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)

Squamous cell carcinomas were induced in the hamster cheek pouch with 9,10-dimethyl-1,2-benzanthracene. The process of carcinogenesis was inhibited by phenylphosphate, an inducer of alkaline phosphatase. Orthophosphate and l-phenylalanine, which inhibit alkaline phosphatase, had a promoting effect on tumor formation. The results are in accordance with those of previous studies on the effect of inducers of alkaline phosphatase on chemical carcinogenesis. The effect of the studied substances on carcinogenesis was apparently unrelated to the presence of phenyl or phosphate groups or of steroid rings. The tumor inhibition or promotion seemed to be related to the potential of the tested substances to induce or inhibit alkaline phosphatase activity.
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PMID:Chemical carcinogenesis in the hamster cheek pouch. Influence of inhibitors and inducers of alkaline phosphatase. 81 3

Tetrakis(hydroxymethyl)phosphonium chloride (THPC) and Pyroset TKP, which is the mixed acetate/phosphate of the same phosphonium base, are widely used in flame-retardant cotton fabrics, particularly in children's sleepwear. THPC degrades thermally and under certain chemical conditions to yield hydrochloric acid and formaldehyde (CH2O). In solution, the latter two compounds are in equilibrium with the known potent carcinogen bis(chloromethyl)ether (BCME). A sample of commercial THPC contained from 4% (at pH 0.4) to 14% (at pH greater than 4.5) free CH2O. The material, as supplied by the manufacter, showed pH 0.4. Gas chromatographic analysis of aqueous commercial THPC did not reveal any peak chracteristic of BCME under conditions where 0.1 ppm of the material can be detected. Application to mouse skin of THPC ( 2 mg in 0.1 ml DMSO) and of Pryset TKP (7 mg in 0.1 ml DMSO), three times per week for 400 days with 20 female ICR/Ha Swiss mice per group, gave one squamous carcinoma in the THPC-treated group. THPC was inactive as an initiating agent in two-stage mouse skin carcinogenesis with phorbol myristate acetate as promoter. Both agents were active as tumor promoters, using a single application of 7,12-dimethylbenz[a]anthracene (20 microng in 0.1 ml acetone) as initiator. With THPC as promoter (2 mg in 0.1 ml DMSO, thrice weekly) 3 of 20 mice bore papillomas which progressed to squamous carcinoma. With Pyroset TKP as promoter (7 mg in 0.1 ml DMSO) 7 of 20 mice bore papillomas of which two progressed to squamous carcinoma.
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PMID:Evaluation of chemical flame retardants for carcinogenic potential. 84 2

Transmission electron microscopic studies have been carried out on psammoma bodies in two benign and seven malignant papillary serous neoplasms of the ovary. Ultrastructurally, psammoma bodies are composed of microcrystals in all respects similar to calcium-phosphate apatite crystals of bone. The formation of psammoma bodies is initiated intracellularly, in both the neoplastic epithelial cells and stromal histiocytes. The initial seeding site of apatite crystals is served by lipid-rich intracellular vesicles. These structures are produced in association with autophagocytosis in the neoplastic epithelial cells and heterophagocytosis of extracellular lipidic material in the stromal histiocytes. Extracellular lipids presumably derive from dehiscent tumor tissue. The close relationship between larger intraepithelial calcific bodies and microfilaments suggests that the latter provide supportive matrix for further intracellular calcification. Large extracellular psammoma bodies result from fused calcific bodies which have been extruded from calcified cells. Mineralization of extracellular collagen fibers is not observed. The results provide supportive evidence to the concept that psammoma bodies in ovarian papillary serous neoplasms and probably in other neoplastic and non-neoplastic conditions are a consequence of dystrophic calcification associated with cellular degeneration.
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PMID:Ultrastructural studies on the morphogenesis of psammoma bodies in ovarian serous neoplasia. 87 45

