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1. Karita M, Tsuchiya H, Kawahara M, Kasaoka S, Tomita K: The antitumor effect of liposome-encapsulated cisplatin on rat osteosarcoma and its enhancement by caffeine. Anticancer Res; 2008 May-Jun;28(3A):1449-57
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  • [Title] The antitumor effect of liposome-encapsulated cisplatin on rat osteosarcoma and its enhancement by caffeine.
  • BACKGROUND: Drug delivery systems are for the purpose of targeting a drug to a specific tissue selectively and at the same time preventing a drug from accumulating in healthy organs.
  • Liposomes have been proposed as useful drug carriers in targeted drug delivery system and are under investigation in several therapeutic fields.
  • The action of CDDP-L on rat osteosarcoma and the enhancing action of caffeine on the antitumor effect of CDDP-L were evaluated.
  • Using osteosarcoma-bearing rats, the retention of CDDP-L in the blood, its intratumor concentration, cytoreductive effect and the enhancing action of caffeine on its antitumor effect were examined.
  • RESULTS: The liposomes were able to remain in the systemic circulation for a long time and to be concentrated in the osteosarcoma, but that action did not produce an effect corresponding to the quantity of cisplatin which was encapsulated reaching the tumor.
  • CONCLUSION: CDDP-L combined with caffeine treatment can produce better results for osteosarcoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Bone Neoplasms / drug therapy. Caffeine / pharmacology. Cisplatin / administration & dosage. Osteosarcoma / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Screening Assays, Antitumor. Drug Synergism. Liposomes / administration & dosage. Liposomes / pharmacokinetics. Male. Rats. Rats, Inbred F344

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  • (PMID = 18630498.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Liposomes; 3G6A5W338E / Caffeine; Q20Q21Q62J / Cisplatin
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2. Brounais B, Chipoy C, Mori K, Charrier C, Battaglia S, Pilet P, Richards CD, Heymann D, Rédini F, Blanchard F: Oncostatin M induces bone loss and sensitizes rat osteosarcoma to the antitumor effect of Midostaurin in vivo. Clin Cancer Res; 2008 Sep 1;14(17):5400-9
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  • [Title] Oncostatin M induces bone loss and sensitizes rat osteosarcoma to the antitumor effect of Midostaurin in vivo.
  • PURPOSE: In cultures, the cytokine oncostatin M (OSM) reduces the growth and induces differentiation of osteoblasts and osteosarcoma cells into glial/osteocytic cells.
  • EXPERIMENTAL DESIGN: Adenoviral gene transfer of OSM (AdOSM) was done in naive and osteosarcoma-bearing rats, alone or in combination with Midostaurin (PKC412), a derivative of staurosporine currently used in cancer clinical trials.
  • Bone variables were analyzed by micro-computed tomography scanner, by histology, and by the levels of various serum bone markers.
  • Osteosarcoma progression was analyzed by the development of the primary bone tumor, evolution of pulmonary metastasis, histology (necrosis and fibrosis), and animal survival.
  • In an osteosarcoma rat model, the combination of AdOSM with PKC412 reduced the progression of the primary bone tumor, pulmonary metastatic dissemination, and increased overall survival, whereas these agents alone had no antitumor effect.
  • Increased tumor necrosis and tissue repair (fibrosis) were observed with this combination.
  • CONCLUSION: These in vivo experiments confirm that systemic OSM overexpression alters osteoblast/osteosarcoma activity.
  • Because OSM sensitizes rat osteosarcoma to apoptosis/necrosis, the use of kinase inhibitors such as Midostaurin in association with OSM could represent new adjuvant treatments for this aggressive malignancy.
  • [MeSH-major] Bone Neoplasms / drug therapy. Oncostatin M / pharmacology. Osteosarcoma / drug therapy. Staurosporine / analogs & derivatives

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  • (PMID = 18765531.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 106956-32-5 / Oncostatin M; 120685-11-2 / 4'-N-benzoylstaurosporine; H88EPA0A3N / Staurosporine
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3. Théoleyre S, Mori K, Cherrier B, Passuti N, Gouin F, Rédini F, Heymann D: Phenotypic and functional analysis of lymphocytes infiltrating osteolytic tumors: use as a possible therapeutic approach of osteosarcoma. BMC Cancer; 2005;5:123
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  • [Title] Phenotypic and functional analysis of lymphocytes infiltrating osteolytic tumors: use as a possible therapeutic approach of osteosarcoma.
  • BACKGROUND: Osteosarcoma is the most common type of primary bone tumor.
  • The use of aggressive chemotherapy has drastically improved the prognosis of the patients with non-metastatic osteosarcomas, however the prognosis of the patients with metastasis is still very poor.
  • Then, new and more effective treatments for curing osteosarcoma, such as immunotherapy are needed.
  • Tumor-infiltrating lymphocytes (TIL) have been involved in the control of tumor development and already assessed with success for the treatment of several cancers including melanoma.
  • While TIL represent a fascinating therapeutic approach in numerous malignant pathologies, there is few report concerning adult bone-associated tumors including osteosarcoma.
  • METHODS: Human TIL were isolated and characterized (phenotype, lytic activity) from twenty-seven patients with bone-associated tumors (osteosarcoma, Ewing's sarcoma, giant cell tumor, chondrosarcoma, plasmocytoma and bone metastases).
  • Similar experiments were performed using rat osteosarcoma model.
  • RESULTS: While TIL with a main CD4+ profile were easily isolated from most of the tumor samples, only TIL extracted from osteosarcoma were cytotoxic against allogeneic tumor cells.
  • Similar data were observed in rat osteosarcoma model where TIL were characterized by a main CD4+ profile and high lytic activity against allogeneic and autologous tumor cells.
  • Moreover, rat TIL expansion was not accompanied by refractoriness to further activation stimulus mainly by tumor antigens.
  • CONCLUSION: These results demonstrated that TIL therapy could be a very efficient strategy for the treatment of adult osteosarcoma.
  • [MeSH-major] Bone Neoplasms / pathology. Lymphocytes / pathology. Osteolysis. Osteosarcoma / pathology

