Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-one consecutive patients with testicular cancer treated with bleomycin, vinblastine, and cisplatin (PVB) were evaluated for acute vascular ischaemic events during chemotherapy. Angina pectoris occurred in 8/21 (38%) patients, a median 5.6 weeks after initiation of chemotherapy and persisted for 2-7 days. Raynaud's phenomenon was detected in seven (33%) subjects, transient ischaemia of the toes was found in six (29%) patients, one patient complained of migraine, but none had major cerebrovascular accidents. Patients with and without angina pectoris and/or Raynaud's phenomenon did not differ in respect of age, histology of tumor or medication. Ischaemia occurred at any time during the course of chemotherapy. No correlation was found between dosage of drugs and time of onset of ischaemic reactions. However, arterial occlusive event is a frequent and common toxicity and a result of treatment with PVB.
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PMID:Acute vascular toxicity after combination chemotherapy with cisplatin, vinblastine, and bleomycin for testicular cancer. 245 30

A case of pituitary apoplexy causing pituitary hemorrhage with extension into the third ventricle is reported. The patient was a 73-year-old, obese female admitted with sudden onset of vomiting and impaired consciousness. Neurological examination revealed that she was stuporous, with marked neck stiffness and a dilated left pupil. A plain skull X-ray showed sellar enlargement and destruction of the dorsum sellae. Computed tomography demonstrated a high-density area in the third and lateral ventricles and a round, high-density mass in the suprasellar cistern. The patient died the next day. Autopsy revealed a large tumor in the sellar and suprasellar areas. The tumor and the hematoma within it compressed the floor of the third ventricle and passed through the lamina terminalis and the hypothalamic region. Histological examination disclosed a basophilic adenoma. The pituitary hemorrhage appeared to be the result of ischemia and necrosis within the pituitary adenoma caused by its acute expansion. The extension of the hematoma into the third ventricle was attributable to the large size of the tumor and its close adhesion to the floor of third ventricle.
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PMID:[Pituitary hemorrhage extending into the third ventricle. Case report]. 248 40

Mesenteric ischemia associated with carcinoid tumors often presents with nonspecific abdominal pain and is usually due to mesenteric branch artery occlusion caused by elastic vascular sclerosis. Mesenteric ischemia was defined by the operative findings of cyanosis or infarction. Eleven patients with intraabdominal metastatic carcinoid tumor were evaluated by angiography. Angiographic narrowing and occlusion of multiple peripheral jejunal and ileal intramesenteric branch arteries was present in 3 patients with mesenteric ischemia, but also occurred in 5 of 8 patients without mesenteric ischemia. Other angiographic abnormalities included staining of the primary tumor (5) or metastases (6), tenting of small mesenteric vessels (5), and occlusion of draining mesenteric veins (2). We conclude that in patients with midgut carcinoid tumors, angiographic narrowing and occlusion of peripheral mesenteric arteries most likely represents elastic vascular sclerosis, is indicative of mesenteric invasion of tumor, but correlates poorly with the presence of ischemia in the subtended bowel. Alternatively, a normal selective arteriogram should exclude mesenteric ischemia as the cause of abnormal pain.
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PMID:Limitations of angiography for mesenteric ischemia caused by midgut carcinoid tumors. 250 47

Ischemia may invalidate hormone-receptor analyses. This study determined the effects of progressive ischemia on steroid hormone-receptor analyses. Breast cancer was induced in 50- to 60-day-old female Holtzman rats by intragastric administration of 25 mg of 7,12-dimethylbenz[a]anthracene. After 90 days, rats were anesthetized and breast tumors were devascularized in vivo. At 0, 30, 60, 90 and 150 minutes, a biopsy specimen from each tumor was taken and rapidly frozen. Steroid binding capacity for estrogen (ER), progesterone (PR), and androgen (AR) receptors was determined by incubation with tracer receptor ligand. Ischemia decreased ER and AR levels by 30 minutes, whereas PR levels were unchanged through 150 minutes of ischemia. Following mastectomy, tylectomy, or breast biopsy, PR may be the most reliable of the hormone receptors for determining endocrine-responsive breast cancer. However, for accurate determination of all hormone receptors, specimens should be frozen in liquid nitrogen immediately, then preserved at -70 degrees C, or processed immediately.
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PMID:Lability of steroid hormone receptors following devascularization of breast tumors. 253 31

