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  • Colorectal carcinoma  (1)
  • Loss of heterozygosity  (1)
  • human immunodeficiency virus (HIV)  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Absence of the Cell Cycle Inhibitor p27Kip1 Protein Predicts Poor Outcome in Patients With Stage I-III Colorectal Cancer (1999)
    Springer
    Annals of surgical oncology 6 (1999), S. 19-25 
    Details
    ISSN: 1534-4681
    Keywords: Colorectal carcinoma ; P27Kip1 protein ; Prognostic markers ; Cell cycle inhibitors.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: The p27Kip1 protein regulates the G1 to S phase transition of cell cycle by binding to and inhibiting the cyclin E/Cdk2 complex. This study explores the prognostic significance of the absence of the p27Kip1 protein in patients with colorectal cancer (CRC). Methods: Formalin-fixed tumor sections from 124 patients who underwent curative resection for stage I-III CRC were analyzed by immunohistochemistry using MoAb anti-p27Kip1. Results: Detectable levels of p27Kip1 protein were found in 86% of tumors. Median follow-up was 55 months. Actuarial 5-year disease-free survival (DFS) and overall survival (OS) were 76% and 85%, respectively, in patients with tumors with p27Kip1 protein expression and 34% and 40%, respectively, in those whose tumors lacked p27Kip1 protein expression (P 〈 .001). At multivariate analysis, tumor stage (III vs. I-II) and p27Kip1 protein status (absence vs. presence) were found to be independent prognostic factors for DFS and OS. Conclusions: Lack of p27Kip1 protein expression in CRC is a negative prognostic marker and may therefore be useful in selecting early-stage patients more likely to benefit from adjuvant treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s10434-999-0019-2
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Occasional loss of constitutive heterozygosity at 11p15.5 and imprinting relaxation of theIGFII maternal allele in hepatoblastoma (1994)
    Springer
    Journal of cancer research and clinical oncology 120 (1994), S. 732-736 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF01194272
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    B cell activation and human immunodeficiency virus infection. V. Phenotypic and functional alterations in CD5+ and CD5− B cell subsets (1993)
    Springer
    Journal of clinical immunology 13 (1993), S. 381-388 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00920013
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    Paper (German National Licenses)
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