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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms behind tumour regression during ischaemic therapy of liver malignancy are not thoroughly elucidated. Ischaemia-reperfusion injury and release of free radicals is one mechanism suggested. The aim of the present study was to explore whether inhibition of hydroxyl radicals, by complex binding Fe with desferrioxamine (DFO), counteracted the retardation in tumour growth rate after HAL and whether DFO in itself had an effect on tumour growth in 2 experimental rat liver tumours. Rats with a hepatoma or an adenocarcinoma were subjected to HAL or to a sham procedure with or without additional injections of DFO daily for 2 or 7 days. HAL had an inhibitory effect on tumour growth rate. The effect of HAL was not counteracted by DFO, while DFO alone caused a decrease in tumour volume. There was an additive effect of DFO and HAL on tumour growth rate in both tumour systems. In vitro there was a growth inhibitory effect of DFO in both tumours, more pronounced in the hepatoma than in the adenocarcinoma. Our findings indicate that the effect of HAL is not mediated by release of oxygen free radicals. In the adenocarcinoma system, an additive effect of DFO and HAL was seen. As a rate-limiting enzyme for DNA synthesis is dependent on iron, depletion of iron can decrease mitotic activity, a mechanism that could explain the effect of DFO on tumour growth.
Int J Cancer 1995 Nov 15
PMID:Influence of hepatic artery occlusion and desferrioxamine on liver-tumour growth. 759 Dec 71

Arterial tumor embolization is a rare but serious complication of neoplastic disease. The majority of these tumors are associated with primary or secondary lung malignancies, originating from pulmonary vein metastasis or from an atrial mass. Malignant germ cell tumors primarily disseminate to the retroperitoneal lymph nodes and lung, and to the brain and liver later in the course of the disease. A germ cell tumor metastasis embolizing to the iliac-femoral arterial system has not yet been reported. We report a metastatic embolism in a patient with disseminated embryonal cell carcinoma causing acute limb ischemia, managed by surgical embolectomy. The sudden development of limb ischemia in a patient with a germ cell tumor should alert the physician to the possibility of tumor embolism.
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PMID:Acute limb ischemia due to malignant arterial embolism from a metastatic germ cell tumor. 760 99

Heat shock protein (HSP) synthesis is induced by hyperthermia and other types of stress in mammalian cells in vitro and in vivo. In the present report we describe that in human erythroleukemic cells, aspirin (400 microM), when administered during or immediately after a hyperthermic treatment, causes an increase in the amount of HSP70 synthesized and prolongs HSP70 synthesis for a period of several hours. This effect is not due to increased HSP70 mRNA stability. In the presence of aspirin, the heat shock transcription factor is maintained in the activated DNA-binding state for a period twice as long as control, an effect which results in enhanced and prolonged HSP70 mRNA transcription. A different cyclooxygenase inhibitor, indomethacin (10(-7) M), also provokes similar effects. The modulation of the heat shock response by aspirin and indomethacin is associated with the ability of these drugs to potentiate the effect of hyperthermia and prolong thermotolerance for a period of 48 h. These results indicate that the use of aspirin and indomethacin should be carefully monitored in cancer patients undergoing hyperthermic treatment. On the other hand, the ability of aspirin to enhance HSP70 synthesis suggests that nonsteroidal anti-inflammatory drugs could potentiate the cytoprotective role of HSPs in pathological states, including fever, inflammation, and ischemia.
Cancer Res 1995 Oct 01
PMID:Aspirin enhances thermotolerance in human erythroleukemic cells: an effect associated with the modulation of the heat shock response. 767 Dec 59

Cells from all organisms have developed a remarkable number of strategies to deal with adverse changes in their environment. One of these protective mechanisms is the heat shock response, or stress response, characterized by the extremely rapid increased expression of a selected group of proteins--the heat shock proteins (hsp)--after a sudden increase in the normal cellular growth temperature. The same response takes place when cells are subjected to a wide variety of other stressors: a) environmental assaults: exposure to heavy metals, alcohols, inhibitors of energy metabolism, amino acid analogues; b) states of disease: ischemia, oxidative injury, infectious diseases, immunity disorders and malignancy. On the other hand, some hsp are believed to play an important role in protein maturation steps and in cellular development and differentiation. The understanding of stress response is still incomplete but the promise of its medical applications for fighting against ischemia, infection, immunity diseases and cancer is clearly on the horizon.
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PMID:[Stress proteins]. 771 18

