adriamycin/nekrosis

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Tumor necrosis factor receptor deficiency exacerbated Adriamycin-induced cardiomyocytes apoptosis: an insight into the Fas connection.

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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

Phospholipase C-delta1 is a critical target for tumor necrosis factor receptor-mediated protection against adriamycin-induced cardiac injury.

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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

Adriamycin sensitizes the adriamycin-resistant 8226/Dox40 human multiple myeloma cells to Apo2L/tumor necrosis factor-related apoptosis-inducing ligand-mediated (TRAIL) apoptosis.

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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

Sensitivity of resistant human tumor cell lines to tumor necrosis factor and adriamycin used in combination: correlation between down-regulation of tumor necrosis factor-messenger RNA induction and overcoming resistance.

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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

Amelioration of adriamycin skin necrosis: an experimental study.

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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

Experimental skin necrosis produced by adriamycin.

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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

Pain relief after free flap reconstruction in adriamycin necrosis on the dorsum of the hand. A case report.

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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.

Recall phenomenon or severe skin and muscle necrosis following Adriamycin extravasation in the hand.

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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

Synergism of Fas-mediated apoptosis and tumor necrosis factor on adriamycin cytotoxicity to transitional cell carcinoma.

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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

DMSO protects against adriamycin-induced tissue necrosis.

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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

Protection against adriamycin-induced skin necrosis in the rat by dimethyl sulfoxide and alpha-tocopherol.

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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

Therapeutic effects of liposomal adriamycin in combination with tumor necrosis factor-alpha.

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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

Endogenous tumor necrosis factor functions as a resistant factor against adriamycin.

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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

Augmented adriamycin sensitivity in cells transduced with an antisense tumor necrosis factor gene is mediated by caspase-3 downstream from reactive oxygen species.

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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

Effects of heparin fractions on the prevention of skin necrosis resulting from adriamycin extravasation: an experimental study.

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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

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