Diffuse carcinomatous leptomeningeal metastases "carcinomatous meningitis") have the usual clinical course involving multifocal nerve root deficits and a variable diffuse encephalopathy. In contrast, we describe a patient with carcinomatous leptomeningeal metastases who presented with clinical signs of meningitis and focal cerebral infarction. Over an 8-month period, multiple cerebral infarctions and cranial neuropathies developed. Postmortem examination of the patient's brain revealed diffuse leptomeningeal infiltration by a signet-ring adenocarcinoma. The extensive involvement of the subarachnoid space with tumor was associated with dense neoplastic infiltration of the Virchow-Robin spaces. These perivascular tumor infiltrates were accompanied by multifocal mural invasion and, less frequently, by intravascular tumor cells obliterating the lumen. Focal hemorrhagic infarcts in the cerebral cortex corresponded to areas of microscopic vasculopathy. This case provides evidence that tumor-associated vasculopathy with resultant ischemia plays a role in the pathogenesis of focal cerebral infarctions in carcinomatous leptomeningeal metastases.
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PMID:Focal cerebral infarctions associated with perivascular tumor infiltrates in carcinomatous leptomeningeal metastases. 255 69

Magnetic resonance (MR) methods have been used to study the metabolic and vascular response of model tumors to tumor necrosis factor (TNF). Magnetic resonance measurements demonstrated acute reductions in tumor blood flow, measured from tumor uptake of D2O, and in tumor adenosine triphosphate (ATP), measured by 31P magnetic resonance spectroscopy (MRS) following administration of TNF. The decrease in ATP generally followed reduction in tumor blood flow, and therefore was probably due to ischemia caused by damage to tumor vasculature. Superficial human tumors have been studied by MRS to characterize their 31P spectra, and to measure metabolic changes during therapy. The ratio of the intensities of the phosphomonoester (PME) and ATP resonances (PME/ATP) was much higher in tumors than in the normal tissue displaced by the tumors. During therapy, decreases in PME/ATP were detected that paralleled, but did not anticipate, decreases in tumor size. In some cases, a transient increase in PME/ATP was detected during therapy, which did not correlate with changes in tumor size, and which may reflect stimulation of cell growth in some tumor zones.
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PMID:Response of tumors to therapy studied by 31P magnetic resonance spectroscopy. 260 30

Cell injury proceeds through a predictable series of stages as it progresses from reversible to irreversible injury (or "point of no return") and ends eventually in cell death. Ion deregulation is strongly implicated in this process and, in particular, the deregulation of cytosolic Ca2+ ([Ca2+]i) which is thought by most to be a critical step in the transition from reversible to irreversible injury. [Ca2+]i is normally maintained at approximately 100 microM, a level 10,000 times lower than for extracellular Ca2+ [( Ca2+]e). Deregulation may affect any of three Ca2+ buffering systems: the plasma membrane, the mitochondria, and the endoplasmic reticulum. Perturbation of [Ca2+]i is intimately related to perturbation of other ions, including, H+, Na+, and K+. In normal cells, [Ca2+]i elevation is also linked to activation of oncogenes as well as cell division, initiation, wound repair, differentiation, and possibly tumor promotion. In all models of acute injury for which we have measured [Ca2+]i, including ischemia, HgCl2 and calcium inophores, [Ca2+]i always became elevated. This elevation results from influx of [Ca2+]e (ionomycin), redistribution from intracellular stores (NEM, KCN), or from both sources (HgCl2). The degree of [Ca2+]i elevation is correlated with the degree of injury (as determined by blebbing and morphological changes) and cell killing. More recently, much work has been focused on the role of [Ca2+]i in neoplasia. Many stimuli, including the promoter TPA and transforming growth factor beta have been shown to affect normal and transformed cells differently. Both cause differentiation in normal human bronchial epithelial cells but stimulate growth in transformed cells. We propose that deregulation of ions, especially [Ca2+]i, plays an important role, if not a key role, in the initiation of acute and chronic cell injury, including neoplasia. Increases in [Ca2+]i appear to accelerate degradative processes and, unless regulated, lead to cell death.
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PMID:The relationship between cellular ion deregulation and acute and chronic toxicity. 264 22

