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  • 1
    Digitale Medien
    Digitale Medien
    Oxford, UK; Malden, USA : Munksgaard International Publishers
    Journal of cutaneous pathology 31 (2004), S. 0 
    ISSN: 1600-0560
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Background:  Insulin-like growth factor-I (IGF-I) is the principal mediator of growth hormone, exerting its effects through binding of the insulin-like growth factor-I receptor (IGF-IR). Post-receptor activation leads to the production of transcription factors involved in cell proliferation, differentiation, transformation, and survival. Data indicate that IGF-IR is involved in tumorigenesis. To our knowledge, this receptor has not been previously studied in primary cutaneous carcinomas.Methods:  Twenty-five cases of primary cutaneous carcinomas consisting of three keratoacanthoma-type squamous cell carcinomas (KAs), two squamous cell carcinomas in situ (SCCs in situ), eight squamous cell carcinomas (SCCs), three conventional basal cell carcinomas (BCCs), two morpheaform basal cell carcinomas (M-BCCs), and seven Merkel cell carcinomas (MCCs) were analyzed for IGF-IR immunohistochemical expression using IGF-IR mouse monoclonal antibody (dilution 1 : 50) using the avidin–biotin–peroxidase complex method.Results:  Normal epidermis was negative for IGF-IR expression. Normal eccrine glands and outer root sheath strongly expressed IGF-IR. All KAs, SCCs in situ, SCCs, and BCCs were negative for IGF-IR expression. Six of seven (86%) of the MCCs stained with IGF-IR strongly, showing cell membrane accentuation and a perinuclear dot-like pattern.Conclusion:  The data suggest that IGF-IR immunopositivity in MCCs might constitute a diagnostic tool in discriminating between SCCs and BCCs. Although the possible pathogenic significance of the perinuclear dot-like staining pattern observed in these neoplasms is unknown, its pattern is similar to what has been previously described with cytokeratin-20 immunostaining.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Oxford, UK; Malden , USA : Munksgaard International Publishers
    Journal of cutaneous pathology 31 (2004), S. 0 
    ISSN: 1600-0560
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Background:  Hamartin and tuberin are inactivating tumor suppressor proteins implicated in the development of gastrointestinal polyps and sporadic and tuberous sclerosis-associated cutaneous angiofibromas. The pattern of expression of these peptides has not been studied in fibroepithelial polyps (FEPs).Design:  The specific aim of the study was to evaluate the immunohistochemical expression of tuberin and hamartin within the epithelium and dermal fibrocytes of 20 cutaneous FEPs compared with the epithelium and dermal fibrocytes of normal skin. The diagnoses were confirmed independently by a dermatopathologist, and the pattern of intensity was assessed by the mean labeling intensity (MLI) of cytoplasmic and/or nuclear staining for each antibody.Results:  Hamartin and tuberin antibodies showed moderate staining of the keratinocytes and fibrocytes of normal skin and the keratinocytes within FEPs. Both antibodies showed diminished staining within the fibrocytes of the FEPs. The MLI of hamartin was 44.3 ± 4.4 for keratinocyte nuclei in normal skin and 51.2 ± 3.7 within the polyps. The MLI of tuberin was 42.9 ± 3.6 within the keratinocyte nuclei of the normal skin compared to 39.7 ± 3.0 for the polyps. The MLI for hamartin within the fibrocytes of the normal skin was 78.9 ± 7.1 compared to 21.6 ± 4.2 within the polyps, p = 0.01. The MLI for tuberin within the fibrocytes of normal skin was 70.6 ± 5.0 compared to 47.1 ± 4.7 within the polyps.Conclusion:  The data suggest that down regulation or loss of tuberin and/or hamartin expression may be permissive to fibrocyte proliferation or promote collagen production leading to FEP formation.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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