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

A 41-year-old woman was diagnosed as having Werner's syndrome associated with bladder cancer. The patient noticed sudden, total gross hematuria in September, 1985. Cystoscopy revealed a papillary tumor with a stalk that was accompanied by a daughter tumor and concealed the left ureteral orifice. The tumors were 25 X 20 X 10 mm and 15 X 10 X 5 mm. Double contrast cystograms, computed tomography and transurethral echo showed no invasion of muscle layer. Intravesical instillation of mitomycin (10 mg), cylocide (300 mg) and adriacin (30 mg) was carried out 3 times per week for 4 weeks. Tumor size was reduced, and then TUR was performed. High power section of the removed bladder tumor showed pathologically PNT, TCC, grade II, INF alpha, pTla, lyo and v(-). The patient had such clinical manifestations as short stature with low body weight, thin limbs and stocky trunk, senile face, early graying hair, highpitched voice, bilateral cataracts, osteoporosis, sclerodermia-like signs, flat feet, tendency toward diabetes mellitus and parental consanguinity. Hyaluronic acid was not detected in the urine. To the best of our knowledge, this seems to be the 30th report describing the association of malignancy with Werner's syndrome in Japan; besides, only one other case of bladder cancer in Werner's syndrome has been reported to date in the world.
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PMID:[A case of Werner's syndrome associated with bladder cancer]. 359 91

Tumor cell attachment to host endothelium appears to be one of the specific steps occurring during the formation of distant metastasis, in which interactions of extracellular matrix molecules between tumor cells and endothelial cells are greatly involved. From mouse mammary carcinoma cells with no apparent lung-colonizing capacity (FM3A P-O), Honma et al. (Gann, 72, 898-905, 1981) selected two variant sublines, P-15A and P-10, for their ability to form lung tumor colonies with relatively high and low efficiencies, respectively. Comparison of their extracellular matrix products indicated that the rate of hyaluronic acid synthesis in both metastatic variants was about 60 times the rate in the parent cells and that there was no apparent association between metastatic ability and the rate of synthesis of other extracellular matrix molecules. Further analysis of the variant cells in vivo and in vitro indicated that the highly metastatic P-15A cells were surrounded by a hyaluronic acid-rich pericellular coat whereas the intermediately metastatic P-10 cells were not, suggesting the involvement of accumulation of hyaluronic acid in the pericellular regions in the potential for metastasis. The extracellular matrix molecules in host endothelium having a capacity to interact with hyaluronic acid were also studied. Bovine pulmonary arterial endothelial cells were metabolically labeled with 35S-methionine. Extraction and subsequent biochemical characterization of the labeled molecules suggested that PG-M-like chondroitin sulfate proteoglycan participated in the binding. These results provide a basis for further investigation of the potential role of interactions of extracellular matrix molecules between host and tumor cells during metastatic processes.
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PMID:[Interaction of extracellular matrix macromolecules between host and metastatic tumor cells]. 360 37

Hyaluronic acid concentrations were measured by a laser nephelometric assay in serum samples from 50 patients with advanced disseminated neoplasm and 50 healthy controls matched for age and sex. The identity of hyaluronic acid was confirmed by a combination of electrophoretic and enzymatic techniques. The mean serum hyaluronic acid concentration for the control group was 1.09 mg/l, with a range of 0-4 mg/l. The mean concentration for patients with neoplastic disease was 10.38 mg/l, with a range of 0-100 mg/l. Sixty two per cent of the patients with disseminated neoplasm had serum hyaluronic acid concentrations above the control range. There was no correlation between the increased concentration of hyaluronic acid and tumour type, serum bilirubin, serum alkaline phosphatase, or serum urea concentrations. There was a higher incidence of hypercalcaemia in patients with increased hyaluronic acid concentrations, but the correlation between hyaluronic acid and calcium concentrations was not significant. In view of the possible role of hyaluronic acid in cellular differentiation and morphogenesis the finding of increased hyaluronic acid concentrations in patients with advanced neoplastic disease may be of fundamental importance in cancer biology.
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PMID:Serum hyaluronic acid in patients with disseminated neoplasm. 361 92

