hTERT was performed. Semi-quantitative evaluation (–, +, 2+, 3+) was carried out.Results:  BCCs showed diffuse p63 expression and SCCs heterogeneous p63 expression with negativity in terminally differentiated squamous cells. All preneoplastic epidermal lesions showed p63 expression in all cell layers. p53 was found in seven of 10 cases of BCCs, all 10 cases of SCCs, and nine of 10 cases of Bowen's disease. AK and porokeratosis revealed focal to moderate p53 expression. Survivin was found in eight of 10 cases of SCCs and eight of 10 cases of Bowen's disease. Six of 10 cases of BCCs revealed weak survivin positivity. AK and porokeratosis showed survivin expression confined to the basal layer. hTERT expression was found in most cases of skin cancers and preneoplastic lesions.Conclusions:  p63 expression may be a marker of basal/progenitor cells and a diagnostic marker in skin tumors. p63 expression is not related to p53 expression in these tumors. This study points to a putative role of survivin and hTERT in the development of certain skin cancers. In addition, our data support the concept of porokeratosis being a premalignant condition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0303-6987.2004.00228.x
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  • 3
    Electronic Resource
    Electronic Resource
    The differential expression pattern of BMP-4 between the dentigerous cyst and the odontogenic keratocyst (2005)
    Oxford, UK : Munksgaard International Publishers
    Journal of oral pathology & medicine 34 (2005), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  Bone morphogenic protein-4 (BMP-4) is widely expressed in oral cavity and involved in tooth morphogenesis, cellular differentiation and proliferation. The purpose of this study was to compare the difference in expression pattern of BMP-4 in odontogenic keratocysts (OKC) and dentigerous cysts (DC).Methods:  We evaluated 77 cysts, OKC (n = 34) or DC (n = 43). The average age of patients with OKC was 29.5 ± 14.4 and that of patients with DC was 36.1 ± 19.4. The male to female ratio was 20:14 for OKC and 27:16 for DC. Ten cases of OKC were recurrences. Expression of BMP-4 was determined by immunohistochemistry and in situ hybridization.Results:  The intensity scales were (−) for invisible or trace staining, (+) for visible staining, and (++) for dense, strong staining. OKCs exhibited the following staining patterns: the epithelium in 15/34 specimens and the mesenchymal cells in 17/34 specimens showed (++) stain. In contrast, the staining pattern of DC was (−) for epithelium in 37/43 specimens. The mesenchymal cells showed (−) degree staining in 30/43 specimens. The difference between the groups studied was significant (P 〈 0.001 in epithelium and mesenchymal cells). When recurrent and non-recurrent OKC were compared BMP-4 was expressed more intensely in the recurrent cases (P = 0.036 in epithelium). The difference in BMP-4 expression in mesenchymal cells was not significant. In situ hybridization demonstrated positive mRNA probes to BMP-4 were localized in epithelium and mesenchymal cells of OKCs and DCs.Conclusions:  BMP-4 was expressed more intensely in OKC when compared with DC, and was more intensely expressed in recurrent cases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.2004.00285.x
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    Paper (German National Licenses)
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