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)

At St. Joseph's Hospital in 1970 and 1971, 100 patients with invasive ductal adenocarcinoma of the breast were analyzed, retrospectively. Microscopic review of the original tumor was conducted in order to determine histologic grade, degree of circumscription and the presence of vascular or lymphatic invasion, or both. Clinical characteristics of the patients were obtained from patient charts and survival determined through follow-up study at St. Joseph's Tumor Registry. When patients were grouped according to the criteria already mentioned, survival time could be predicted with a degree of accuracy similar to the standard criteria of tumor size and nodal involvement. Specifically, patients in whom tumors had no adverse histologic criteria (that is, low grade, well circumscribed and no vascular or lymphatic invasion) had a 73 per cent ten year survival rate, while those with three adverse criteria (high grade, poorly circumscribed, with lymphatic invasion) had a 33 per cent ten year survival rate. Similarly, 14 per cent of the patients without any adverse histologic criteria had nodal involvement, while 44 per cent of those patients with any adverse criteria proved to have positive nodes. It is suggested that the evaluation of the criteria described provides the surgeon with a reliable means of predicting survival time, based upon the results of the original specimen taken at biopsy. The use of these histologic characteristics has significant potential as it relates to the planning of both primary and adjuvant therapy, based upon evaluation of the specimen. Currently, it should be used in conjunction with axillary dissection and determination of nodal involvement. With further refinement and confirmation of these findings, the potential exists for accurate prognostication prior to axillary dissection.
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PMID:Tumor histology as a prognostic determinant in carcinoma of the breast. 632 Apr 81

Various anticoagulant were assessed in order to develop a transport media for bovine blood which would improve leukocyte stability. The effects of time, disease in the donor and different personnel and laboratory equipment were also tested. The transport media most effective for leukocyte stability was found to be Titriplex IV. This is a modification of Titriplex I by the inclusion of acetylsalicyclic acid to prevent cellular clumping and by the removal of methylene blue. Anticoagulant citrate dextroseformalin-ASA performed equally well for transport but cellular morphology was impaired. Febrile or neoplastic disease in the donor animal did not alter the efficiency of the formalin containing anticoagulants.
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PMID:An anticoagulant for transport of bovine blood. 677 30

Aspirin and indomethacin, administered systemically by oral route, were found to delay the development of hamster buccal pouch epidermoid carcinomas induced by thrice weekly topical applications of a 0.5 percent solution of 7,12-dimethylbenz(a)anthracene (DMBA) in mineral oil. Forty male and female Syrian hamsters (Mesocricetus auratus) were divided into four equal groups. In Group 1 animals the left buccal pouch was painted thrice weekly with DMBA. Group 2 animals were painted thrice weekly with DMBA and received 12 mg. aspirin daily by oral route. Group 3 animals were painted thrice weekly with DMBA and received 1 mg. indomethacin daily by oral route. Group 4 animals were maintained as untreated controls. Two animals in each of the four groups were killed with ether at 8, 10, 12, 13, and 14 weeks after the start of the experiment. At the time of sacrifice the buccal pouches were photographed and the average number of tumors and the average size of tumors in each group were noted. The left and right buccal pouches were dissected, fixed in 10 percent formalin, sectioned in paraffin, and stained with hematoxylin and eosin. Autopsies were also performed on each animal. Both left and right buccal pouches and major organs were studied histologically. Both aspirin and indomethacin in the dosages used were found to delay DMBA buccal pouch carcinogenesis. A suggested mechanism of action is the inhibition of prostaglandin synthesis by the role of both aspirin and indomethacin as inhibitors of prostaglandin synthetase. Indomethacin appeared to exert a greater tumor-inhibiting effect than aspirin in the dosages used.
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PMID:Delay in hamster buccal pouch carcinogenesis by aspirin and indomethacin. 679 84

