vincristine/inflammation

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Sensory and inflammatory colonic changes induced by vincristine in distinct rat models of colitis.

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Preclinical and clinical studies show that gastrointestinal (GI) inflammation can evoke sensory changes occasionally far from the original inflammatory site. Animal models of colitis with either trinitrobenzenesulphonic acid (TNBS) or mustard oil (MO) produce distinct patterns of somatic and

Inflammatory breast cancer: enhanced local control with hyperfractionated radiotherapy and infusional vincristine, ifosfamide and epirubicin.

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Local control rate for inflammatory breast cancer (IBC) is < 50% with standard chemotherapy-radiotherapy regimen. Nineteen women (age range 40-65, median 50 years) with IBC (18 patients) or with a primary tumour of > 10 cm (one patient) received a novel treatment comprising hyperfractionated

Antiallodynic and anti-inflammatory effects of intrathecal R-PIA in a rat model of vincristine-induced peripheral neuropathy.

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There exists a limited number of studies investigating the correlation between spinal adenosine A1 receptors and Vincristine-induced peripheral neuropathy (VIPN). This study explored the role of intrathecal N6-(2-phenylisopropyl)-adenosine R-(-)isomer (R-PIA) in neuropathic pain

Vincristine-related neuropathy versus acute inflammatory demyelinating polyradiculoneuropathy in children with acute lymphoblastic leukemia.

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The objective of this study was to evaluate whether electroneurography could help in differentiating between vincristine-induced neuropathy and acute inflammatory demyelinating polyradiculoneuropathy. We performed electroneurography in 7 children from September 2006 to March 2009 admitted to receive

Nonsteroidal Anti-Inflammatory Drugs Prevent Vincristine-Dependent Cancer-Associated Fibroblasts Formation.

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Vincristine is used in the clinical treatment of colon cancer, especially in patients diagnosed in the advanced phase of cancer development. Unfortunately, similar to other agents used during antitumor therapy, vincristine might induce chemoresistance. Studies of this process focus mainly on the

Involvement of inflammatory mediators in neuropathic pain caused by vincristine.

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Elucidation of the mechanism of neuropathic pain caused by vincristine is required because long-term treatment with this anticancer agent often causes neuropathic pain. We refer to the involvement of inflammatory mediators in vincristine-induced neuropathic pain in this review. Several reports using

Protective effect of Acorus calamus L. in rat model of vincristine induced painful neuropathy: an evidence of anti-inflammatory and anti-oxidative activity.

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The study investigates the protective effect of Acorus calamus L. (AC) in vincristine-induced painful neuropathy. Vincristine (75μg/kg, i.p. for 10 consecutive days) was administered to induce painful neuropathy in rats. Various tests were performed to assess the degree of painful neuropathy at

Bergapten Ameliorates Vincristine-Induced Peripheral Neuropathy by Inhibition of Inflammatory Cytokines and NFκB Signaling.

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Bergapten, a furanocoumarin derivative found in a variety of medicinal plants, is documented to possess anti-inflammatory activity. However, whether bergapten is useful in alleviating the symptoms as well as the progress of peripheral neuropathy is not yet studied. The current investigation has been

Suppressing BRD4 exhibits protective effects against vincristine-induced peripheral neuropathy by alleviating inflammation and oxidative stress

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Vincristine (VCR) is a well-known anticancer drug, and frequently causes painful neuropathy and impairs the quality of life of patients. However, the molecular mechanisms revealing VCR-induced neuropathy are still unclear, and effectively therapeutic strategy is still necessary.

Inflammatory and Neuropathic Gene Expression Signatures of Chemotherapy-Induced Neuropathy Induced by Vincristine, Cisplatin, and Oxaliplatin in C57BL/6J Mice.

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Vincristine, oxaliplatin, and cisplatin are commonly prescribed chemotherapeutic agents for the treatment of many tumors. However, a main side effect is chemotherapy-induced peripheral neuropathy (CIPN), which may lead to changes in chemotherapeutic treatment. Although symptoms associated with CIPN

Potentiation of methotrexate-induced gastrointestinal toxicity by non-steroidal anti-inflammatory drugs (NSAIDs) and vincristine.

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Inhibition of intestinal nutrient absorption by the folate antagonist methotrexate (MTX) and the effects of several organic acid drugs and vincristine on MTX-induced gastrointestinal toxicity were investigated. Male Swiss-Webster mice received MTX, 25 mg/kg, i.p. once daily for 4 successive days.

Immune reconstitution inflammatory syndrome mimics a relapse of AIDS-related Burkitt lymphoma.

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Immune reconstitution inflammatory syndrome (IRIS) is associated with clinical manifestations that can overlap with the patients with acquired immunodeficiency disease (AIDS)-related non-Hodgkin's lymphoma. We herein report a case of AIDS-related Burkitt lymphoma which was successfully treated with

Vincristine-induced dermal toxicity is significantly reduced when the drug is given in liposomes.

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A problem associated with the intravenous delivery of vincristine concerns drug extravasation at the site of injection or infusion. This can result in extensive local soft-tissue damage. A new formulation of vincristine has recently been developed based on encapsulation of the drug in liposomes. The

Translation of TRAF1 is regulated by IRES-dependent mechanism and stimulated by vincristine.

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TRAF1 is a member of the TRAF family, which plays important roles in signal transduction that mediate cell life and death in the immune response, inflammatory and malignant diseases. It is known that TRAF1 transcription is inducible by various cytokines, but little is known about the regulation of

Protective effect of a specific PAF antagonist on vincristine-induced experimental retinopathy.

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The alkaloid vincristine displays considerable toxicity, particularly for the retina. This type of retinopathy being an inflammatory disease, we measured the effects of a new hetrazepine platelet activating factor antagonist, BN 50730, on a vincristine-induced retinopathy in the rat. Retinal

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