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

Leach, R. H. (Wellcome Research Laboratories, Beckenham, Kent, England), and M. Butler. Comparison of mycoplasmas associated with human tumors, leukemia, and tissue cultures. J. Bacteriol. 91:934-941. 1966.-Mycoplasmas originally isolated by various workers from tissue cultures prepared from or inoculated with tumor or leukemic cells fell into four groups; each related to existing species or serotypes. These were Mycoplasma pulmonis, M. fermentans, M. hominis, and the GDL serotype, the last two being well known as contaminants of uninoculated cell lines. All the test strains were able to grow well in certain tissue cultures, and some caused cytopathic effects and acidity. These observations are discussed in terms of the relationship of these strains to the malignant tissues with which they were originally associated. The variable results obtained in certain biological tests on these strains emphasized the need for standardization of the conditions under which such tests may be employed to assist in identification of Mycoplasma species.
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PMID:Compraison of mycoplasmas associated with human tumors, leukemia, and tissue cultures. 592 67

The effect of chronic dietary wheat bran supplementation on the pH of gastrointestinal contents was examined in thirty-one Sprague-Dawley rats. Ten control rats received a fiber-free diet while twenty-one rats were fed the same diet plus a 20% wheat bran supplement. The fiber-fed rats developed a greater acidity of intestinal contents: cecal pH was 6.30 +/- 0.33 in the controls (P less than 0.01). These changes in gastrointestinal pH may be of relevance to the nutrient modulation of gastric and colonic tumor development.
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PMID:Dietary wheat bran lowers colonic pH in rats. 627 14

The effect of hyperthermia at 42.5 degrees C on a human melanoma xenograft in athymic mice was studied. The tumours were heated in vivo in a water-bath. Tumour growth delay and single-cell survival in vitro were used as endpoints. Qualitative information regarding heat-induced vascular damage was obtained from microangiographic analysis. Tumour growth delay after a given treatment was considerably longer than that expected from the cell survival measured in vitro immediately after treatment. Experiments in which removal of the tumours was delayed revealed that tumour cells were continuously dying for at least 24 hr after heat treatment. The volume of the tumour vasculature was considerably reduced after treatment, suggesting that the delayed cell death was attributed to vascular occlusion which resulted in an insufficient supply of oxygen and nutrients and an increased tumour acidity. The present work indicates that at least two mechanisms may be involved in heat-induced cell inactivation in our xenograft: firstly, direct cytotoxic effect of heat; secondly, indirect effect following heat-induced vascular damage.
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PMID:Tumour growth delay, cell inactivation and vascular damage following hyperthermic treatment of a human melanoma xenograft. 654 85

Changes in tumor tissue oxygenation and acidity were determined using ultramicroelectrodes, and presented in histogram fashion. The effect of Hyperthermia and HpD phototherapy were tested. It was found that both modalities affect tumor microcirculation, causing a marked drop in oxygen availability. Tissue pH is decreased by Hyperthermia, but not by phototherapy. These effects are long lasting at least for 24 hours after treatment.
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PMID:Impact of microcirculation and physiologic considerations on clinical hyperthermia. 663 97

Changes in tumor tissue oxygenation and acidity were determined using ultramicroelectrodes, and presented in histogram fashion. The effect of Hyperthermia and Hpd photo-therapy were tested. It was found that both modalities affect tumor microcirculation, causing a marked drop in oxygen availability. Tissue pH is decreased by Hyperthermia, but not by phototherapy. These effects are long lasting, at least for 24 hours after treatment.
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PMID:Changes in tissue oxygenation and acidity induced by localized microwave hyperthermia and hematoporphyrin phototherapy, an update. 663 40

The intratissue pH of SCK tumor and leg muscle of unanesthetized mice were determined before, during and after hyperthermia with the use of bulb type pH microelectrodes having pH-sensitive hemisphere 20-40 micron in outer radius. Intratumor pH was heterogeneous throughout tumor (range, 6.60-7.38; average, 6.96), and was more acidic than the intramuscle pH of mouse leg (average, 7.46). Hyperthermia at 43.5 degrees C for 30 min induced a further increase in acidity (decrease in pH of about 0.2 units) in tumor but not in muscle. The heat-induced acidity in tumor lasted for 12 hr following hyperthermia and then recovered to almost control pH value 24 hr after heating. The cause of the increase in acidity in the heated tumors is not clear, but it appears to result from an increase in the contents of acidic metabolites and a sluggish drainage of them due to induced vascular damage. The increased acidity in the heated tumors may inhibit the repair of thermal damage and sensitizes the tumor cells to subsequent heating.
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PMID:Changes in acidity of mouse tumor by hyperthermia. 670 33

