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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 118 (1992), S. 141-146 
    ISSN: 1432-1335
    Keywords: v-mos ; Acute retrovirus ; Tumour clonality
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Moloney murine sarcoma virus (M-MSV) induces rapidly growing tumours in adult mice of most conventional strains. Rats are less susceptible to M-MSV oncogenesis, but the few rhabdomyosarcomas that do develop after viral inoculation of newborn animals closely resemble conventional malignancies: they develop after a long latency, grow progressively, and metastasize to regional lymph nodes and lungs. Southern blot analysis with a v-mos-specific probe of M-MSV-induced tumours in both species demonstrated an oligo-, monoclonal pattern of exogenous v-mos integration only in the rat system, while mouse tumours were not clonal in origin. Furthermore, the same type of analysis of lymph node and lung metastases showed that cell clones already present in the primary rat lesion colonized secondary sites during tumour progression. Apparently, Moloney murine leukemia virus (M-MuLV) was not involved in rhabdomyosarcoma pathogenesis since M-MuLV-specific DNA sequences could not be demonstrated in three of the six rat tumours. Finally, in all mouse tumours, unintegrated linear M-MSV proviruses could be readily detected.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1335
    Keywords: Loss of heterozygosity ; Loss of imprinting ; Hepatoblastoma ; IGFII-H19
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2592
    Keywords: CD5 ; B lymphocytes ; AIDS ; human immunodeficiency virus (HIV) ; anti-HIV antibody
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
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