Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrial fibrillation has proved to be a frequent complication after thoracotomy for lung cancer. In order to study the possibility that metabolic changes are the trigger mechanism of these arrhythmias, free fatty acids (FFA), glycerol, triglycerides, serum insulin and glucose were determined pre- and postoperatively in patients both with and without this postoperative complication. In the primary series of patients, FFA were found to be increased immediately after the start of the atrial fibrillation, partly in relation to the morning values and partly to the 24-hour curve. This is a possible expression of an increased lipolysis in a causal relationship to the arrhythmia. In another series of patients, the degree of lypolysis was demonstrated using the glycerol values. With this method, no signs of increased lipolysis were found in connection with the onset of atrial fibrillation. Thus, changes in the lipoid metabolism were not found to be the trigger mechanism of the postoperative atrial fibrillation. Reduced values of serum insulin and glucose were not demonstrated either during the uncomplicated postoperative period or at the start of atrial fibrillation.
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PMID:Metabolic studies following thoracotomy for lung cancer with particular reference to postoperative atrial fibrillation. 117 96

The cytotoxic properties of a ricin A chain immunotoxin made with the mouse monoclonal antibody SWA20, recognising a family of sialoglycoprotein antigens selectively expressed by human small-cell lung cancer (SCLC), were examined using a panel of tumour cell lines in tissue culture. SWA20-ricin-A-chain was selectively toxic to the SW2, NCI-H69 and GLC-8 SCLC cell lines, inhibiting the incorporation of [3H]leucine by 50% at a concentration of 0.2-2 nM, but had no selective activity against the NCI-H23 and NCI-H125 lung adenocarcinoma or the control CEM T-lymphoblastoid cell lines. The SWA20 immunotoxin intoxicated the SW2 cell line rapidly, inhibiting [3H]leucine incorporation by 50% within 2 h compared with 0.5 h for ricin. Analysis of the effects of SWA20-ricin-A-chain on the growth of SW2 cells using a limiting-dilution clonogenic assay revealed that the immunotoxin could eliminate 95% of clonogenic malignant cells. Although SWA20-ricin-A-chain was found to be rapidly active against the majority of tumour cells, its action was limited by the presence of insensitive cells expressing low levels of the target antigen.
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PMID:Cytotoxic properties of a ricin A chain immunotoxin recognising the cluster-5A antigen associated with human small-cell lung cancer. 132 29

Pseudomonas cepacia is a gram negative rod, having no fermentative activity on glucose. This organism was detected in the sputum, throat swab, or throat washing of 22 inpatients treated between January, 1990, and December, 1990, at the First Department of Internal Medicine, Kagawa Medical School. The primary diseases for which these 22 patients were hospitalized were leukemia in 12, malignant lymphoma in 5, lung cancer in 2, myelodysplastic syndrome in 1, and embryonal cell carcinoma in 1. Twelve of the 22 patients had episodes of pneumonia which complied clinically with the diagnostic criteria provided to facilitate the National Nosocomial Infection Study. The complication of pneumonia occurred in 7 patients with leukemia, 2 with malignant lymphoma, 2 with lung cancer, and 1 with myelodysplastic syndrome. In 10 of these 12 patients, the organism was detected before the onset of pneumonia. All 22 patients in whom the organism was demonstrated had received antibiotics. The antibiotics which was most frequently used to treat these patients 1 month before detection of Pseudomonas cepacia were amikacin and ceftizoxime, which were used in 13 patients. Of the antibiotics in which the susceptibility to Pseudomonas cepacia was, evaluated, minocycline was effective in 100% (21/21), ceftazidime in 50% (11/22), and ofloxacin in 27.3% (6/22). Physicians should be especially aware of the possibility of colonization and nosocomial respiratory infection by Pseudomonas cepacia in patients with severe underlying diseases.
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PMID:[Nosocomial respiratory infection caused by Pseudomonas cepacia in immunocompromised hosts]. 138 85

