Anticancer research
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Anticancer research · May 2003
ReviewImmune responses to human tumors: development of tumor vaccines.
Strong evidence has been accumulated demonstrating that tumor cells in humans and animal are recognized in general as non-self by the immune system and they are able to induce an immune response which often leads to their elimination. In humans, this evidence includes: (a) The development of T-cell lines and clones with antitumor activity (cytotoxic or helper) which is restricted to autologous tumor cells or to cells expressing the same tumor peptide/HLA epitope; (b) the presence of oligoclonal T cells infiltrating many tumors; (c) the identification and molecular cloning of tumor antigens and of peptides derived from these antigens, which elicit HLA-restricted immune responses. Their discovery provided the ultimate proof for the presence of specific immune responses in human tumors. ⋯ This approach can be effective when an immune response can not be elicited in vivo. The progress made towards the development of tumor vaccines and approaches for adoptive immunotherapy has been substantial. Additional studies need to be carried out to develop new and effective tumor vaccines and adoptive immunotherapy methods.
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Anticancer research · May 2003
Review Comparative Study5-HT3-receptor antagonists in the control of delayed-onset emesis.
Nausea and vomiting are typical side-effects of cancer therapy. The management of acute-onset emesis (< 24 hours post-treatment) has improved markedly in recent years and the 5-HT3-receptor antagonists are widely regarded as the antiemetic 'gold standard' during this period. ⋯ Available data indicates that the 5-HT3-receptor antagonists are at least as good as conventional antiemetics in controlling delayed-onset emesis, and that their efficacy in this setting may be improved by the addition of a corticosteroid. As a result, antiemetic guidelines recommend the addition of a 5-HT3-receptor antagonist for the treatment of delayed emesis, particularly for high-risk patients.
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Anticancer research · May 2003
ReviewT-antigen of human polyomavirus JC cooperates withIGF-IR signaling system in cerebellar tumors of the childhood-medulloblastomas.
Polyomaviruses are implicated in a number of cancers, and the transforming activity of their early protein, large T-antigen, has been documented in a variety of cell types and in experimental animals (1). Although the pathways by which T-antigen induces uncontrolled cell growth are not fully defined, T-antigen mediated inactivation of tumor suppressors, p53 and pRB, is well-documented in some malignancies (2). Here we postulate that functional interaction between the insulin-like growth factor (IGF-IR) and the T-antigen of human polyomavirus JC (JCV T-antigen) may contribute to the process of malignant transformation in medulloblastomas: (i) the IGF-IR signaling system is strongly activated in medulloblastoma cell lines and medulloblastoma biopsies; (ii) the cytoplasmic protein, insulin receptor substrate 1 (IRS-1), is translocated to the nucleus in the presence of JCV T-antigen; (iii) molecular characterization of the interaction between IRS-1 and JCV T-antigen indicates that the binding involves the N-terminal portion of IRS-1 (PH/PTB domain) and the C-terminal region of JCV T-antigen (aa 411-628); and finally (iv) competition for the IRS-1-JCV T-antigen binding attenuates anchorage-independent growth of T-antigen positive medulloblastoma cells in culture. Based on these findings, we propose a novel role for IRS-1 in JCV T-antigen-mediated deregulation of cellular equilibrium, which may involve uncoupling of IRS-1 from the surface receptor and translocation of its function to the nuclear compartment of the cell.