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  • Artikel: DFG Deutsche Nationallizenzen  (1)
  • 2000-2004  (1)
  • 1980-1984
  • 1965-1969
  • 1930-1934
  • 1925-1929
  • Bcl-x  (1)
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  • Artikel: DFG Deutsche Nationallizenzen  (1)
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  • 2000-2004  (1)
  • 1980-1984
  • 1965-1969
  • 1930-1934
  • 1925-1929
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  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Archives of dermatological research 292 (2000), S. 225-232 
    ISSN: 1432-069X
    Schlagwort(e): Key words Melanoma ; Melanoma-metastases ; Bcl-2 ; Bcl-x ; Bax
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Apoptosis is an important cofactor in the pathogenesis of a plethora of malignancies. However, little is known about modulation of the expression of bcl gene family in melanocytic tumors. To determine the role of bcl-2, bcl-x and bax in melanocytic tumors we investigated the differential expression of these genes via RT-PCR in tissue samples from human ¶benign nevi, primary melanomas and melanoma metastases in comparison with normal skin. Bcl-2 was strongly expressed in 14/16 metastases (87.5%), whereas only 7/13 primary melanomas (53%), 7/15 nevi (46%) and 7/16 normal tissue samples (43%) showed expression of bcl-2 (P 〈 0.05). There was a strong indication of a correlation between tumor thickness and bcl-2 expression in nodular malignant melanomas. Expression of bcl-x was found in 16/16 melanoma metastases (100%), 11/13 primary melanomas (84%), 12/15 nevi (80%) and 10/16 normal tissue samples (62%) (P 〈 0.05). Bcl-xL expression increased from primary melanoma to melanoma metastases, whereas bcl-xS showed a decreasing expression level during melanoma progression. No differences in bax expression were seen between melanoma metastases, primary melanoma, nevi and normal tissue. Immunohistochemical investigations of another 53 tissue samples showed similar results. Our results strongly indicate that bcl-2 and bcl-xL gene expression increases with progression of malignant melanoma. Bcl-2 and bcl-xL expression could reflect an increased malignant potential caused by an inhibition of apoptosis and growth advantage for metastatic melanoma cells.
    Materialart: Digitale Medien
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