Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029463 (osteosarcoma)
16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytologic and cytochemical examination of eighteen cases of round-cell sarcoma of bone allowed classification of these tumors into four cytologic groups. Additional cytochemical examinations based on the PAS and D-PAS reactions, and the demonstration of the activity of peroxidase, naphtol-ASD-Chloracetate esterase, alpha-naphthylacetate esterase, naphthol-AS-acetate esterase with and without sodium fluoride inhibition, acid and alkaline phosphatases yielded no evidence of uniform behavior among the individual groups or within any single group. The studies showed that a positive glycogen reaction cannot be used as a basic criterion for the classification of such tumors as Ewing's sarcoma and for regarding them as a uniform tumor group. It is possible that a pool of tumors is involved, including tumors of monocytic and probably of lymphocytic origin, reticulum-cell sarcoma, tumors of myelocytic and erythroplastic origin, stem-cell tumors, and endothelial-cell tumors. Histologic examination alone is not sufficient for the classification of round-cell sarcomas of bone, and it should be supplemented by cytologic and cytochemical or histochemical methods. Osteosarcomas (23 cases) and chondrosarcomas (8 cases) display cells which are characteristic for these tumors and which could be correlated with their benign counterparts, osteoblasts and chondroid cells. The histologically recognizable degree of malignancy of chondrosarcoma can be evaluated better with the cytologic than with the histologic technic. Indications of the possibilities of differential diagnosis based on the cytologic pictures of benign and malignant osteoplastic and chondroplastic tumors, giant-cell tumors and chordoma are discussed.
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PMID:Cytologic and cytochemical behavior of primary malignant bone tumors. 18 69

PTH-related peptide (PTHrP) has been shown to be the major mediator of hypercalcemia of malignancy, but may also exert effects on cell growth and differentiation. The Leydig cell tumor H-500, when implanted in Fischer rats, produces abundant PTHrP and eventually causes the death of the host animal. In the present study we have used antisense RNA technology to block the effects of PTHrP in H-500 Leydig tumor cells in vivo. The full-length rat PTHrP complementary DNA encoding amino acid -36-->141 was subcloned as an EcoRI-BglII insert in the antisense orientation into the mammalian expression vector pRc/CMV to produce the plasmid pRc-PAS. This plasmid was then stably transfected into the H-500 Leydig tumor cells with a Lipofectin reagent. After selection with the neomycin derivative G-418, a stable cell line, H-500-PTHrP-AS, was obtained which showed 80% inhibition of endogenous PTHrP messenger RNA compared to wild-type or vector-only transfected H-500 cells. Conditioned culture medium from these experimental cells showed a marked decrease in PTHrP immunoreactivity and in the ability of the medium to stimulate adenylate cyclase in UMR-106 rat osteosarcoma cells. Furthermore, inhibition of PTHrP production resulted in a significant increase in the doubling time of the H-500 cells. Transfection of the experimental plasmid into Rat-2 fibroblasts, which do not produce PTHrP, had no effect on cell growth. Control and experimental cells were then implanted sc into male Fischer rats. Animals were killed at timed intervals, and their tumor volumes were determined. Experimental animals receiving cells transfected with antisense PTHrP plasmid showed near-normal levels of plasma calcium and decreased expression of tumoral PTHrP messenger RNA. These animals also showed a 30-70% lower tumor volume during the course of the experiment compared to control animals. These studies have demonstrated that PTHrP can play a role as a promoter of tumor growth in vitro and in vivo.
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PMID:Regulation in vivo of the growth of Leydig cell tumors by antisense ribonucleic acid for parathyroid hormone-related peptide. 758 90

A case of myositis ossificans in 15-year old boy that occurred as a complication of the recurrent synovia hemangioma of the left knee was presented. The alteration was diagnosed as: osteosarcoma, chondrosarcoma and chondromyxoid fibroma by the pathologists from other institutions. The diagnosis of myositis ossificans was established using numerous histochemical and immunochemical methods (PAS, PAS diastasis, Alcian blue, Masson trichrom, von Kossa, Azur A, Toluidin blue, Goldner, method by Peris, Citokeratin, S-100, NSE and Vimentin). The presence of zonal phenomenon, as the one observed in the presented case, is one of the most significant criteria for differentiation of myositis ossificans from osteosarcoma.
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PMID:[Myositis ossificans in recurrent synovial hemangioma of the knee]. 1083 65

Structural changes in the extracellular matrix (ECM) are necessary for cell migration during tissue remodeling. MMPs, VEGF, Ki-67 (proliferative protein), and constituents of ECM play a critical role in angiogenesis and underlie neoplastic invasion and metastasis. This prompted us to investigate the effect of a diet containing lysine, proline, arginine, ascorbic acid, and green tea extract (NM) on the growth of tumors induced by implanting human osteosarcoma MNNG in athymic nude mice and the expression of MMPs, VEGF, Ki-67 and fibronectin in these tumors, as well as the production of mucin (by PAS staining). We also investigated the effect of the supplemented diet on serum ascorbic acid, total protein content, alkaline phosphatase activity, and liver enzymes. Athymic male nude mice (n = 12) were inoculated with 3 x 10(6) osteosarcoma cells MNNG-HOS and randomly divided into group A (fed a regular diet) and group B (fed a regular diet supplemented with 0.5% NM). Four weeks later, the mice were sacrificed. Results showed that NM inhibited the growth and reduced the size of tumors in nude mice. Histological evaluation revealed increased mitotic index, MMP-9, and VEGF secretion in the control group tissues. Results demonstrate that the nutrient mixture of lysine, proline, arginine, ascorbic acid, and green tea extract tested strongly suppressed the growth of tumors without adverse effects in nude mice, suggesting potential as an anticancer agent.
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PMID:Effect of ascorbic acid, lysine, proline, and green tea extract on human osteosarcoma cell line MNNG-HOS xenografts in nude mice: evaluation of tumor growth and immunohistochemistry. 1701 99

Klotho is originally discovered as an anti-aging gene and knock-out of klotho accelerates aging in mice. Subsequent studies support the anti-carcinogenesis role of klotho in a variety of human malignancies. The present study investigated the role of klotho on growth and metastasis of osteosarcoma cells. The osteosarcoma cells were transduced with lentivirus particles encoding klotho or scramble control. The reconstructed osteosarcoma cells were injected into the femoral medullary cavity of nude mice to establish a xenograft animal model. The anti-tumor properties of klotho were evaluated in terms of tumor growth, apoptosis, glycogen production, and pulmonary metastasis. Lentivirus-mediated overexpression of klotho significantly decreased tumor volume and weight in osteosarcoma mice. Determination of PCNA and Ki67 expression revealed that overexpression of klotho inhibited cell proliferation in tumor tissues obtained from osteosarcoma xenografts. PAS staining also showed that overexpression of klotho significantly decreased the production of glycogen in osteosarcoma. Moreover, TUNEL positive cells were significantly increased after lentivirus-mediated overexpression of klotho. Furthermore, lentivirus-mediated upregulation of klotho reduced the number of pulmonary metastatic lesions in mice compared to control mice. These findings demonstrated that elevated klotho could inhibit osteosarcoma cell growth and pulmonary metastasis in vivo, suggesting that klotho may be a valuable therapeutic target for osteosarcoma.
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PMID:Overexpression of klotho suppresses growth and pulmonary metastasis of osteosarcoma in vivo. 3261 56