A murine monoclonal antibody, VM-1, which binds to basal cells of normal human epidermis, reduces the ability of human squamous cell carcinoma cells (SCL-1) derived from the skin to attach and spread on collagen by about 50% and causes cell rounding. Similar effects have been previously shown using normal human keratinocytes. The attachment of cell lines derived from human lung squamous cell carcinomas (SW1271 and SW900), melanoma A375, glioblastoma 126, and fibrosarcoma HT1080 is also inhibited by this antibody. VM-1 antibody does not bind to normal human fibroblasts, benign nevus cells, or the human B-cell-derived line 8866. VM-1 antibody inhibits the growth of SCL-1 cells in vitro as measured by cell numbers and [3H]thymidine ([3H]TdR) incorporation. It is not cytolytic in the presence of complement as measured by 51Cr release. Repeated treatment of SCL-1 cells with VM-1 antibody significantly reduces the proportion of SCL-1 cells that attach to collagen. In addition, after treatment of SCL-1 cells with VM-1 antibody, several proteins can no longer be demonstrated by gel electrophoresis of the cell-free supernatant. The VM-1 antibody effect on attachment and spreading is partially reversed by pretreatment of the collagen surface with laminin and fibronectin, but not with the carbohydrates chondroitin-6-sulfate or hyaluronic acid or with the protein lysozyme. By fluorescence staining, the antigen recognized by VM-1 antibody is membrane-bound and Triton X-100 extractable. The VM-1 antigen is excluded from Bio-Sil TSK-400 and sediments at about 10.5 S. It has a covalent molecular weight on the order of 10(6). Proteinase K digestion produces VM-1 antibody reactive fragments, assumed to be polysaccharides, with a polydisperse molecular weight distribution in the range 5000 to 30,000. The VM-1 antigen is partially lost from solution on boiling and is no longer detectable in the aqueous or organic phase after chloroform-methanol extraction. The properties of the VM-1 antigen are consistent with those of a proteoglycan involved in attachment and spreading of keratinocytes and certain tumor cells on collagen.
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PMID:Inhibition of attachment and growth of tumor cells on collagen by a monoclonal antibody. 369 49

A previously described method for determination of hyaluronic acid is modified for the analysis of pleural and ascitic fluids. After 20 microL of the acellular supernate is precipitated with ethanol, the precipitate is digested overnight with chondroitinases and chondroitin sulfatases. The content of hyaluronic acid-derived disaccharide is then analyzed by "high-performance" liquid chromatography. The high sensitivity (detection limit, less than 0.1 microgram of hyaluronate-derived uronic acid per milliliter) and reproducibility (SD = 4% of the mean) enable accurate determination of hyaluronic acid, even in effusions from patients without signs of mesothelioma. The range of values obtained for pleural and ascitic fluids from patients without signs of this kind of tumor is the same as that found by using other techniques, being slightly higher in those patients showing signs of tissue destruction. The concentrations of hyaluronic acid were considerably increased in most, but not all, of the cases of mesothelioma.
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PMID:Liquid-chromatographic determination of hyaluronic acid in pleural and ascitic fluids. 370 19

A case of recurrent and metastasizing subcutaneous myxopapillary ependymoma of the sacrococcygeal region in a 44-year-old man is reported. The tumor was characterized light microscopically by numerous papillary projections, lined by epithelium-like cells, with a variable degree of polymorphism. Histochemical analysis relating to glucosaminoglycans indicated the presence of hyaluronic acid and chondroitin-4- and/or 6-sulfate. Using immunoperoxidase techniques, glial fibrillary acidic protein (GFAP) and S-100 protein were demonstrated within the tumor cells. Ultrastructurally, the tumor cells were characterized by an abundance of intermediate cytoplasmic filaments, prominent interdigitating cytoplasmic projections, the formation of desmosomes and external lamina-like material. The growth pattern in the tissue culture of this tumor is described, and the ultrastructural appearance of the cultured cells revealed features similar to the primary and recurrent tumor. Chromosome analyses by the G-banding technique of early generations of cultured tumor cells revealed a normal diploid stemline without gross chromosomal deviations. Among the different variant cells and clones recorded, those with X chromosome deviations were of special interest since gonosomal deviations have previously been observed in other types of glioma. The differential diagnosis against adenopapillary carcinoma, chordoma and malignant teratoma is briefly discussed.
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PMID:Metastasizing myxopapillary ependymoma of the sacrococcygeal region. A clinico-pathologic, light- and electronmicroscopic, immunohistochemical, tissue culture, and cytogenetic analysis of a case. 371 5