To investigate ischemic potentiation of thermal cell killing, mammary carcinomas transplanted to the legs or tails of C3H mice were treated with hyperthermia using rubber-lined compression cuffs. During treatment, warm water was circulated through the cuffs under pressure so that blood flow to the contained tumor-bearing limbs was interrupted. Ninety min at 41.5, 42.0, or 42.5 degrees and pressures between 60 and 135 mm Hg destroyed about 50% of tumors but damaged the normal tissues. Damage increased with the degree of compression. Intermittent pressure application was therefore adopted (five 18-min periods at 80 to 90 mm Hg alternating with four periods of 5 min at zero pressure). This favored the normal tissues, a high cure rate being maintained (73%) with damage to normal tissue virtually eliminated. The most satisfactory explanation of these results is a selective heat sensitivity, augmented by ischemia, on the part of tumor blood vessels. The success of intermittent treatment is then attributable to progressive impairment of the blood supply to the tumors, preventing the heat dissipation and relief of conditions such as acidity and nutrient deficiency which would otherwise result from periodic restoration of the circulation.
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PMID:Treatment of mouse mammary tumors using combined hyperthermia and ischemia. 685 Jun 44

Insulin binding and responsiveness in primary cultures of R3230AC rat mammary tumor cells were studied as a function of the hydrogen ion concentration of the culture medium. When insulin binding was assayed at pH 7.4, cultures that were maintained for a sufficient length of time in acidic medium demonstrated a significant increase in insulin receptor concentration compared to control cultures. The increase in insulin binding, which occurred as cultures approached confluency, was attributed to the increased acidity rather than nutrient depletion of the culture medium. In contrast, maximum binding was observed when the pH of the assay buffer was above 8.0, independent of the culture conditions. Binding of Concanavalin A, reflecting more generalized cell surface glycoproteins, decreased as cultures approached confluency, but was unaffected by the pH of either the culture medium or the assay buffer. The effect of pH on insulin responsiveness was studied. Insulin receptors generated by acidic culture conditions demonstrated insulin-induced down-regulation. Regardless of the pH environment, all cells demonstrated the same amount of insulin binding after exposure to 10(-6) M insulin. Under the in vitro conditions employed, cultured cells did not demonstrate a significant response to added insulin by alteration in growth, substrate transport, or incorporation of precursors into macromolecules, although the basal rates of these parameters were lower in cells maintained in acidic pH environments. The data presented indicate the necessity of considering the pH of the culture medium in studies of receptor regulation. It is possible that tumor cells, due to increased lactic acid production, may be especially prone to these changes.
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PMID:Effect of environmental hydrogen ion concentration on regulation of insulin receptors in cultured R3230AC mammary carcinoma cells. 685 36

When injected at tracer levels into the blood, radiogallium as 67Ga-citrate binds to, and it transported to the site of the tumor by, transferrin. The process by which transferrin-bound Ga is converted to tumor-bound Ga is not fully understood, but may involve the differential physiology of neoplasms compared with normal tissues. Based on the slight acidity known to be exhibited by the extracellular fluid of many animal and human tumors, we have studied the effect of pH on stability and dissociation of the Ga-transferrin complex and on the uptake of Ga by tumor cells in vitro and animal tumors in vivo. When plasma from rabbits injection 67Ga-citrate was dialyzed at pH 6.5-7.5, dissociation of Ga from transferrin showed an inverse pH-dependence. A similar inverse dependence on pH was observed for the uptake of Ga by L1210 leukemia cells and Ehrlich ascites cells incubated with Ga-transferrin complex. Tumor uptake of Ga in rats bearing Walker-256 carcinosarcoma or Murphystum lymphosarcoma whose tumor pH had been further lowered by administration of glucose showed a statistically significant increase over control rats receiving no glucose. These results demonstrate that the stability of the Ga-transferrin complex is pH-dependent and suggest that dissociation of this complex due to decreased pH at the tumor site may be one factor involved in tumor localization and binding of Ga.
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PMID:Effect of pH on tumor cell uptake of radiogallium in vitro and in vivo. 689 27

The pH distributions in transplanted neural (TV1A, BT1A) and hepatic (HV1A3) tumors and in brain and kidney of BDIX rats were analyzed as a function of serum glucose concentration (SGC), tumor size, and tissue architecture. Tissue damage during pH measurements in vivo could be minimized by the use of pH microelectrodes with tip diameters of less than or equal to 10 micrometers. In normoglycemic rats, the pH in TV1A tumors was only slightly lower than in brain or kidney. However, at 6 hr after the induction of hyperglycemia by continuous i.v. infusion of glucose, the average pH in TV1A tumors had fallen to 6.7 at an SGC of 27 mM and to 6.1 at an SGC of 50 mM. A similar glucose-mediated pH reduction was observed in BT1A and HV1A3 tumors. No significant increase in tissue acidity occurred in brain and kidney. The pH in tumors had reached its minimum at 2 hr after the onset of high-dose glucose infusion (SGC, 50 mM) and could be maintained at this level in hyperglycemic rats for at least 48 hr. In hyperglycemic hosts, an increased retention of acidic metabolites in the tumor tissue with decreasing vascular density was reflected by a tumor size (age)-dependent pH reduction and a higher degree of intratumoral pH variation. In partially necrotic tumors, pH values as low as 5.2 were recorded. Oral administration of NaHCO3 to tumor-bearing rats had no effect on the average pH in TV1A tumors.
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PMID:Tumor-selective modification of cellular microenvironment in vivo: effect of glucose infusion on the pH in normal and malignant rat tissues. 706 23


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