The lung is particularly exposed to various inhaled toxic products whose toxicity can be at least partly mediated by the generation of free radicals. Oxidants burden can also result from lung metabolism of xenobiotics or from activation of phagocytes. Free radicals are mainly derived from an univalent sequential reduction of molecular oxygen. Mitochondria is the main location of intracellular production which may also result from auto-oxidation of small molecules or function of some enzymes. To prevent the deleterious effects of free radicals produced by normal metabolism, cells are equipped with an antioxidant system composed of enzymes (superoxide dismutase, catalase, glutathione peroxidase) and non enzymatic substances such as glutathione, iron chelators, vitamin E and C, ceruleoplsamin). Targets of free radicals toxicity are phospholipids by initiation of lipid peroxidation, proteins which may be activated or inactivated via oxidation of sulfhydryl residues. Another target is DNA with possible strand breaks or mutation. Transcription activities can be also altered and it has been recently reported that some transcription factors such as NF-kB can be activated by oxidants. Under these circumstances free radicals may be considered as second messengers. Lung oxygen toxicity has been largely studied. Oxygen-induced lung lesions are non specific. It is possible to induce a resistance to 100% O2 by the pre-exposure of animals to 85% O2. This tolerance phenomenon is associated with an increased lung content in antioxidant substances. The mechanisms of gene regulation of antioxidant enzymes are still poorly understood in eukaryotes. Overproduction of free radicals in the lung is also involved in various clinical settings such as ischemia-reperfusion, exposure to ozone or NO2, acute respiratory distress syndrome, drug induced lung toxicity, pathogenesis of COPD, asthma, cancer and ageing. The precise role of free radicals among other mechanisms of lung injury is still unclear. A better knowledge of free radicals mechanisms of toxicity and of antioxidant regulation is needed to develop antioxidant therapeutic strategies.
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PMID:[Free radicals and respiratory pathology]. 773 56

The FMRFamide-related peptides F1 and F2, originally isolated from lobster pericardial organs, have been shown to exert cardioexcitatory effects on isolated or semi-isolated crustacean hearts. The present study sought to determine the in vivo effects of F1 and F2 on cardiac and circulatory performance of Cancer magister using a pulsed-Doppler technique. In general the effects of F1 and F2 were similar; however, F1 was more potent and its effects were of longer duration than those exerted by F2. Infusion of either F1 or F2 caused a decrease in heart rate and subsequent periods of acardia. These decreases in rate occurred concurrently with a short-term increase in stroke volume of the heart, followed by a longer-term decrease in stroke volume. Hemolymph flow rates through the anterior aorta, anterolateral arteries, sternal artery, and posterior aorta also showed the same trend, with an initial short-term increase in flow rate followed by a longer-term decrease with periods of ischemia. Hemolymph flow through the paired hepatic arteries simply decreased, but recovery to pretreatment levels was faster than in the other arterial systems. Threshold for these responses occurred at circulating concentrations between 10(-9) mol.l-1 and 10(-8) mol.l-1 for F1 and somewhat higher, between 10(-8) mol.l-1 and 10(-7) mol.l-1, for F2.
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PMID:The FMRFamide-related peptides F1 and F2 alter hemolymph distribution and cardiac output in the crab Cancer magister. 774 90

Tamoxifen is the anti-estrogen the most widely used in breast cancer. The duration of its prescription, as adjuvant treatment, tends to increase (5 years, and even more) and now it is used in chemoprevention. A slight increase of thromboembolic complications was noted in some studies. This article evaluates the frequency of thromboembolic accidents (TEA) in 441 postmenopausal patients treated by an association of conservative radiosurgery, tamoxifen +/- chemotherapy, for a breast carcinoma T0, T1T2 < 4 cm. Nineteen patients (4.3%), all in remission, presented a TEA, between 1 and 44 months after the beginning of the tamoxifen treatment. We observed seven pulmonary embolisms (PE), 11 deep venous thromboses (DVT) and an acute arterial ischemia. Two patients aged 74 and 80 years died, the others had a favourable evolution under anticoagulant treatment. Among these 19 patients, six presented known risks factors (phlebitis, cardiovascular disorders) and ten had a "favouring circumstance" aggravating the risk of TEA (surgical operation, severe infection, fracture). Their median age was 65 years (61 for all the 441 patients). We noted eight cases of breast lobular cancer (42%) among these 19 patients (11% for all the patients). Among postmenopausal patients, the indication of tamoxifen must be evaluated according to the benefits expected in those with high risk factors of TEA (history of heart failure, obesity, spread varix, age > 65 years). In case of DVT and/or PE, this treatment seems contra-indicated. In case of "favouring circumstances", a hypocoagulant or systematic anticoagulant treatment must be proposed. In case of combined chemotherapy, it is better to start tamoxifen at the end of the treatment. These simple prophylactic measures should allow to reduce significantly the risk of TEA in postmenopausal patients with adjuvant anti-estrogenotherapy.
Bull Cancer 1995 Jan
PMID:[Thromboembolic accidents in postmenopausal patients with adjuvant treatment by tamoxifen. Frequency, risk factors and prevention possibilities]. 774 16