Although it is generally accepted that altered nutrient intake and metabolism are responsible for the progressive loss of body weight observed in most advanced cancer patients, there is still considerable controversy regarding the contributory role of changes in both resting energy expenditure (REE) and glucose metabolism. Several studies suggest increases in both REE and glucose appearance in advanced cancer patients compared with healthy control subjects, whereas others revealed no changes in either metabolic parameter. We measured REE with indirect calorimetry and glucose kinetics with a primed constant infusion of D-[U-14C]glucose and D-[6-3H]glucose over the last 4 h of a 24-h fast in 32 advanced lung cancer patients immediately after diagnosis and before any chemotherapy or radiotherapy and in 19 healthy volunteer subjects. REE for the lung cancer group was not significantly different from that in the control group (1535.8 +/- 78.0 vs. 1670.2 +/- 53.9 kcal/day, respectively, p = 0.151). When REE was expressed as a function of body weight, or lean body mass, no differences between the two groups were observed. The rate of glucose appearance was 9.88 +/- 0.36 mumol.kg-1.min-1 in the cancer patients and 10.15 +/- 0.53 mumol.kg-1.min-1 in control subjects (p = 0.667), of which 50.4 versus 58.2%, respectively, was oxidized. The amount of glucose recycled was 13.54 +/- 1.22% in cancer patients and 15.08 +/- 0.99% in control subjects (p = 0.394). The amount of VCO2 from direct oxidation of glucose was 23.39 +/- 0.74% in cancer patients and 27.45 +/- 1.36% in control subjects (p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose metabolism in advanced lung cancer patients. 149 56

In 1919, glucose intolerance became the earliest recognized metabolic abnormality in cancer patients. Prior to the development of severe malnutrition, colon, gastric, sarcoma, endometrial, prostate, localized head, neck, and lung cancer patients had many of the metabolic abnormalities of type II (noninsulin dependent) diabetes mellitus. These metabolic abnormalities include glucose intolerance, an increase in both hepatic glucose production (HGP) and glucose recycling, and insulin resistance. In a study of over 600 cancer patients, a diabetic pattern of glucose tolerance test was noted in over one-third of the patients. An increased rate of HGP, commonly seen in diabetics, has been noted in almost all types of cancer patients studied to date. Etiology of the increased glucose production in the cancer patient is not known, but abnormalities in the counter regulatory hormones, especially growth hormone, may contribute to the development of abnormal glucose metabolism. A second possible stimulus for the increase in HGP could be the glucose needs of the tumor. Abnormally high glucose utilization rates in small amounts of tumor tissue have recently been described. This suggests that small tumors may have large needs for glucose calories. An increase in anaerobic glycolysis in the tumor tissue can increase lactate production in the tumor-bearing human, thus supplying substrate to the liver to increase glucose production rates. In this paper, the nature of abnormal glucose metabolism in cancer patients is described.
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PMID:A review of cancer cachexia and abnormal glucose metabolism in humans with cancer. 150 7

Oncogenes of the myc family c-raf-1 and K-ras have been reported to modulate radiosensitivity. We examined the possible relationship between in vivo radiosensitivity to single-dose irradiation with 3-10 Gy, and activity of these proto-oncogenes in 2 sets of small-cell lung cancer (SCLC) xenografts, the CPH and the GLC series. CPH-54A and CPH-54B are in vitro-derived subclones of a SCLC cell line, while the GLC tumours were established as cell lines from a patient during longitudinal follow-up. Both tumours were later transferred into nude mice. CPH-54A was more sensitive to single-dose irradiation than CPH-54B, while, with respect to the 3 GLC tumours examined, GLC-16 was most sensitive, followed by GLC-14 and GLC-19. The CPH tumours expressed similar amounts of c-myc and c-raf-1 mRNA, and neither expressed N-myc or L-myc. GLC-14 expressed N-myc and c-raf-1 mRNA but no c-myc. GLC-16 and GLC-19 expressed identical amounts of c-raf-1 and high levels of c-myc mRNA, but neither expressed N-myc or L-myc. None of the tumours was mutated at codon 12 or K-ras. Our results show that SCLC xenografts with different radiosensitivity may express identical amounts of some of the proto-oncogenes reported to modulate radiosensitivity. Thus, factors other than activation of the examined proto-oncogenes must be involved in causing the differences in radiosensitivity found in the SCLC xenografts. Possible long-term effects of irradiation on proto-oncogene expression was examined in xenografts of GLC-16, following regrowth after single-dose irradiation. No long-term difference in expression of c-raf-1 or c-myc mRNA was detected between control tumours and tumours irradiated with 5 or 10 Gy.
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PMID:Radiosensitivity of small-cell lung cancer xenografts compared with activity of c-myc, N-myc, L-myc, c-raf-1 and K-ras proto-oncogenes. 165 70

