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

The C-cell is the source of the hypocalcemic polypeptide hormone, calcitonin. Sequential increments in calcitonin response to provocative calcium and pentagastrin infusions have been used to identify family members at high risk for the development of medullary thyroid carcinoma, a neoplasm of C-cell origin. Correlative light microscopic and immunohistochemical studies have permitted the identification of a spectrum of C-cell proliferative abnormalities ranging from C-cell hyperplasia (CCH) to invasive medullary thyroid carcinoma. Ultrastructurally, both normal and hyperplastic C-cells occupied an intrafolliculat localization, being separated from the interstitium by the follicular basal lamina and from the luminal colloid by extensions of the follicular cell cytoplasm. These relationships were maintained in areas of advanced hyperplasia where C-cells often completely encircled and displaced the follicular epithelium. Nodular CCH was characterized by the complete obliteration of the follicular space by C-cells. In these areas, prominent reduplications as well as occasional defects in the basal lamina were noted. Some of the solid C-cell nodules adjacent to areas of medullary thyroid carcinoma appeared to form by gradual replacement of follicles by C-cells and did not represent sites of intrathyroidal vascular or lymphatic extension. Two major cell types were noted in cases of CCH. One cell type which was filled with secretory granules measureing 280 nm. in diameter (type I) predominated in areas of diffuse CCH and was also found in control thyroid glands. The larger number of secretory granules in this cell type together with the relative lack of development of granular endoplasmic reticulum and Golgi regions suggested that these cells were in the storage phase of their secretory cycle. The second cell type had fewer secretory granules, which measured 130 nm. in diameter (type II), and was characteristically located in areas of nodular CCH. Type II granules were found in cells with cytologic evidence of active protein synthesis and secretion. Variations in granule morphology and cell ultrastructure may be correlated with functional variations in C-cell populations.
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PMID:C-cell hyperplasia. An ultrastructural analysis. 83 36

Review of 40 cases of retinoblastoma revealed that histologic evidence of calcification was noted in 38 of the 40 tumors, whereas only three of 16 roentgenograms were positive for calcium. Calcificaton detected by roentgenograms and histopathologic examination correlated poorly with quantitative determination for tumor calcium. Compared to control eyes, however, eyes with retinoblastoma contain large amounts of calcium (1.2 vs. 218 mug/ml. ash). This calcification, though frequently not observed in standard roentgenograms, should be detected by the newer diagnostic modalities such as hypocycloidal polytomography, computerized transaxial tomography, ultrasonography, and radionuclide scintigraphy with technetium diphosphonate, a bone-scanning agent.
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PMID:Calcification in retinoblastoma. 84 82

Metronidazole (0.6 mg/gm) was injected intraperitoneally at 12 hour intervals for 10 days into C3H/HeJ mice with established C3HBA mammary adenocarcinomas. Tumor growth, total white cell count and body weight were decreased by 3 days. Heart rate and rectal temperature were depressed most following the initial injections but were less depressed by 10 days. Hemoglobin and hematocrit were not changed. Plasma assays of total protein, uric acid, bilirubin, alkaline phosphatase and calcium were not affected. It was not possible to separate the tumors treated with metronidazole from control tumors, based on cellular differences. Blood vessels in most of the tumors in the drug treated animals were larger and appeared engorged with blood.
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PMID:Effect of metronidazole on the C3H/HeJ mouse and growth of the C3HBA mammary adenocarcinoma. 85 27

The findings presented indicate that localized calcifications can sometimes develop within squamous cell carcinoma of the cervix. Apparently, these deposits develop via calcium salt loading from epithelial necrosis within the cell complexes of the tumor. This means that, with microcalcifications in a metastasis of a squamous cell carcinoma, the pathologist evaluating biopsies should also consider the possibility of metastases of a tumor from the area of the cervix.
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PMID:[Microcalcifications in squamous cell carcinoma of the cervix (author's transl)]. 87 Mar 85

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 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

In rabbits bearing the prostaglandin-producing VX2 carcinoma, the plasma concentration of 13,14-dihydro-15-keto-PGE2 (PGE2-M) was elevated within one week after tumor implantation and preceded the development of hypercalcemia. Both the rate of rise and magnitude of the increase were greater for the metabolite than for PGE2; at the time of peak hyercalcemia (about 4 to 5 weeks after tumor implantation), the increase over basal in plasma PGE2-M was about 75 fold whereas it was previously shown that the increase in PGE2 was less than 2 fold. Indomethacin, which inhibits PGE2 synthesis in VX2 cells in culture, lowered in parallel plasma calcaium and PGE2-M in tumor-bearing rabbits. Administration of hydrocortisone to rabbits bearing the VX2 tumor prevented the development of hypercalcemia when given at the time of tumor implantation and reversed the elevated plasma calcium in previously untreated animals; the steroid hormone also lowered plasma concentrations of PGE2-M. These findings are consistent with our hypothesis that the hypercalcemic syndrome in VX2 tumor-bearing rabbits is due to the secretion of PGE2 by the tumor.
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PMID:Plasma concentrations of 13,14-dihydro-15-keto-prostaglandin E2 in rabbits bearing the VX2 carcinoma: effects of hydrocortisone and indomethacin. 89 22

Prostaglandin biosynthesis and metabolism were studied in the VX2 carcinoma-bearing rabbit, an animal model of prostaglandin-mediated hypercalcemia. All the identification and quantification of the prostaglandins were done by gas chromatography-mass spectrometry. The tumor incubated in vitro converted exogeneous arachidonic acid principally to PGE2. Biosynthesis from endogenous precursor lipids yields mainly PGE2 and PGF2alpha. The 100,000 x g supernatant fluid of the tumor did not contain any metabolizing enzymes. Significant hypercalcemia developed between the first and second week after tumor implantation. The levels of the major plasma metabolite of PGE2, 15-keto-13,14-dihydro-PGE2, became elevated at one week, had risen 25-fold by the end of the second week, and at the fourth week were elevated to 256 times the pre-incubation levels. The concentration of 15-keto-13,14-dihydro-PGF2alpha in plasma rose in parallell but to a lesser degree. 7alpha-hydroxy-5,11-diketotetranor-prostane-1,16-dioic acid, the major urinary metabolite of the E prostaglandins, was elevated two weeks after tumor implantation and rose until the fifth week. Indomethacin treatment lowered both serum calcium and the plasma level of 15-keto-13,14-dihydro-PGE2.
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PMID:Prostaglandin-mediated hypercalcemia in the VX2 carcinoma-bearing rabbit. 89 23

Peculiarities of Ca2+ accumulation in tumor mitochondria (TM) under different experimental conditions were studied. In the absence of penetrating anions TM were shown to accumulate Ca2+ five times less than liver mitochondria do, this difference being even more in the presence of acetate. pi abolishes the observed defects in Ca2+ transport while increasing considerably the Ca2+-capacity of TM. Besides, as distinct from liver mitochondria, Pi produces a stabilizing effect upon the membrane permeability of TM, which can be responsible for the increase in the TM Ca2+-capacity.
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PMID:[Ca2+ ion transport in the mitochondria of Ehrlich ascites tumor cells]. 90 25

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


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