Lack of potentiation of vincristine-induced neurotoxicity by VP-16–213

Dv, Jackson; Hb, Wells; Dr, White; Hb, Muss; Richards, Fred; Mr, Cooper; Jj, Stuart; Ek, Pope; Cl, Spurr

doi:10.1097/00000421-198306000-00013

Cited by 17 publications

(2 citation statements)

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“…A mild peripheral neuropathy was reported in 1-20% of patients receiving etoposide alone (1,4,8,18), although this finding has been challenged by others (14). The possible enhancement of vincristine-induced peripheral neuropathy by etoposide has also been questioned (12,25). A single case of etoposideinduced central nervous system toxicity, character-ized by acute dystonia, an extrapyramidal side effect, has also been reported (2).…”

Section: Introductionmentioning

confidence: 99%

Etoposide- and BMY-40481-Induced Sensory Neuropathy in Mice

et al. 1994

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The effects of high toxic doses of the anticancer drugs, etoposide and its phosphate derivative, BMY- Ultrastructurally, ganglion cell bodies had focally extensive dilation of the rough endoplasmic reticulum, mitochondrial swelling, increased numbers of phagolysosomes and prominent aggregations of microfilaments (globular filamentous bodies). Ultrastructural axonal changes occurred primarily in large, myelinated fibers and consisted of axonal swelling or loss, thinning of myelin sheaths, and a decrease in the number of organelles. This is the first report of etoposide-related sensory neuropathy in laboratory animals, a model that may be useful for the study of etoposide-related peripheral neuropathy in humans.

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Section: Introductionmentioning

confidence: 99%

Etoposide- and BMY-40481-Induced Sensory Neuropathy in Mice

et al. 1994

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“…In one series in which patients with recurrent malignant brain tumors who had progressed after receiving BCNU and Vincristine were treated with standard doses of VP-16, 17% were noted to have responses and 34% had stable disease [2]. Recent data have demonstrated synergistic antitumor activity between Vincristine and VP-16 [3] without added toxicity [4].…”

Section: Introductionmentioning

confidence: 99%

VP-16, vincristine and procarbazine with radiation therapy for treatment of malignant brain tumors

1990

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Twelve patients aged 34 to 65 with malignant gliomas were treated with VP-16, Procarbazine, Vincristine and concurrent radiation therapy. There were 9 patients with glioblastoma multiforme and 3 with anaplastic astrocytoma. All patients had a subtotal resection or biopsy as the initial procedure. Six patients (1 anaplastic astrocytoma) have developed progressive disease. Mean time to tumor progression was 46 weeks. This combined modality treatment program was associated with reversible hematologic toxicity which was severe in 2 patients. These data compare favorably to data obtained from similar patients treated with radiation therapy and BCNU.

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Neuromuscular disorders in systemic malignancy and its treatment

Stübgen

1995

Muscle and Nerve

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Neuromuscular dysfunction in patients with known or suspected malignancy has three basic etiologies: (1) a direct effect of the neoplasm, either by compression or infiltration; (2) a "remote," or paraneoplastic, effect of cancer; or (3) a side effect of anticancer treatment, radiation or chemotherapy. A variety of clinical features or syndromes are due to damage either at the level of the neuron (anterior horn cell or dorsal root ganglion neuron), nerve root(s), brachial or lumbosacral plexus, peripheral nerve (motor, sensory, and/or autonomic), neuromuscular junction, or muscle. A complex clinical picture evolves when dysfunction in due to more than one cause at more than one anatomical site.

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Lack of potentiation of vincristine-induced neurotoxicity by VP-16–213

Cited by 17 publications

References 0 publications

Etoposide- and BMY-40481-Induced Sensory Neuropathy in Mice

Etoposide- and BMY-40481-Induced Sensory Neuropathy in Mice

VP-16, vincristine and procarbazine with radiation therapy for treatment of malignant brain tumors

Neuromuscular disorders in systemic malignancy and its treatment

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