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  • Loss of heterozygosity  (1)
  • human immunodeficiency virus (HIV)  (1)
  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Journal of cancer research and clinical oncology 120 (1994), S. 732-736 
    ISSN: 1432-1335
    Schlagwort(e): Loss of heterozygosity ; Loss of imprinting ; Hepatoblastoma ; IGFII-H19
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract The 11p15.5 chromosomal region contains one or more loci involved in congenital developmental abnormalities and in the genesis of embryonal tumors, such as Wilms' tumor, embryonal rhabdomyosarcoma, and hepatoblastoma. In these tumors, a loss of constitutive heterozygosity, selectively involving a specific parental allele, suggests both the presence of onco-suppressor genes and a phenomenon of genomic imprinting. We present evidence that both genetic events could be occasionally involved in hepatoblastoma. In fact, loss of heterozygosity at 11p15.5 could be documented in 3 of 13 patients with hepatoblastoma, and in 2 cases the paternal origin of the residual allele in the tumor was assessed. Moreover, imprinting of the paternal IGFII allele and the maternal H19 allele was confirmed in normal tissues of 5 informative patients. Finally, imprinting relaxation of IGFII was detected in the tumor tissue of 1 patient.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1573-2592
    Schlagwort(e): CD5 ; B lymphocytes ; AIDS ; human immunodeficiency virus (HIV) ; anti-HIV antibody
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract B cell dysregulation is a hallmark of human immunodeficiency virus infection. Since B lymphocytes comprise two distinct subpopulations, CD5+ and CD5− cells, we addressed their individual phenotypic and functional behavior. Seropositive patients with both limited and advanced disease progression had an increased percentage of peripheral blood CD5+ B cells, compared to seronegative controls (20.1±2.1 and 22.7±5.7, respectively, vs 17.0±3.4 in controls); however, due to the lymphopenia and reduced number of circulating B cells in infected individuals, the absolute number of CD19+ CD5+ lymphocytes was actually reduced. Although HIV-specific antibodies were synthesized spontaneouslyin vitro only by CD5− B cells, a 10-fold lower degree of spontaneous, non-HIV-specific activation was also displayed by unstimulated CD5+ B cells. These findings indicate that B cell dysregulation during HIV infection involves both the CD5− and the CD5+ B cell compartments; moreover, in view of the putative role of CD5+ B cells in autoimmune phenomena and IL-10 production, these data reinforce the possibility that B cell dysfunction might be causally involved in AIDS pathogenesis.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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