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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five smokers had erythrocyte masses sufficiently larger than normal to pose a problem in the differential diagnosis of polycythemia. Evaluation excluded lung disease, shunt physiology, hemoglobin with increased oxygen affinity, erythropoietin-producing tumor, renal disease, or polycythemia rubra vera as the primary cause of erythrocytosis in these patients. All were found to have levels of carboxyhemoglobin sufficient to cause clinically significant hypoxemia and to account for the increased erythrocyte masses. In two patients the erythrocytosis improved when they stopped smoking. Heavy smoking is a reversible cause of polycythemia and should be considered in the differential diagnosis of this problem.
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PMID:Smoking as a cause of erythrocytosis. 23 31

Direct measurements using 200 micron oxygen cathode electordes have been made in tumour and subcutaneous tissues of anaesthetized C3H mice treated with misonidazole. In air-breathing animals a six-fold increase in tumour oxygen cathode readings was observed by 23 min after i.p. injection of misonidazole at 0.5 mg/g body weight. A similar rise, but of 2.5 times, was observed for the subcutaneous tissues. Comparison of tumour oxygen readings for drug-treated and control mice breathing 100% O2 at different pressures showed markedly increased levels for the drug-treated animals. Tumour response to radiation was measured for 250 kV X-rays and 15 MeV electrons. In each case, when a dose of radiation was combined with pre-treatement with misonidazole an increased radiation response was observed when compared with the same dose of radiation given alone. At the highest dose (40 Gy) there was a suggestion of an increased normal tissue reaction. The significance of the measurements is discussed.
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PMID:Oxygen cathode measurements and radiation response in tumour-bearing mice treated with misonidazole. 27 16

Visible light and oxygen enhanced both chromosome instability and malignant transformation of mouse cells in culture. Nine cell lines were initiated from 8 pools of 10- to 13-day C3H embryos. Each cell line was divided into sublines, which were either maintained shielded from light or were exposed for 3 or 24 hours to fluorescent light (approximately 150 foot-candles) two or three times weekly. Cultures of the sublines were also maintained with either a gaseous phase of 0-1% oxygen or atmospheric (18%) oxygen. Each line was monitored for cytologic manifestations of malignant neoplastic transformation, and 8 lines were monitored for chromosome alterations. Seven lines were assayed for tumorigenicity by intraocular implantation into syngeneic hosts. Repeated light exposure and/or high oxygen increased the frequency of minute chromosomes, which result from chromatid breaks, and also increased the rate of shift from diploid to heteroploid state. Four cell lines showed no cytologic changes indicative of neoplastic change during the test period. Two of these were assayed in vivo and failed to grow as tumors. In the remaining 6 lines, cytologically neoplastic colonies appeared earlier or more abundantly in the light-exposed cultures and/or those gassed with high oxygen. In 3 of these lines, tumors developed only from the light-exposed cultures; in the other 2, tumor latency periods were significantly shorter in the cultures exposed to light or gassed with atmospheric oxygen.
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PMID:Role of photosensitization and oxygen in chromosome stability and "spontaneous" malignant transformation in culture. 29 51

TCD50 values for thermally resistant tumors have been significantly reduced. The therapeutic ratio has been improved for some tumor-normal tissue situations and treatment protocols, but not for others. The oxygen enhancement ratio (OER) for hyperthermic damage may be congruent to 1; if this is true for tumor cells in vivo, the combination of hyperthermia and radiation should improve the therapeutic ratio to the extent that hypoxic cells are critical. There does not appear to be a differential response to hyperthermia by the normal foot or tumor growing in the foot pad for the following two parameters: (a) relationship between heating time to produce the specified response and the level of heating, and (b) effect of fractionation of hyperthermia.
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PMID:Hyperthermic effects on animal tissues. 32 6

Laboratory data from studies of hyperthermia as a potential antitumor agent indicate that: (a) tumor cells may be more sensitive to heat than normal tissue; (b) hyperthermia enhances response to irradiation and can increase the therapeutic ratio; (c) cells are most sensitive to hyperthermia during the S-phase, when they are resistant to ionizing radiations; (d) the oxygen effect is absent for hyperthermic cell killing, and radiation effects are less oxygen-dependent when potentiated by heat treatment; and (e) biological damage changes more rapidly at temperatures above 43 degrees C. Methods of heat production and dosimetry need to be refined further before these findings can be put to practical use in tumor therapy.
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PMID:Prospects for hyperthermia in human cancer therapy. Part II: implications of biological and physical data for applications of hyperthermia to man. 32 8