Circulating macrophages and metastatic tumor cells can penetrate the vascular endothelium and migrate from the circulatory system to extravascular compartments. Both activated murine macrophages and different metastatic tumor cells (B16-BL6 melanoma; ESb T-lymphoma) attach, invade, and penetrate confluent vascular endothelial cell monlayer in vitro, by degrading heparan sulfate proteoglycans in the subendothelial extracellular matrix. The sensitivity of the enzymes from the various sources degrading the heparan sulfate proteoglycan was challenged and compared by a series of inhibitors. Activated macrophages demonstrate a heparanase with an endoglycosidase activity that cleaves from the [35S]O4 = -labeled heparan sulfate proteoglycans of the extracellular matrix 10 kDa glycosaminoglycan fragments. The macrophages do not store the heparanase intracellularly but it is instead found pericellularly and requires a continuous cell-matrix contact at the optimal pH for maintaining cell growth. The degradation of [35S]O4 = -labeled extracellular matrix proteoglycans by the macrophages' heparanase is significantly inhibited in the presence of heparan sulfate (10 micrograms/ml), arteparon (10 micrograms/ml), and heparin at a concentration of 3 micrograms/ml. In contrast, other glycosaminoglycans such as hyaluronic acid, dermatan sulfate, and chondroitin sulfate as well as the specific inhibitor of exo-beta-glucuronidase D-saccharic acid 1,4-lactone failed to inhibit the degradation of sulfated proteoglycans in the subendothelial extracellular matrix. Degradation of this heparan sulfate proteoglycan is a two-step sequential process involving protease activity followed by heparanase activity. However, the following antiproteases--alpha 2-macroglobulin, antithrombin III, leupeptin, and phenylmethylsulfony fluoride (PMSF)--failed to inhibit this degradation process, and only alpha 1-antitrypsin inhibited the heparanase activity. B16-BL6 metastatic melanoma cell heparanase, which is also a cell-associated enzyme, was inhibited by heparin to the same extent as the macrophage heparanase. On the other hand, heparanase of the highly metastatic variant (ESb) of a methylcholanthrene-induced T lymphoma, which is an extracellular enzyme released by the cells to the incubation medium, was more sensitive to heparin and arteparon than the macrophages' heparanase, inhibited at concentrations of 1 and 3 micrograms/ml, respectively. These results may indicate the potential use of heparin or other glycosaminoglycans as specific and differential inhibitors for the formation in certain cases of blood-borne tumor metastasis.
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PMID:Murine macrophage heparanase: inhibition and comparison with metastatic tumor cells. 380 31

A new human rhabdomyosarcoma cell strain, designated KYM-1, has been established from a neck tumor found in a 9-month-old infant. The cultured cells were round and mainly free-floating or in a moniliform pattern with a population doubling time of 75 hours. In stained preparations, the cells were pleomorphic and had a single round or oval nucleus in non-striated cytoplasm. However, the intracellular presence of myogenic markers was clearly shown by enzyme-immunochemical stains. An ultrastructural feature of the KYM-1 cells was the presence of numerous intermediate filaments in the perinuclear area and around the Golgi complexes which were associated with abundant cell organelles and aggregates of glycogen granules. High viscosity of the spent culture medium was attributed to hyaluronic acid, identified by electrophoresis and hyaluronidase digestion, and immunological and biochemical analyses revealed that the increased concentration of plasminogen activator activity found in the culture medium was almost wholly of the tissue plasminogen activator type. The KYM-1 cells also contained high concentrations of alkaline phosphatase activity. Tumorigenicity of the cells was confirmed by heterotransplantation into hamsters treated with anti-thymocyte serum.
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PMID:Characterization of a human rhabdomyosarcoma cell strain in tissue culture. 383 Feb 65

In a four-year-old boy a malignant teratoid medulloepithelioma of the ciliary body was removed by means of an 11.0 X 11.0 mm "block excision". Two years later the patients visual acuity was 0.6. The lesion originates in the nonpigmented ciliary epithelium, extending along the lens equator to the pupillary zone and through the iris stroma into the anterior chamber. The tumor shows tubular structures with hyaluronic acid, "retinal rosettes", and areas with ganglion and GFAP-positive glial cells. The immunohistochemical demonstration of the glial fibrillary acidic protein is also of diagnostic value for the classification of tumors of the nonpigmented ciliary epithelium.
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PMID:[Malignant teratoid medulloepithelioma of the ciliary body and glial fibrillary acidic protein. Clinical, histochemical and immunohistochemical findings]. 390 50

Myxoma of the jaw is classified as an odontogenic tumor although final proof for an odontogenic origin is lacking. In the present study glycosaminoglycans (GAG's) in the extracellular matrix of a jaw myxoma were analyzed and compared with known data on GAG's in dental tissues. It was noted that the GAG's formed approximately 1% of the total tumor weight and 17% of the dry weight. Hyaluronic acid formed 72.4% of the GAG-fraction. Neither this high GAG-content nor the high fraction of hyaluronic acid are found in dental tissues and it is concluded that the myxoma matrix differs from the matrix in dental pulp and periodontal ligament.
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PMID:Glycosaminoglycans in myxoma of the jaw: a biochemical study. 392 72


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