adriamycin/necrosis

Cardiomyopathy is a major dose-limiting factor for applications of Adriamycin, a potent chemotherapeutic agent. The present study tested the hypothesis that increased tumor necrosis factor (TNF)-alpha signaling via its receptors protects against Adriamycin-induced cardiac injury. We used mice in

The clinical application of adriamycin, an exceptionally good chemotherapeutic agent, is limited by its dose-related cardiomyopathy. Our recent study showed that tumor necrosis factor-alpha (TNF-alpha) receptors mediated cytoprotective signaling against adriamycin-induced mitochondrial injury and

The newly discovered member of the tumor necrosis factor superfamily, Apo2L/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), has been identified as an apoptosis-inducing agent in sensitive tumor cells but not in the majority of normal cells, and hence it is of potential therapeutic

A number of human tumor cell lines of various histological origin were examined for their sensitivity and resistance to tumor necrosis factor-alpha (TNF) and Adriamycin (ADR). Six ovarian lines, and one each of a renal, lung, and B-cell line, were tested for putative mechanisms of resistance to

Skin necrosis following subcutaneous Adriamycin extravasation is a significant clinical problem. In this study Adriamycin dilution and various drugs were tested for their ability to ameliorate this toxic effect. When Adriamycin was diluted to a concentration of less than or equal to 0.25 mg/ml, no

Skin ulceration caused by extravasation of Adriamycin follows a severely protracted course accompanied by considerable morbidity. To develop an animal model of Adriamycin ulceration, we compared intradermal injection of Adriamycin to injection beneath the panniculus carnosus with varying drug

A free flap transfer in a case of Adriamycin necrosis on the dorsum of the hand is reported. The advantages of this method of reconstruction are discussed.

A 56-year-old male, following pneumonectomy for oat cell carcinoma, was receiving Adriamycin intravenously. Early in his treatment schedule, the intravenous Adriamycin was alleged to have infiltrated, and was promptly stopped. However, treatment was continued through the veins of the other arm at

OBJECTIVE To explore the accurate Fas antigenic expression in transitional cell carcinoma (TCC) cells and and compare its synergistic modulation on adriamycin cytotoxicity with alpha-tumor necrosis factor (TNF-alpha). METHODS The expression of Fas antigen in normal urothelium and TCC cell lines was

Inadvertent extravasation of Adriamycin (Adria) can result in severe tissue necrosis. The mechanism of this tissue damage is believed to be the release of free radicals into the tissue. Topical applications of dimethylsulfoxide (DMSO) used after Adria extravasation have been shown to decrease ulcer

Extravasation of Adriamycin during i.v. infusion can cause serious local complications. We have used a rat skin model to study the protection afforded by dimethyl sulfoxide and alpha-tocopherol (vitamin E) against Adriamycin-induced skin necrosis. Topical daily application of 1 ml dimethyl sulfoxide

Liposomes as drug carriers in cancer chemotherapy have attracted considerable interest. To enhance the therapeutic effect of Adriamycin entrapped in liposomes (Lip-ADM) on human solid tumors, we investigated the therapeutic effects of Lip-ADM in combination with recombinant human tumor necrosis

One of the mechanisms of cytotoxicity by tumor necrosis factor (TNF) and heat is the induction of reactive oxygen molecules. Cells producing endogenous tumor necrosis factor (enTNF) show resistance to the cytotoxicity of exogenous TNF and heat by inducing manganous superoxide dismutase (MnSOD) to

While transduction of an antisense tumor necrosis factor (TNF) gene sequence can augment the cytotoxicity of adriamycin (ADM) in human cancer cells, the specific effect of introducing this sequence on the signal transduction pathway leading to cell death remains unclear. In ADM-resistant pancreatic

Extravasation of a chemotherapeutic agent is one of the most frequent complications in cancer patients. Full-thickness skin necrosis often occurs after extravasation. Alternative approaches to treatment are local wound care, elevation, and hypothermia. It was shown that heparin prevents skin