The Dunning R3327H rat prostatic adenocarcinoma appears to be an appropriate animal model for studying prostatic cancer. This report contains a detailed characterization of this tumor at the morphologic, biochemical, and therapeutic levels. Electron micrographic, histologic, and histochemical studies clearly establish the adenocarcinoma nature of this tumor. The histology of the R3327H tumor is similar to well-differentiated human prostatic cancer. The biochemical and enzymatic profile of the tumor indicates its origin from the rat dorsolateral prostate. The cell kinetics and growth rates of this tumor following a variety of hormonal manipulations (castration, estrogens, androgens, and antiandrogens) have established that 70%-90% of the cells in this tumor require androgens for their growth. However, 10%-30% of the cells are capable of growth in the absence of androgens. Both cell types are present in the initial tumor inoculum and these different cell types possess similar growth rates. The predominance of the androgen-sensitive cells accounts for the relatively greater size of the tumor achieved in the intact male animal at a given growth time. After the tumor is well established in an intact animal, subsequent estrogen therapy or castration resulted in a marked diminution in tumro volume. This was followed by a subsequent relapse. In addition, estramustine phosphate was also shown to cause shrinkage in the tumor volume.
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PMID:Characterization of the Dunning R3327H prostatic adenocarcinoma: an appropriate animal model for prostatic cancer. 87 32

A 25-year-old white woman with sporadic hypophosphatemic rickets presented with a 7 year history of chronic mild hypercalcemia, osteitis fibrosa cystic and hypercalcemic nephropathy. Serum immunoreactive parathyroid hormone was elevated by greater than 100-fold and a 3.5 g parathyroid tumor was found at operation. Survey of the literature reveals that of 9 previous cases in which hypercalcemic hyperparathyroidism occurred in association with hypophosphatemic rickets, only two had classical x-linked familial hypophosphatemic rickets. It appears more than likely that this unusual combination of skeletal diseases represents the chance occurrence of primary hyperparathyroidism in patients with underlying x-linked familial hypophosphatemic rickets rather than a complication of phosphate therapy.
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PMID:Hypercalcemic hyperparathyroidism in hypophosphatemic rickets. 87 68

The effects of platinum complexes, selected for their potent anti-tumor activities, have been studied on rat liver mitochondria. Among the mitochondrial properties which have been studied, the most marked effects of platinum complexes were obtained on functions linked to the inner membrane. cis-Pt(II)(3,4-diaminotoluene) dichloride is shown to stimulate state 4 respiration. It inhibits the phosphate transport into mitochondria, decreases the accumulation of Ca2+, and induces a more rapid release of the accumulated Ca2+. A release of Mg2+ from mitochondria incubated in the absence of added divalent cations, and an efflux of divalent cations from mitochondrial membranes are also observed. All these results indicate a profound modification of the of the permeability of mitochondrial membrane.
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PMID:Effect of an anti-tumor platinum complex, Pt(II) diaminotoluene, on mitochondrial membrane properties. 88 18

Uptake of phosphate (32P) in L cells was modulated by reaction with anti-L cell antibody. A biphasic response was noted with high, cytotoxic concentrations inhibiting 32P uptake and low, cytostimulatory concentrations stimulating 32P uptake. Stimulation of 32P uptake was dependent upon multivalent binding as immune IgG and F(ab')2 were effective, but univalent Fab' was ineffective in enhancing 32P uptake into cells. Antibody stimulation of 32P uptake appeared to be an energy independent process and to take place by activation of 32P membrane transport with an increased Vmax (19.3 pmoles/min to 25.3 pmoles/min), but the same Km (0.22 mM). Isolation and measurement of cellular (primarily membrane) phospholipids demonstrated a dramatic increase of (2-fold) specific radioactivity in phosphatidylinositol. Early turnover of phosphatidylinositol may be an important signal for tumor cells to grow at an enhanced rate when exposed to cytostimulatory concentrations of antibody.
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PMID:Humoral immunostimulation. VIII. Increased incorporation of phosphate and turnover of phosphatidylinositol in cells treated with antibody. 89 29