The Baumgartner perfusion apparatus has been applied to the study of the interaction of platelets and tumor cells and their attachment to subendothelial structures. Cells derived from an anaplastic murine tumor (Hut 20 line) induced platelet aggregation and were included in platelet thrombi that deposited on vascular subendothelium in perfusion experiments with heparinized human blood. In contrast, perfusion of blood samples containing cells from a line derived from a human epithelial carcinoma of the lung (A549 line), which did not interact with platelets, resulted in the deposition of platelets alone, with no tumor cells or blood cells other than platelets being observed in the thrombus. Extremely large platelet-tumor cell thrombi were found at the vascular surface in Hut 20 perfusions using vessel segments which had been treated with alpha-chymotrypsin. These large heterogeneous thrombi perturbed blood flow through the system and entrapped both erythrocytes and white cells. In order to quantitate the deposition of tumor cells, Hut 20 cells were labeled with 125I-deoxyuridine and perfused in whole blood at a concentration of 3.7x10(5)/ml. Tumor cell incorporation into platelet-tumor cell thrombi on chymotrypsinized segments yielded about 30,000 cpm/mg of vascular tissue but this value was reduced some 2 orders of magnitude by the inclusion of PGE1 (1 ng/ml of perfusing blood; 2.8 microM) in parallel samples. Aspirin at 100 microM reduced tumor cell-dependent platelet aggregation but did not decrease the platelet-dependent deposition of radiolabeled Hut 20 cells on vascular subendothelium, suggesting the release reaction may not be of major significance in this interaction. Tumor cell-induced platelet aggregation was not observed in a perfusion experiment using blood from a patient with severe von Willebrand's disease. However addition of 0.1 vol of ABO-compatible, heterologous plasma as a source of factor VIII to the von Willebrand blood sample restored the platelet-dependent deposition of radiolabeled tumor cells to control values.
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PMID:The use of a perfusion model for studying aggregation and attachment of platelets and tumor cells at subendothelial surfaces. 711 4

The influence on transpulmonary passage by an inhibitor of platelet aggregation, aspirin, and/or anabolic steroid, (Nandrolone decanoate), was investigated in syngeneic CBA mice. An increase of extrapulmonary metastases was used as a measure of increased redistribution of tumor cells from lungs to other organs. Aspirin alone did not reduce metastasis formation in lungs and did not significantly increase transpulmonary passage of tumor cells. The anabolic steroid increased the metastasis crop only in the lungs. However, treatment with the two compounds together increased the metastases in lungs and extrapulmonary organs. The results disclosed that in this system inhibition of platelet aggregation did not reduce metastasis formation but in combination with another drug, an anabolic steroid, it increased the number of experimental metastases.
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PMID:Influence of aspirin and/or anabolic steroid (nandrolone decanoate) on experimental metastasis formation. 734 91

The effect of non-steroidal anti-inflammatory drugs (NSAIDs), acetylsalicylic acid (commonly known as aspirin), salicylic acid, piroxicam and indomethacin on the growth of rat glioma cells (RG 2) in vitro and aspirin in vivo was studied. The in vitro studies reveal that aspirin and salicylic acid strongly inhibit growth of rat glioma (RG 2) cells in concentrations used in medicine for treatment of rheumatic diseases. On the other hand, indomethacin and piroxicam had no effect, indicating that the inhibitory effect on tumor growth is not due to the inhibition of prostaglandin synthesis. The synthesis of ATP was markedly reduced (34% of control) in the presence of drugs, whereas protein synthesis measured as 3H-leucine incorporation was slightly more inhibited (73% of control) than cell growth. Aspirin administered to Fischer 344 rats inhibited growth of RG 2 cells inoculated into the caudate nucleus in vivo, both when administered the day before inoculation of tumor cells and when tumors had formed, i.e. 5 days post inoculation.
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PMID:Growth inhibition of rat glioma cells in vitro and in vivo by aspirin. 756 4

Analgesic nephropathy has long been considered a potentially preventable cause of renal disease. Early reports were described in patients who consumed analgesics containing phenacetin. In recent data, the removal of phenacetin from analgesic preparations resulted in a reduction in analgesic-induced end stage renal disease in Europe and Australia. However, a reduction in the incidence of analgesic nephropathy has not occurred uniformly, suggesting that phenacetin is not the sole cause. Current data raise concerns regarding adverse renal effects of acetaminophen and nonsteroidal antiinflammatory drugs. Aspirin taken alone may be of least concern. The diagnosis of analgesic nephropathy is suggested in subjects with chronic renal failure, a history of daily consumption of analgesic preparations, small bumpy kidneys, and renal papillary necrosis or chronic interstitial nephritis. However, the spectrum of disease may be changing, because these agents also may increase the risk of cardiovascular disease and chronic renal disease due to nephrosclerosis, glomerulonephritis, and diabetes mellitus. Potential pathogenetic mechanisms in analgesic nephropathy include direct cellular injury induced by analgesics, prostaglandin inhibition with reduction or redistribution of renal blood flow, and interesting new concepts regarding the role of caffeine in increasing oxygen demand and reducing oxygen supply in the medulla. The primary goal of therapy is discontinuation of analgesic consumption. Because of the association between analgesic intake and uroepithelial tumors, surveillance of patients for neoplasm is suggested.
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PMID:Case report: analgesic nephropathy: a soda and a powder. 757 21