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  • (PMID = 16188028.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1262697
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4. Geng S, Sun B, Liu S, Wang J: Up-regulation of connexin 43 and gap junctional intercellular communication by Coleusin Factor is associated with growth inhibition in rat osteosarcoma UMR106 cells. Cell Biol Int; 2007 Nov;31(11):1420-7
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  • [Title] Up-regulation of connexin 43 and gap junctional intercellular communication by Coleusin Factor is associated with growth inhibition in rat osteosarcoma UMR106 cells.
  • Numerous researches has suggested the possibility of connexins as potential anti-tumour targets for chemoprevention and chemotherapy.
  • We investigated the ability of Coleusin Factor (CF, also named FSK88) to regulate the Cx43 expression and GJIC level in rat osteosarcoma UMR106 cells.
  • The results have demonstrated that CF increased the mRNA and protein expression of Cx43 in both in a dose- and timedependent manner, and concomitant with up-regulation of Cx43, CF treatment up-regulated the diminished GJIC level in UMR106 cells as assayed by dye transfer experiments.
  • In addition, Cx43 distribution at the plasma membrane was also enhanced dramatically by CF treatment.
  • [MeSH-major] Colforsin / analogs & derivatives. Colforsin / metabolism. Connexin 43 / metabolism. Gap Junctions / metabolism. Osteosarcoma / metabolism. Up-Regulation

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  • (PMID = 17681476.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Connexin 43; 1F7A44V6OU / Colforsin
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5. Tomoda R, Seto M, Hioki Y, Sonoda J, Matsumine A, Kusuzaki K, Uchida A: Low-dose methotrexate inhibits lung metastasis and lengthens survival in rat osteosarcoma. Clin Exp Metastasis; 2005;22(7):559-64
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  • [Title] Low-dose methotrexate inhibits lung metastasis and lengthens survival in rat osteosarcoma.
  • Lung metastasis is the most crucial event affecting the treatment of osteosarcoma and is dependent on tumor angiogenesis.
  • To improve the prognosis for patients with osteosarcoma, prevention of lung metastasis is essential.
  • Low-dose methotrexate is a useful drug for treating a variety of diseases.
  • We investigated the inhibitory effect of methotrexate on lung metastasis in a rat osteosarcoma cell line with high metastatic potential, S-SLM.
  • We also evaluated the effect of methotrexate on the proliferation of endothelial cells and S-SLM osteosarcoma cells in vitro.
  • Methotrexate significantly inhibited the proliferation of endothelial cells at a lower concentration than that of S-SLM osteosarcoma cells.
  • These data suggest that low-dose methotrexate inhibited lung metastasis of osteosarcoma through its antiangiogenic activity.
  • Our results indicate that low-dose methotrexate is a promising drug for tumor dormancy therapy in patients with osteosarcoma and lung metastasis.
  • [MeSH-major] Bone Neoplasms / drug therapy. Lung Neoplasms / secondary. Methotrexate / therapeutic use. Osteosarcoma / drug therapy
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / therapeutic use. Cell Division / drug effects. Cell Line, Tumor. Disease Models, Animal. Dose-Response Relationship, Drug. Male. Neoplasm Metastasis / pathology. Neoplasm Metastasis / prevention & control. Rats. Rats, Inbred F344. Survival Analysis