Oncogenic osteomalacia is a syndrome in which unexplained osteomalacia remits after resection of a coexisting mesenchymal tumor. We have investigated the mechanism by which a giant cell tumor of bone caused biopsy-proved osteomalacia in a 42-yr-old woman. The biochemical abnormalities were: hypophosphatemia; decreased renal tubular maximum for the reabsorption of phosphate per liter of glomerular filtrate; negative calcium and phosphorus balance; hyperaminoaciduria; and subnormal calcemic response to exogenously administered parathyroid hormone. Malabsorption, hypophosphatasia, fluorosis, and acidosis were excluded as causes of the osteomalacia. Serum 25-hydroxycholecalciferol was normal (27+/-1 ng/ml). However, the serum concentration of 1alpha,25-dihydroxycholecalciferol was low (1.6+/-0.1 ng/100 ml). Oral administration of physiological amounts of 1alpha,25-dihydroxycholecalciferol resulted in resolution of the biochemical abnormalities of the syndrome and healing of the bone pathology. We suggest that tumor-induced inhibition of 1alpha,25-dihydroxycholecalciferol synthesis caused the osteomalacia. The causal role of the tumor was proved by demonstrating that resection was accompanied by roentgenographic evidence of bone healing and maintenance of normal serum phosphorus; renal tubular maximum for the reabsorption of phosphate; calcium and phosphorus balance; aminoaciduria; and calcemic response to exogenous parathyroid hormone.
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PMID:Osteomalacia due to 1alpha,25-dihydroxycholecalciferol deficiency. Association with a giant cell tumor of bone. 90 49

Uninvolved gastric mucosa from duodenal ulcer, gastric ulcer, and gastric cancer patients was incubated with [1-14C]glucose and [6-14C]glucose in order to assess the relative contributions of the pentose phosphate pathway and Krebs cycle to glucose metabolism. [14C]Glucose counts retained by the tissue, glycolysis, and pyruvate formation were also measured. Tumor tissue from the cancer patients was included in the study. Less than 1.2% of the glucose entering the tissues was metabolized via the pentose phosphate pathway; suggesting that this pathway plays a minor role in energy production from glucose. The major determinant of energy production was the Krebs cycle. Its contribution to glucose metabolism was greatest in the body mucosa of duodenal ulcer patients, less in the uninvolved body mucosa of gastric ulcer patients, and lower still in the corresponding body mucosa of gastric cancer patients. The low levels of Krebs cycle activity seen in the latter tissue resembled those of uninvolved antral mucosa. The smallest Krebs cycle contribution was seen in tumor tissue. [14C]Glucose counts retained by the tissue and glycolysis both tended to vary inversely with Krebs cycle activity among the tissues studied. Thus, both were small in the body mucosa of noncancer patients and somewhat larger in the body mucosa of cancer patients, in uninvolved antral mucosa and in tumor tissue.
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PMID:Krebs cycle, pentose phosphate pathway, and glycolysis in the uninvolved gastric mucosa of peptic ulcer and gastric cancer patients. 91 74

Estracyt (estramustine phosphate) injected intraperitoneally, 100 mg, per Kg. three days a week for four weeks, retarded growth of the R-3327 tumor in intact rats and in orchiectomized rats given androgen. The growth inhibition was accomplished by reduction of tumor deoxyribonucleic acid concentration and of the activities of acid phosphatase, leucine aminopeptidase, and other hydrolases. Histologic examination revealed cellular necrosis particularly prominent in the orchiectomized, androgen-treated rats. Estracyt did not affect the uptake of 65-Zn in the tumors but markedly reduced the high uptake in the dorsolateral prostate. There was no accumulation of 3H or 14C in the tumors after intravenous administration of 3H, 14C-labeled Estracyt, but the isotope concentrations decreased much in the same way as they decreased in the dorsolateral prostate. The isotopes were retained in the ventral prostate, where their concentrations were approximately twenty times higher than those in the muscle four hours after injection. The results demonstrate the value of the R-3327 tumor in the evaluation of drugs of potential clinical use for the treatment of prostatic cancer. The results also show that Estracyt has an antitumor effect which is not dependent on the antigonadotropic action of the drug.
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PMID:Inhibitory effects of Estracyt on R-3327 rat prostatic carcinoma. 91 34


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