diphenylhydantoin/neoplasms

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Toxicology and Carcinogenesis Studies of 5,5-Diphenylhydantoin (CAS No. 57-41-0) (Phenytoin) in F344/N Rats and B6C3F1 Mice (Feed Studies).

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5,5-Diphenylhydantoin and its sodium salt are primarily used in the treatment of grand mal and psychomotor seizures, often in combination with other anticonvulsants, including phenobarbital. 5,5-Diphenylhydantoin is a suspected human carcinogen and was one of three compounds selected by the NTP to

Comparative enhancing effects of phenobarbital, amobarbital, diphenylhydantoin, and dichlorodiphenyltrichloroethane on 2-acetylaminofluorene-induced hepatic tumorigenesis in the rat.

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Earlier studies showed that phenobarbital feeding enhanced hepatic tumorigenesis in rats previously fed 2-acetylaminofluorene for a brief period. As part of an investigation of the mechanism of this enhancement, the present study evaluated the relative enhancing abilities of amobarbital,

Growth-inhibitory effect of diphenylhydantoin on murine astrocytomas.

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In previous work reported from this laboratory we found that diphenylhydantoin (DPH) inhibited the growth of 7 of 10 tissue-cultured human astrocytoma cell lines in a microtiter system. In this report we describe significant growth inhibition by DPH of two murine astrocytoma tissue cultures and

5,5'-Diphenylhydantoin (phenytoin) attenuates the action of 3,5,3'-triiodo-L-thyronine in cultured GC cells.

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We have previously reported that 5,5'-diphenylhydantoin (DPH) inhibits total cellular and specific nuclear T3 binding by cultured GC cells, a rat pituitary tumor cell line that produces GH. DPH decreased competitively the rate of T3 accumulation by GC cells and noncompetitively inhibited specific

Induction of a novel Ca2+-dependent chymotrypsin-like serine protease by tumor promoters in rat livers.

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Induction of a microsomal Ca2+-dependent serine protease by hepatic tumor promoters was studied. Male F344 rats were fed a diet containing one of the following promoting agents: phenobarbital (CAS: 50-06-6), dichlorophenyltrichloroethane (CAS: 50-29-3), butylated hydroxytoluene,

Phase I trial of vinorelbine and diphenylhydantoin in patients with refractory carcinoma.

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The anti-epileptic diphenylhydantoin (DPH; Dilantin) selectively enhances the in vitro cytotoxicity of vinca microtubule poisons in both parent sensitive and multi-drug resistant (MDR) human tumor cells. The in vivo clinical activity of this combination has not been fully evaluated. OBJECTIVE To

The in vivo cytotoxic activity of procarbazine and procarbazine metabolites against L1210 ascites leukemia cells in CDF1 mice and the effects of pretreatment with procarbazine, phenobarbital, diphenylhydantoin, and methylprednisolone upon in vivo procarbazine activity.

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An in vivo assay of the activity of procarbazine, N-isopropyl-alpha-(2-methylhydrazino)-p-toluamide hydrochloride, and several metabolic intermediates against IP-implanted L1210 leukemia cells in CDF1 male mice is described. Treatment of tumor-bearing mice with procarbazine at doses of 300-500 mg/kg

The effects of diphenylhydantoin on murine astrocytoma radiosensitivity.

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Diphenylhydantoin is a well known anticonvulsant used primarily in the treatment of epilepsy. The prophylactic use of diphenylhydantoin has been suggested for certain cerebral metastases, and it is routinely administered to prevent seizures induced by intracranial neoplasms and/or surgery. Patients

Inhibition of metabolic cooperation by the anticonvulsants, diphenylhydantoin and phenobarbital.

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High densities of 6-thioguanine-sensitive Chinese hamster V79 cells reduce the recovery of co-cultured 6-thioguanine-resistant cells through a form of intercellular communication (metabolic cooperation). Diphenylhydantoin and phenobarbital, suspected human and animal teratogens and tumor promoters,

Tumor promotion by an anticonvulsant agent, phenytoin, in mouse liver: correlation with CYP2B induction.

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To investigate the liver tumor promoting effects of phenytoin (5,5-diphenylhydantoin; DPH), 5 week old male D2B6F1 mice were given a single i.p. dose of 90 mg N-nitrosodiethylamine (NDEA)/kg body wt in tricaprylin. Control groups received tricaprylin alone. After 2 weeks, the mice were given a diet

Therapeutic potential for phenytoin: targeting Na(v)1.5 sodium channels to reduce migration and invasion in metastatic breast cancer.

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Voltage-gated Na(+) channels (VGSCs) are heteromeric membrane protein complexes containing pore-forming α subunits and smaller, non-pore-forming β subunits. VGSCs are classically expressed in excitable cells, including neurons and muscle cells, where they mediate action potential firing, neurite

Phenytoin: 80 years young, from epilepsy to breast cancer, a remarkable molecule with multiple modes of action.

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In 1908 phenytoin (5,5-diphenylhydantoin) was first synthesized as a barbiturate derivative in Germany by professor Heinrich Biltz (1865-1943) and subsequently resynthesized by an American chemist of the pharmaceutical company Parke-Davis in 1923 in Detroit. Screening phenytoin did not reveal

Effects of liver-tumor promoters on phalloidin sensitivity of rat hepatocytes.

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Hepatocytes were isolated by a collagenase perfusion method from male F-344 rats fed a diet containing 0.05% phenobarbital (PB), 0.05% dichlorophenyltrichloroethane (DDT), 0.25% ethyl-alpha-p-chlorophenoxyisobutyrate (CPIB), 0.02% methapyrilene hydrochloride (MP), 0.05% amobarbital (AB) or 0.05%

Interaction of nitrofurantoin with diphenylhydantoin.

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Left-sided motor seizures in a patient with an operated brain tumor were controlled with 300 mg/d DPH. The introduction of antimicrobial therapy with nitrofurantoin caused a fall of serum DPH levels and the recurrence of seizures, at the same time serum gammaGT values were increased. These changes

[Differential diagnosis of infratentorial atrophies by computed tomography (author's transl)].

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Computed tomographical findings are documented for 140 patients with different cerebellar atrophic or heredodegenerative processes. There are idiopathic cerebellar atrophies, so called alcoholic and paraneoplastic cerebellar atrophies, cerebellar atrophies associated with nutritional deficiency

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