Metabolic disturbances of Na, K, Ca and glucose as paraneoplastic syndrome were reviewed on the basis of recent progress of such areas. These abnormalities usually occur due to the production of hormones or other physiologically active substances by tumor tissues. Hyponatremia is the most common abnormality of Na metabolism in patients with cancers such as lung cancer, malignant lymphoma, thymoma and so on. Usual cause of hyponatremia as paraneoplastic syndrome is inadequate secretion of Antidiuretic Hormone (SIADH), which brings dilution hyponatremia associated with water intoxication. Recently hyponatremia due to abnormal secretion of atrial natriuretic peptide has been noted. Ca metabolism disturbance associated with cancer is usually observed as hypercalcemia and it is said that such hypercalcemia is seen in about 10% of cancer patients. Main cause of hypercalcemia associated with cancer is local osteolytic hypercalcemia (LOH) due to bone metastasis or humoral hypercalcemia of malignancy (HHM). The most common etiology of HHM is the production of Parathormone (PTH) related peptide (PTH-rP) massively secreted from cancer tissues. PTH-rP has been recently well investigated and its molecular, mRNA and gene structure have been already determined. The progress of this area is very rapid and PTH-rP will be assayed in the clinical laboratory in near future. As for glucose metabolism disturbance as paraneoplastic syndrome, hypoglycemia is the most common abnormality. This type of hypoglycemia has been noted in relation with excessive production of somatomedin.
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PMID:[Metabolic disturbance as paraneoplastic syndrome]. 182 8

Distribution of 57Co-bleomycetin in organs and tissues of rats with experimental short-term hyperglycemia was studied. Hyperglycemia was induced by intraperitoneal administration of 40 per cent glucose solution in doses of 1 to 10.4 g/kg. The labeled antitumor antibiotic was also administered intraperitoneally (0.2-0.8 MBq per animal). The data on both the external radiometry in the area under the animal limb and the radiometry of separate organs and tissues showed that hyperglycemia markedly altered pharmacokinetics of the labeled antibiotic and retarded its elimination. With respect to the lungs it even increased the drug tropism and accumulation. This information may be useful in radionuclide diagnosis and therapy in particular of lung cancer. The time course of glucose concentration in blood was not an adequate criterion of hyperglycemia influence since the influence of hyperglycemia on retarding the drug elimination was also observed when the level of glucose in blood did not differ from the initial one.
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PMID:[57Co-bleomycetin distribution in the body of experimental animals with hyperglycemia]. 244 78

An alteration in the serum elastase 1 level in a previously non-diabetic patient, who unfortunately developed the hyperosmolar hyperglycemic non-ketotic syndrome (HHNS), was observed after intravenous hyperalimentation for 6 days. The patient underwent the therapy because of the occurrence of severe persistent anorexia which appeared as a side effect of treatment of lung cancer with combined anticancer drugs. In parallel with progressive dehydration, levels of serum elastase 1 and urine glucose became greatly elevated at an earlier stage of HHNS. A slight increase in serum alpha 1-antitrypsin was observed. However, there were no significant changes in serum amylase activity and serum alpha 2-macroglobulin level before or during HHNS. The elevation of the serum elastase 1 level was considered to be due to serum electrolyte abnormalities and the defect of serum alpha 2-macro-globulin elevation. Rehydration therapy with half-normal saline solution immediately produced negative urine glucose, but the serum elastase 1 level only gradually normalized after improvement of HHNS.
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PMID:Significance of increased serum elastase 1 level during the hyperosmolar hyperglycemic non-ketotic syndrome. 244 40

Human tumors were transplanted into athymic nude mice. From blood samples in the final stage of their passages we observed that in some of these lines, human lung cancer lines mostly, blood glucose generally decreased with increasing size of the tumor grafts. This observation was the reason for further investigations. Eight out of 13 human lung cancer lines caused a decrease of blood glucose in grafted mice. The extent of decrease was directly correlated with the proliferation of grafts. The results raise hope that the model of human malignant tumors, xenotransplanted and passaged into athymic nude mice, could be helpful in research on IGF and related substances.
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PMID:Lowering of blood glucose in athymic nude mice and rats, grafted with human lung cancers. 251 47


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