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mitomycin c/nekrose

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Fanconi anemia C protein acts at a switch between apoptosis and necrosis in mitomycin C-induced cell death.

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Deregulation of apoptosis seems to be a hallmark of the Fanconi anemia (FA) syndrome. In order to further define the role of the FA protein from complementation group C (FAC) in apoptosis, we characterized parameters modified during the mitomycin-C (MMC)-induced apoptotic program. It is shown that

Hyperbaric oxygen therapy for mitomycin C-induced scleral necrosis.

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Intraoperative or postoperative use of mitomycin C is one of the treatment options to reduce the recurrence of pterygia. Scleral necrosis, a potentially blinding complication after mitomycin C use, has been among great concern in ophthalmic practice. A patient is presented in whom scleral necrosis

[Bladder necrosis after an immediate post-operative mitomycin C instillation].

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Administration of intravesical chemotherapy by mitomycin C decreases the risk of recurrence in non-muscle-invasive bladder tumours. We report the case of a man, who presented a full bladder necrosis after an immediate adjuvant mitomycin C instillation. The failure of resection of the necrotic area

Kidney cortical necrosis induced by mitomycin-C: a morphologic experimental study.

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Experimental studies on mitomycin-C nephrotoxicity are scanty and mention the occurrence of cortical hemorrhage, tubular necrosis, or hydronephrosis secondary to papillomatous hyperplasia of the uroepithelium. To our knowledge, only one experimental study has mentioned morphological lesions similar
The instillation of chemotherapeutic agents after transurethral resection of bladder tumor as an adjuvant treatment in bladder tumors is accepted as being safe if there is no associated bladder perforation. Mitomycin C (MMC) is a widely used agent for the adjuvant treatment of bladder tumors. A
OBJECTIVE To validate the methodology of isolated hypoxic hepatic perfusion (IHHP) using balloon catheter techniques and to gain insight into the distribution of tumor necrosis factor-alpha (TNF), melphalan, and mitomycin C (MMC) through the regional and systemic blood compartments when applying
BACKGROUND Addition of tumour necrosis factor-alpha (TNF) to hypoxic abdominal perfusion (HAP) and hypoxic pelvic perfusion (HPP) with chemotherapeutic agents for treatment of un-resectable malignancies may lead to similar enhanced anti-tumour effects as are observed when TNF is added to isolated
OBJECTIVE The majority of patients with juvenile idiopathic arthritis-related uveitic glaucoma require surgery to control intraocular pressure. Trabeculectomy with mitomycin C (MMC) is a major treatment option, although both chronic inflammation and young age increase risk of filtration failure.

Hyperbaric oxygen therapy for mitomycin C-induced scleral necrosis.

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Intraoperative or postoperative use of mitomycin C is one of the treatment options to reduce the recurrence of pterygia. Scleral necrosis, a potentially blinding complication after mitomycin C use, has been among great concern in ophthalmic practice. A patient is presented in whom scleral necrosis

Delayed tissue necrosis due to mitomycin C.

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We report about a patient having received intravenous mitomycin C without evidence of tissue injury until three months following its extravasation. After drinking alcoholic beverages 3 months later he developed a severe ulcer at the site of the previous extravasation. There are only a few reports

Intra-arterial infusion of mitomycin C in treatment of breast cancer: occurrence of skin necrosis in irradiated patients.

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Eight previously irradiated breast cancer patients with local recurrences were treated with intra-arterial infusions of 8 mg/m2 mitomycin C given at 3-week intervals. The mean time interval between radiotherapy and intra-arterial chemotherapy was 38 months (range 2-60). In five cases a temporary

Delayed tissue necrosis associated with mitomycin-C administration.

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Necrosis of the glans penis: a rare complication of intravesical therapy with mitomycin c.

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Chemotherapy amplifies production of tumor necrosis factor.

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Several chemotherapeutic agents exert cytotoxicity through the generation of reactive oxygen species (ROS), and our laboratory has shown that ROS increase tumor necrosis factor (TNF) production. Therefore, we hypothesized that cis-dichlorodiammine platinum (CDDP), mitomycin-C, and doxorubicin

Reversal of lethal, chemotherapeutically induced acute hepatic necrosis in rats by regenerating liver cytosol.

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In this report we further evaluate the role of regenerating liver cytosol (RLC) as a stimulator of hepatic regeneration by assessing its effect on survival, liver function, and hepatic regeneration in a model of in vivo isolated perfusion of the rat liver with high concentrations of cytotoxic drugs
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