The use of hepatic artery ligation or permanent dearterialization as the sole procedure for the palliation of patients with malignant hepatic tumors has no proved value. The combination with cytotoxic drug administration via the portal route may offer some advantage. The use of transient dearterialization with one longer ischemic period has been successful in the treatment of metastatic carcinoid disease with carcinoid syndrome but ineffective in the treatment of other hepatic tumors. New knowledge of the effects of transient ischemia on the formation of arterial collaterals and the pathophysiologic mechanisms in cellular injury has led us to further refinement of this therapeutic principle. The first results of repeated short periods of ischemia are promising and give some hope for the future palliation of this group of tumor patients.
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PMID:Status of ischemic therapy for hepatic tumors. 264 21

PAF is a phospholipid formed from the action of phospholipase A2 upon cellular membranes in response to immunologic or hypoxic stimuli. PAF does not exist in its active form as a storage product within cells, but is synthesized rapidly after phospholipase A2 activation. A potent lipid released by multiple cell types in mammalian systems, the emerging perspective is that PAF is a major endogenous mediator influencing the pathogenesis and outcome of ischemia and conditions of circulatory shock. These effects appear to be especially relevant to the syndrome of MSOF during critical illness. All of the major criteria for validation of a shock factor have been fulfilled for PAF. First, PAF has been measured in biological fluid of animals during shock states, although this is not an easy task since PAF is formed in minute amounts and is rapidly metabolized. Nevertheless, combinations of high pressure liquid chromatography (HPLC) and bioassay methods employing washed rabbit platelets have been successfully utilized in this regard. Second, synthetic PAF has been injected into cell suspensions, isolated tissues, and live animals, where it produces most of the effects attributed to endogenous PAF released by immunologic or hypoxic stimuli. These studies have shown that PAF exerts a variety of pathophysiologic actions, including (1) cardiodepression (that is, a negative inotropic effect), (2) reductions in systemic blood pressure, (3) leakage of fluid from the microvasculature, (4) bronchoconstriction, and (5) platelet aggregation. All of these actions of PAF can initiate or exacerbate shock and ischemic injury in multiple organ systems. Third, specific PAF receptor antagonists have been found to markedly attenuate the severity of endotoxic, anaphylactic, hemorrhagic, and traumatic shock, as well as acute myocardial ischemia. In all these conditions, a variety of PAF receptor antagonists (including PAF analogues and structurally dissimilar substances) have improved survival and have retarded pathophysiologic processes believed to be important in causing tissue injury. These processes include lysosomal membrane damage and proteolysis. Moreover PAF receptor antagonists attenuate the release of secondary toxic factors in shock, such as myocardial depressant factor. Thus, administration of specific PAF receptor antagonists early in the course of circulatory shock and organ ischemia may prove to be useful therapeutic agents in a variety of life-threatening disorders. In addition to having direct actions, PAF appears to function as a pivotal agent in a chain of mediators producing tissue injury. Recent evidence suggests that tumor necrosis factors (i.e., cachectin) stim
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PMID:Induction of tissue injury and altered cardiovascular performance by platelet-activating factor: relevance to multiple systems organ failure. 265 Aug 21

Several of the features of magnetic resonance imaging (MRI) are advantageous for diagnostic examination of the musculoskeletal system. For example, the excellent depiction of bone marrow makes it a very sensitive method for identifying trauma, tumor, ischemia and infection of the marrow space. In addition, the high-contrast discrimination of soft tissues and the ability to make thin-section images in any plane allows for the depiction of abnormalities involving the muscles, ligaments, tendons, and neurovascular structures. The major disadvantages are the nonspecificity of many of the findings, the high cost of examinations, and the limited number of available MRI units. MRI is most appropriately utilized when it can be expected to provide diagnostic information not available from less-expensive noninvasive diagnostic methods and when the results of the examination may significantly affect patient management. To get the most out of the examination, it should be performed and interpreted with knowledge of clinical findings and results of other imaging tests, especially plain roentgenograms. To date, MRI has proved to be most useful for the evaluation of the spine, shoulder, hip, and knee.
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PMID:Magnetic resonance imaging of the musculoskeletal system. An overview. 266 85


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