The nitroxides are stable, low molecular weight free radical compounds which are freely membrane permeable. These properties make the nitroxides valuable for the study of and possible protection against oxidative stresses. It is becoming increasingly clear that oxidative stress is important to the pathogenesis of cancer as well as to the development of treatments for cancer. Several nitroxides have been shown to interrupt the toxicity of oxidative stress with the protection against H2O2 toxicity and possibly ischemia/reperfusion injury being of primary importance. With respect to radiation, the nitroxides have afforded both in vitro and in vivo protection. The redox activity of the nitroxides may allow for the differential activity of these agents in normal versus tumor tissues. Further study of these compounds may yield a nitroxide with clinical applications as well as provide insight into the mechanisms of radiation cytotoxicity. Finally, the nitroxides have allowed us to explore the mechanisms of action of several chemotherapeutic agents. Understanding these processes is important to the process of ameliorating the toxicity of therapies and to the rationale design of future agents.
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PMID:New directions for free radical cancer research and medical applications. 777 Dec 56

Cardiac toxicity was first noted in patients receiving Taxol during continuous cardiac monitoring, which was performed because of the high incidence of serious hypersensitivity reactions noted early in phase I trials. After cardiac events were documented, patients with cardiac disease and those on medications known to alter cardiac conduction were excluded from most trials. The cardiac events reported with Taxol from the initiation of NCI-sponsored clinical trials through August 1992 are summarized. Adverse cardiac events were reviewed in four clinical databases: 1) the Cancer Therapy Evaluation Program's Adverse Drug Reaction database following treatment of more than 3400 patients; 2) all cardiac toxicities in patients on GOG-111 who were randomized to cisplatin plus either Taxol or cyclophosphamide; 3) cardiac toxicity in 198 patients who received 618 courses of Taxol with or without cisplatin during continuous cardiac monitoring; and 4) cardiac toxicities reported for the first 696 patients on NCI TRC-9103 for ovarian cancer. Published reports of studies of taxine's cardiac effects, and of cardiac toxicity associated with yew poisoning, Cremophor EL, and H1 and H2 antagonists, are also reviewed. In patients without significant cardiac risk factors, asymptomatic sinus bradycardia is frequent (approximately 30%). Heart block and conduction abnormalities occur infrequently and are often asymptomatic. The casual relationship of Taxol to atrial and ventricular arrhythmias and cardiac ischemia is less clear because many patients had other conditions known to be associated with cardiac events. Nevertheless, the incidence of serious cardiac events was low. Routine cardiac monitoring is not required for patients without risk factors. There are, however, insufficient data to make treatment recommendations for patients with cardiac disease and those taking medications that alter cardiac conduction. To maximize patient safety and the clinical database, physicians who administer Taxol should continue to be alert to potential cardiac toxicities associated with Taxol.
J Natl Cancer Inst Monogr 1993
PMID:A reassessment of cardiac toxicity associated with Taxol. 791 18

The effect of ischemia-reperfusion, induced by the transient embolic agent degradable starch microspheres (DSMs) on tumor tissue was investigated from the standpoint of active oxygen species. Rabbits with VX2 carcinoma received regional infusion of DSMs by transcatheter angiography, and it was confirmed that DSMs occluded tumor vessels. Blood flow in the tumors decreased rapidly immediately after the DSM treatment and returned to the original level within 40 min. The size of tumors did not change after a single infusion of DMS, while five repeated DSM treatments led to a significant reduction in tumor size. This reduction in tumor size was prevented by the treatment of rabbits with superoxide dismutase and catalase, indicating that the generation of active oxygen species in the tumor was involved in the mechanism of action of DSMs. Thiobarbituric acid-reactive substances also increased in the tumors after DSM infusion, and this increase was also inhibited by treatment with superoxide dismutase and catalase. In conclusion, the antitumor effect of the transient embolic agent DSM is secondary to the phenomenon of ischemia-reperfusion injury. In addition, active oxygen species and lipid peroxidation are possible causes of ischemia-reperfusion injury.
Cancer Res 1994 Oct 01
PMID:Antitumor effect of ischemia-reperfusion injury induced by transient embolization. 792 11


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