A clinical study was started in order to examine the suitability of the Thrombostat (in vitro bleeding test) (IVBT) as a diagnostic tool to prevent perioperative bleeding due to aspirin (ASA) and/or platelet function disorders of other origins. This report is based on preliminary data. Eighty three patients who had ingested ASA in the last two weeks and/or with a history of bleeding and/or documented hemorrhagic disorders requiring distinct urological operations, were included in the study. In all patients the IVBT with CaCl2, in addition to common coagulation tests, were performed. Thirteen patients stopped ASA ingestion until IVBT became normal and did not show any increased bleeding tendency. The residual patients were classified by the various operations. The following operation groups were formed: Male genitals (n = 11), inguinal/suprapubic operations (n = 7), transurethral tumor resections of the bladder (TURB) (n = 17), transurethral prostate resection (TURP) (n = 12), tumor nephrectomy (n = 8), radical prostatectomy (n = 9). Thirty six patients with a history of ASA use, but normal IVBT, served as control group (C). Thirty one patients with a history of ASA ingestion had normal in vivo bleeding times (BT) and abnormal IVBT with CaCl2 (A). Seven patients had a bleeding history and/or documented hemorrhagic disorders (B). None of the patients (A) with abnormal IVBT but normal BT displayed clinically relevant bleeding. However, the blood loss was somewhat higher compared to the controls (C), especially in patients with TURB and radical prostatectomy (not significant).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemostaseological management of urological operations in patients taking aspirin using the Thrombostat 4000. 766 Jan 58

Epidemiological studies have suggested that increased intake of calcium (Ca) or aspirin (ASA) is associated with a reduced risk for colon cancer. To delineate a possible mechanism of action, the present study used male F344 rats in an azoxymethane (AOM)-induced colon tumor model to study the single and interactive effects of Ca and ASA on cholic acid-promoted experimental colon carcinogenesis. Following initiation with AOM, a promotion diet containing 0.5% cholic acid was fed for 34 weeks until the adenoma development stage. Cholic acid was used as a surrogate for high-fat diets and to promote carcinogenesis. Diets were supplemented with CaCO3 (2% Ca by weight), 250 p.p.m. ASA, or both. After 34 weeks, the diets were switched during the progression stage and rats were killed at week 51. Several intermediate endpoints were examined during the course of AOM carcinogenesis to determine their reliability as predictors of colon cancer risk. Intermediate endpoints included colon crypt height measurement, colon mucosal ornithine decarboxylase (ODC) and colon mucosal protein kinase C (PKC) activities. The biomarkers were examined at the beginning of the study at 2 weeks, and thereafter at 5, 15, 30 and 40 weeks of dietary treatment. Animals were necropsied at week 51 and tumor incidence and numbers were analyzed for correlation with biomarkers. Survival was highest in the group fed CaCO3 during the promotion stage and tumor burden was lowest in groups fed CaCO3 during this stage. Supplementation during the progression stage was ineffective. The cholic acid promotion model resulted in increased ODC which was inhibited by intervention during the promotion stage with Ca, but not ASA. PKC was also activated by cholic acid feeding, and this effect was modulated by intervention in the promotional stage with Ca or ASA. Colon tumor incidence and burden was increased by cholic acid promotion and decreased by Ca, but not affected by ASA. In summary, Ca is a more effective chemopreventive agent in cholic acid-promoted colon carcinogenesis than ASA, impacting both incidence and tumor number. Colonic ODC, but not PKC may be a suitable predictor of risk and response in chemoprevention trials for colon cancer.
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PMID:Chemopreventive effects of calcium but not aspirin supplementation in cholic acid-promoted colon carcinogenesis: correlation with intermediate endpoints. 772 52

Cephalic duodenopancreatectomy is certainly the operation of choice in cases of adenocarcinoma of the pancreatic head. We evaluated the results of this operation in order to justify its indication and to pinpoint the factors that have an influence on the patients' prognosis after the operation. From 1982 to 1992, 386 patients were hospitalized in our department with the diagnosis of pancreatic cancer, all histological types included. Of these, 21 men and 18 women, mean age 65 years, underwent cephalic duodenopancreatectomy for adenocarcinoma. Associated with these operations were 3 liver metastasis excisions, 2 vascular resections, 1 colectomy and 1 splenectomy. All the tumors were operated on whenever technically possible, except those associated with distant metastasis. Postoperatively, only one patient died (on the 29th day, of viral meningitis). Postoperative morbidity was 51% with 23% local complications. There was one leakage of the anastomosis. Age, weight loss, history of pancreatitis or cirrhosis, anesthetic risk (ASA) and tumor staging were not found to be factors increasing the risk of postoperative complications. Survival after 1 year was 34% and after 5 years 6%. The degree of histological differentiation was the only factor that had any significant influence on the postoperative survival rate in our study. We conclude that cephalic duodenopancreatectomy is the treatment of choice which is capable of improving the quality, and to a lesser extent the length, of survival of patients suffering from pancreatic cancer, with acceptable postoperative mortality and morbidity rates.
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PMID:[Cephalic duodenopancreatectomy for pancreatic adenocarcinoma]. 774 Feb 89


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