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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 105 (1983), S. 79-82 
    ISSN: 1432-1335
    Keywords: Head and neck cancer ; CDDP ; Radio enhancement ; Toxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A combination of radiotherapy and daily administration of cis-dichlorodiammineplatinum (II) (CDDP) was given to six patients with locally advanced solid tumors including regional lymph-node metastases. Four of these patients had esophageal cancer (two with supraclavicular lymph-node metastases), one patient had oropharyngeal cancer (T4N1M0), and one had recurrent cancer of the tongue with involvement of the skin of the neck. Radiotherapy in fractionated daily doses was given to three patients and the other three received superfractionated (two fractions/day) doses; CDDP was given within 15 min after radiotherapy at a dose of 8 mg/m2 for fractionated and 4 mg/m2 for superfractionated treatment. Evaluation of response in irradiated fields showed complete tumor control, as judged from histological examination in three patients, partial tumor regression in two (recurrent carcinoma of the tongue), and no response in one. One patient showed tumor progression in irradiated fields 7 weeks after treatment and two developed distant metastases. Due to severe leukopenia (〈2,000/mm3) occurring after the 3rd week of treatment, treatment was postponed in one patient and discontinued in two. Sepsis occurred in two patients and two patients developed severe thrombocytopenia (25,000/mm3 and 44,000/mm3). All patients needed red cell transfusions during therapy. Serum levels of sodium, potassium, calcium, and magnesium dropped in all patients, whereas renal function was stable. Only one patient showed severe gastrointestinal toxicity, expressed in vomiting and diarrhea. These preliminary data warrant further evaluation of this regimen, but it is clear that the treatment requires intensive supportive care.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-7373
    Keywords: Taxol ; Cremophor EL ; Org 2766 ; neuropeptidergic cells ; microtubules ; peptide secretion ; Lymnaea stagnalis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cerebral ganglia of the freshwater snailLymnaea stagnalis were incubatedin vitro in 10 μM Taxol for 8 and 24 h. Cremophor EL (0.1%) was used as a diluant. The tissue was processed for electron microscopy. Various ultrastructural parameters were assessed quantitatively. Cremophor EL appeared to seriously affect the cell somata of the multipeptidergic caudodorsal cells. In the Cremophor-controls the mean area of Golgi zones, the percentage dense material (neuropeptides) in these zones, the number of large electron dense granules (these are involved in neuropeptide processing) and the mean nuclear heterochromatin clump size, were significantly smaller than in the Ringer-controls, whereas the number of lipid droplets was higher. All these parameters, except for the lipid droplets, were not different in the Cremophor-controls and the Taxol-treated specimens. After 24 h treatment, but not after 8 h, Cremophor EL furthermore induced an increase in the number of axonal microtubules. It is argued that the results might signify activation of the neurons by Cremophor EL. Taxol induced a significant increase in the number of microtubules in axons and cell somata. Furthermore an increase in the number of Golgi zones was observed, suggesting activated neuropeptide synthesis. In all groups immunostaining with antibodies to neuropeptides produced by the caudodorsal cells was normal. Release of neuropeptide (exocytosis) from axon endings was elevated after Taxol treatment, and exceptionally high in specimens cotreated with Taxol and Org 2766 (incubation time 22 h). The effect of Org 2766 and Taxol on the number of microtubules was cumulative. It is argued that transport of neuropeptide granules from the cell somata to the axon terminals was not affected by Taxol. It is concluded that Taxol neurotoxicity is probably not due to impeded microtubular axonal transport.
    Type of Medium: Electronic Resource
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