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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Der Onkologe 5 (1999), S. 238-251 
    ISSN: 1433-0415
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zytostatika sind Medikamente, die zur Behandlung von bösartigen Erkrankungen in der Klinik wie auch in der Praxis zum Einsatz kommen. Die gewünschte Wirkung, nämlich die Vernichtung von Tumorzellen, ist oft nur unter Inkaufnahme toxischer Reaktionen erreichbar. Diese toxischen Reaktionen betreffen in erster Linie den Patienten. Die Klinik dieser unerwünschten Reaktionen gehört zum Inhalt der ärztlichen Tätigkeit am Patienten. Diese Aspekte der medikamentösen Tumortherapie sollen hier unberücksichtigt bleiben. Es soll vielmehr versucht werden, die Gefahren, die beim Umgang mit Zytostatika bestehen, darzustellen und Hinweise zu ihrer Vermeidung bzw. Minderung zu geben.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cancer chemotherapy and pharmacology 18 (1986), S. S1 
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Antitumor activity (increase in lifespan and cure) was greater for ifosfamide (IFO) in several experimental tumors, some of which were primarily resistant to cyclophosphamide (CYC). IFO has been shown to be active in anthracycline-resistant and in adriamycin/cisplatin-resistant sublines of an Ehrlich ascites tumor, as well as in tumor cells primarily resistant to CYC. The few comparative controlled clinical trials available suggest superior single-agent activity of IFO compared with CYC in soft tissue sarcoma and ovarian cancer. Combination chemotherapy with IFO has been effective in second-line treatment of sarcomas, malignant lymphomas, lung cancer, and testicular cancer, most of them pretreated with or refractory to CYC. Although it is difficult to obtain clinical proof that there is no cross-resistance between IFO and CYC, IFO has been shown to be active in multirefractory malignant lymphomas, in small cell lung cancer not responding to adriamycin, vincristine, and etoposide, and in soft tissue and bone sarcomas. Testicular cancer and pancreatic cancer are some of the tumors in which IFO activity is currently being evaluated and in which CYC has so far failed to show sufficient clinical activity. More comparative controlled clinical trials are needed in ovarian cancer, breast cancer, malignant lymphomas, sarcomas and cervical cancer, in which IFO has already shown sufficient single-agent activity. Due to its lower level of cross-resistance with a variety of heterocyclic products, but also with other alkylating agents, in addition to its use in induction chemotherapy, IFO is an important second-line agent in many clinical situations.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 117 (1991), S. S164 
    ISSN: 1432-1335
    Keywords: Ifosfamide plus mesna ; Toxicity ; Continuous infusion ; Short-term infusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In clinical practice and in most ongoing studies in adult and pediatric tumours, daily short-time infusions of ifosfamide (IFO) on 2–5 consecutive days with cycle doses between 6 g/m2 and 12 g/m2 are used at present. The continuous i.v. infusion of IFO/mesna over 1–5 days is still experimental. Since mesna prevents IFO-induced urotoxicity, the IFO dose could be increased to 16 g/m2 per cycle. As the dose and schedules of IFO/ mesna were increased and varied, CNS and renal toxicity became more evident. CNS toxicity seems not to be dependent on i.v., but on oral dosing of IFO. Renal dysfunction and previous administration of cisplatinum predispose for CNS toxicity. The incidence or severity of CNS toxicity does not increase with subsequent courses of IFO i.v. The nephrotoxicity of IFO is dependent on IFO dose, diuresis, mesna dose and whether there has been previous cisplatinum and seems to involve preferentially the tubulus system, leading to 25 cases of Fanconi renal syndrome as published in 1988–1990. Fanconi's syndrome depends on the cumulative IFO dose, the previous administration of nephrotoxic drugs such as cisplatinum and the age of the children. Studies are continuing to determine the least nephrotoxic dose and schedule of IFO plus mesna. Leucopenia and thrombopenia are well-known dose-dependent side-effects of IFO, with similar incidence after i.v. short-time and continuous infusion.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary In the ultraviolet (UV)-mutable bacterium, Myxococcus xanthus, dose response curves for the induction of rifampicin-resistant (Rifr) mutants were compared with dose response curves for Weigle(W)-reactivation of the UV-irradiated phage Mx4 at a phage survival of 5x10−6. In most strains examined, including a uvr mutant, these curves are largely similar. Unexpectedly the UV-sensitive strain M. xanthus Bt, which is unable to perform W-reactivation, is nevertheless UV-mutable. This result may indicate that the repair pathway involved in phage reactivation is only partly responsible for UV-mutagenesis or alternatively is not able to act on phage DNA in M. xanthus Bt cells. N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) treatment of M. xanthus cells also results in marked W-reactivation of the UV-irradiated phage Mx4 at the same survival of 5x10−6. The MNNG-stimulated phage reactivation is of the same order of magnitude as the UV-stimulated phage reactivation. Also the dose response curves for the induction of Rifr mutants by MNNG and the MNNG-stimulated phage reactivation are quite similar. This coincidence may indicate that misrepair mutagenesis is involved in both UV and MNNG-mutagenesis. It is suggested that M. xanthus is a useful organism with which to study misrepair mutagenesis in bacteria.
    Type of Medium: Electronic Resource
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