Environmental lung injury may take the form of acute tracheobronchitis, asthma, pulmonary edema, chronic bronchitis, emphysema, allergic pneumonitis, fibrosing alveolitis, pleurisy, and neoplastic disease. Environmental factors eliciting these responses include irritant gases and fumes, oxidants, organic allergens, inorganic dust, bacterial enzymes, and high partial pressures of oxygen. The basic pulmonary reactions to these toxic agents--bronchoconstriction, vasoconstriction, increased vascular permeability, inflammation, carcinogenesis--may be mediated, aggravated, or modulated by biologically active substances. These humoral agents include biogenic amines (e.g. histamine): peptides (e.g., bradykinin, vasoactive intestinal peptide, and spasmogenic lung peptide); enzymes (e.g., proteases, superoxide dismutase, and mixed function oxidases); and acidic lipids (e.g., prostaglandins, prostaglandin endoperoxides, and thromboxanes).
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PMID:Environmental injury of the lung: role of humoral mediators. 35 83

Studies on volunteers have shown that the gas hypoxic mixture containing 10% of oxygen and 90% of nitrogen (GHM-10) renders a protective action on the genetic apparatus of human skin cells but provides no protection of the peripheral blood leucocytes, which show the identical character of metabolic processes as neoplastic cells. Under clinically performed distant x-ray therapy for breast cancer the inhaling of GHM-10 was found to render the antiradiation protective action on different normal tissues (skin, subcellular connective tissue, muscle tissue, mammary gland tissue), but it fails to protect the tumor tissue and regional lymph nodes involved. The clinical observations were supported by pathomorphological examination of the operation material.
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PMID:[Radiation protection using a gaseous hypoxic mixture in oncological practice]. 38 Jan 57

Disturbances in the functional properties of tumor mitochondria have been studied during the course of induction of haemorrhage brought about by endotoxin in the murine Crocker sarcoma (S 180). Extensive impairment of function was already present in mitochondria isolated from control tumors, as shown by low respiratory control ratios. The existing mitochondrial damage intensified promptly in response to injection of endotoxin long before the onset of haemorrhage at 4 h. The nature of the additional damage took two forms, depending on the duration of exposure to endotoxin; first, at 30 min, a true uncoupling of oxidative phosphorylation was seen, largely reversible in vitro by pre-treatment of the isolated organelles with bovine serum albumin (BSA). Second, at 1 h and later, oxygen utilisation in the presence of succinate, ADP and inorganic phosphate (Pi) was depressed. The pre-addition of BSA consistently lowered respiration rates with succinate and Pi in all preparations. The extent of endogenous inhibition of the adenine nucleotide translocase appeared unaltered by endotoxin in vivo.
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PMID:Early mitochondrial damage in the induction of haemorrhagic necrosis in the Crocker sarcoma (S 180) by endotoxin. 38 16

In ten specimens of resected pulmonary tissue, a little known and underscribed form of aspergillosis called tumor-like blocked pulmonary cavity with liquid content infected with aspergilli was observed. This designation was based on the finding in the specimens of tumor-like cavitary structures with blocked bronchus and contents from which abundant growth of aspergillus fumigatus was invariably obtained in cultures. Nine of the ten specimens were bronchiectasis, and one was a bronchogenic cyst. The scant literature was review, emphasizing features characteristic of this form of mycetoma and differences from the typical and frequently encountered form of ordinary pulmonary aspergilloma. The serologic response and its long duration were attributed to biological properties of aspergilli in this form caused by inaccessibility of oxygen and by occlusion of the bronchial lumen.
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PMID:A trial of isolating a tumor-like form of pulmonary cavities infected with aspergilli. II. Intra- and postoperative, morphologic and serologic data. 38 68

Significant recent achievement in radiotherapy are presented, with brief discussions of brachytherapy, clinical dose-rate effects, ultrafractionation, and total and half-body irradiation. Reports on radiation modifiers, including hyperbaric oxygen, chemical radiosensitizers, and normal tissue protective agents are briefly summarized, while the potential of local and systemic hyperthermia is discussed in greater detail. Recent reports of local tumor control in so-called "radioresistant tumors," such as salivary gland tumors, adenocarcinomas of the breast, prostate and pancreas, malignant melanoma and malignant carcinoid, are summarized. Current status of heavy particle radiotherapy is discussed in detail. Results of initial clinical trials of neutron beam therapy are summarized, and a brief review of proton beam clinical trials and pion beam facilities is included. Recent reports defining the role of combined irradiation and surgery in rectal and breast cancer, and in soft tissue sarcomas, are discussed. Reports of enhanced radiation toxicity seen with concomitant or sequential chemotherapy and radiotherapy are detailed, including CNS toxicity seen with methotrexate and cytosine arabinoside, cardiotoxicity with adriamycin, and pulmonary toxicity with bleomycin. New or improved diagnostic techniques with special relevance to radiotherapy treatment planning, including CT scanning, histerography, internal mammary lymphoscintigraphy, and upper extremity lymphangiography are described.
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PMID:Recent advances in radiotherapy. 40 98


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