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At least 19 recordsLinked to original sources
PubMed1978

Antineoplastic agents. 1. Synthesis and antineoplastic activities of chloroethyl- and methylnitrosourea analogues of thymidine.

A new class of chloroethyl- and methylnitrosourea analogues of thymidine, 5a,b, 6, 10, and 11, has been synthesized from the corresponding amino nucleosides, 2 and 7. The 3'-chloroethyl and 3'-methyl derivatives, 10 and 11, inhibited L1210 cell growth in culture (ED50 = 1.5 and 1.0 micrometer, respectively) more effectively than 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) (ED50 = 4 micrometer) and the 5'-nitrosourea analogues. Neither the alkylating nor the carbamoylating activities of these compounds correlated with their biological activity.

Alkylating Agents↗
PubMed1975

Effects of antineoplastic agents on wound healing in mice.

The influence of antineoplastic agents on wound healing was evaluated in an experimental model employing surgical incisions in the skin of mice. A single injection in the therapeutic dose range of various clinically active antitumor agents was administered immediately following operation and the breaking strength of skin wounds was measured 3, 7, and 21 days later. Vincristine and methotrexate decreased wound strength at 3 days but not on days 7 or 21. Actinomycin D interfered with early phases of wound healing and had less effect on later phases. Treatment with bleomycin had no effect on wound strength at days 3 or 21 but prevented an increase in wound strength from day 3 to day 7; 1,3-bis(2-choroethyl)-1-nitrosurea (BCNU) decreased wound strength at all time points after operation, whereas 5-Fluorouracil had no significant effect at any time. The presence of a large tumor mass had no direct effect on wound strength nor did it modify the effect on wound strength of an antineoplastic agent, cyclophosphamide. These findings are discussed, taking into account the experimental and clinical literature on the effects of antitumor drugs on wound healing.

Animals↗
PubMed1975

The bioavailability in man of ICRF-159 a new oral antineoplastic agent.

The bioavailability of the antineoplastic agent, ICRF-159, has been examined in 12 patients receiving the drug in single and subdivided dose schedules in an attempt to account for the differences in toxicity found with the different schedules clinically. Recovery of radioactivity in the urine after single large doses (13.3-19.4 g) was 8.5 +/- 3.0% of the administered dose. After doses of 3.8-5.55 g recovery was 22.7 +/- 10.5% and after the same dose subdivided into 3 equal aliquots it was 52 +/- 8.7%. Unrecovered radioactivity was largely accounted for in the faeces. Plasma radioactivity levels in 2 patients after high and low dose were equivalent. Toxicity of the drug paralleled urinary recovery of radioactivity. It is concluded that schedule dependence of toxicity of ICRF-159 is at least partly due to bioavailability factors.

Administration, Oral↗
PubMed1979

[Cis-diamminedichloroplatinum(II). A new antineoplastic agent derived from the group of heavy metal complexes (author's transl)].

Platinum coordination complexes represent a new class of antineoplastic agents among which only cis-diamminedichloroplatinum(II) (cis-DDP) has undergone extensive clinical trials. Cis-DDP and some of its congeners share the potential to form DNA-crosslinks with the group of bifunctional alkylating agents, yet cross-resistance is incomplete. The prominent dose-limiting nephrotoxicity can be effectively circumvented by forced diuresis. Cis-DDP not only displays outstanding activity against non-seminomatous testicular cancer but also has a broad spectrum of clinical activity. It ranks very high in activity against bladder cancer and head and neck tumors. Since myelosuppression by cis-DDP is mild, it combines well with other antineoplastic agents. Synergism has been experimentally shown for cyclophosphamide and several other antineoplastic agents. For testicular cancer combination chemotherapy including cis-DDP has become accepted treatment. The simple geometry of platinum coordination complexes allows substitutions of leaving and remaining ligands with anorganic or organic moieties thus altering pharmakokinetic, antineoplastic, and toxic properties in comparison to the parent compound. Mechanism of action, pharmacology, and clinical use of cis-DDP as well as of potentially useful congeners are discussed in this review, since cis-DDP is expected to be available for general use in medical oncology in the near future.

Animals↗
PubMed1979

Cutaneous irritation in the topical application of 30 antineoplastic agents to New Zealand white rabbits.

Of 30 antineoplastic agents studied for their primary irritation potential in rabbits, 9 showed some potential for irritation. Five of these 9 agents produced a significant dermal irritation. None of the irritation observed was considered to be irreversible skin damage. The study further showed a strong correlation between irritation observed by the Draize method and acute inflammation evaluated histopathologically. There was a tendency toward increased epidermal thickness of irritated skin sites. None of the agents produced gross or microscopically visible lesions in the internal organs observed.

Administration, Topical↗
PubMed1977

Antineoplastic agents and their oral manifestations.

The use of antineoplastic agents is rapidly increasing. A general classification of these drugs and their mechanisms of action is presented. Many of the drugs have an adverse effect on oral tissue, and the practicing dentist today must be well acquainted with these effects. A discussion of the features of these reactions and their management is presented.

Antineoplastic Agents↗
PubMed1979

Adequacies and inadequacies in assessing murine toxicity data with antineoplastic agents.

Previous retrospective analyses have suggested a very positive correlation in toxic doses of antineoplastic agents between mice and humans. Additional toxicological information has now been accumulated and reveals a noticeable variability in the existing data base. Nevertheless, it is likely that mouse toxicological studies will become a principal determinant for estimating initial doses to be used in humans. Recognition of the factors responsible for differences in determinations of toxic dose levels in mice will enhance the proper utilization of this approach.

Animals↗
PubMed1979

[Pharmacokinetics of antineoplastic agents (author's transl)].

The general basis of pharmacokinetics are summarized with the clinical aims of a better utilisation of drugs by the application pharmacokinetic data. The subject is illustrated by some antineoplastic agents especially on high dose methotrexate regimens and clinical use of 5 FU. A pharmacokinetic model may be described with the first agent but for 5 FU no specific model has yet been demonstrated. Some examples of studies on adriamycin and cytosine arabinoside are then given.

Antineoplastic Agents↗
PubMed1978

Tyramine-like effect of cyclocytidine (2,2'-anhydro-1-beta-arabinofuranosylcytosine hydrochloride), an antineoplastic agent.

Since cyclocytidine (2,2'-anhydro-1-beta-arabinofuranosylcytosine hydrochloride) was introduced as an antineoplastic agent for the treatment of lymphatic leukemia, sinus acceleration and an increase in systemic blood pressure has been reported as its systemic effects in the clinical cases. These cardiovascular effects of cyclocytidine were observed also in anesthetized dogs, but not in reserpine-pretreated animals. Increases in heart rate and in systemic blood pressure were prevented by propranolol and phentolamine, respectively. The mechanism of these sympathomimetic effects was further analysed in the excised, blood-perfused canine sinoatrial node and papillary muscle preparations with a support dog. Positive chronotropic and inotropic responses to cyclocytidine were abolished by desipramine, propanolol, and pretreatment with reserpine but not by tetrodotoxin and hexamethonium. The tyramine-like actions of cyclocytidine at adrenergic neuronal terminals were discussed in conjunction with the uptake mechanism of the drug into the tumor cells.

Ancitabine↗