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  • (PMID = 16475026.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
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6. Yoshitani K, Honoki K, Morishita T, Kido A, Miyauchi Y, Mii Y, Takakura Y: Growth inhibition of rat osteosarcoma and malignant fibrous histiocytoma cells by tyrosine kinase inhibitor STI571. In Vivo; 2003 May-Jun;17(3):255-8
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  • [Title] Growth inhibition of rat osteosarcoma and malignant fibrous histiocytoma cells by tyrosine kinase inhibitor STI571.
  • We have recently established rat osteosarcoma and malignant fibrous histiocytoma (MFH) cell lines.
  • RT-PCR analysis revealed that MFH and osteosarcoma cell lines expressed high and very low levels of PDGFR alpha respectively, and that all cell lines expressed similar levels of PDGFR beta.
  • The effect of STI571 on cellular growth measured by MTS colorimetric dye reduction showed that the growth of each cell line was inhibited in a dose- and time-dependent manner.
  • These data suggested that STI571 tyrosine kinase inhibitor plays a role in blocking or slowing the rate of growth of MFH and osteosarcoma cells expressing tyrosine kinase type receptor.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Histiocytoma, Benign Fibrous / drug therapy. Osteosarcoma / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Animals. Benzamides. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Imatinib Mesylate. Proto-Oncogene Proteins c-kit / genetics. RNA, Messenger / genetics. Rats

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  • (PMID = 12929576.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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7. Sneddon WB, Syme CA, Bisello A, Magyar CE, Rochdi MD, Parent JL, Weinman EJ, Abou-Samra AB, Friedman PA: Activation-independent parathyroid hormone receptor internalization is regulated by NHERF1 (EBP50). J Biol Chem; 2003 Oct 31;278(44):43787-96
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  • Parathyroid hormone (PTH) regulates extracellular calcium homeostasis through the type 1 PTH receptor (PTH1R) expressed in kidney and bone.
  • Using a combination of radioligand binding experiments and quantitative, live cell confocal microscopy of fluorescently tagged PTH1Rs, we show that in kidney distal tubule cells and rat osteosarcoma cells, which lack NHERF1, the synthetic antagonist PTH-(7-34) and naturally circulating PTH-(7-84) induce internalization of PTH1R in a beta-arrestin-independent but dynamin-dependent manner.
  • [MeSH-major] Phosphoproteins / physiology. Receptor, Parathyroid Hormone, Type 1 / metabolism
  • [MeSH-minor] Actins / metabolism. Amino Acid Motifs. Animals. Arrestins / metabolism. Bone and Bones / metabolism. Cell Line. Cyclic AMP / metabolism. Cytoskeleton / metabolism. DNA, Complementary / metabolism. Dynamins / metabolism. Endocytosis. Genes, Dominant. Humans. Immunoblotting. Inositol Phosphates / metabolism. Kidney / metabolism. Ligands. Mice. Microscopy, Confocal. Microscopy, Fluorescence. Mutation. Precipitin Tests. Protein Structure, Tertiary. Protein Transport. Rats. Sodium-Hydrogen Antiporter. Time Factors

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  • (PMID = 12920119.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-54171; United States / NIDDK NIH HHS / DK / DK-62078
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Arrestins; 0 / DNA, Complementary; 0 / Inositol Phosphates; 0 / Ligands; 0 / Phosphoproteins; 0 / Receptor, Parathyroid Hormone, Type 1; 0 / Sodium-Hydrogen Antiporter; 0 / beta-arrestin; 0 / sodium-hydrogen exchanger regulatory factor; E0399OZS9N / Cyclic AMP; EC 3.6.5.5 / Dynamins
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8. Chipoy C, Berreur M, Couillaud S, Pradal G, Vallette F, Colombeix C, Rédini F, Heymann D, Blanchard F: Downregulation of osteoblast markers and induction of the glial fibrillary acidic protein by oncostatin M in osteosarcoma cells require PKCdelta and STAT3. J Bone Miner Res; 2004 Nov;19(11):1850-61
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  • [Title] Downregulation of osteoblast markers and induction of the glial fibrillary acidic protein by oncostatin M in osteosarcoma cells require PKCdelta and STAT3.
  • The effects of OSM on proliferation and differentiation of osteosarcoma and nontransformed osteoblasts were analyzed.
  • OSM downregulates osteoblast markers but induces the glial fibrillary acidic protein by the combined activation of PKCdelta and STAT3, offering new lines of therapeutic investigations.
  • INTRODUCTION: Oncostatin M (OSM) is a multifunctional cytokine of the interleukin-6 family implicated in embryonic development, differentiation, inflammation, and regeneration of various tissues, mainly the liver, bone, and the central nervous and hematopoietic systems.
  • One particularity of OSM relies on its growth inhibitory and pro-differentiating effects on a variety of tumor cell lines such as melanoma, providing arguments for a therapeutic application of OSM.
  • The objective of this study was to analyze the effects of OSM on osteosarcoma cell lines proliferation and differentiation.
  • RESULTS: OSM inhibits the growth of rat osteosarcoma cell lines as well as normal osteoblasts, in correlation with induction of the cyclin-dependent kinases inhibitor p21WAF1.
  • This inhibitory effect is restricted to mature osteoblasts and differentiated osteosarcoma because OSM effectively stimulates osteoblast markers and bone nodule formation in early, but not late, bone marrow mesenchymal stem cell (BMSC) cultures.
  • In osteosarcoma cells or BMSC, OSM induces expression of the glial fibrillary acidic protein (GFAP) as well as morphological and ultrastructural changes, for example, elongated shape and bundles of microfilaments in cell processes.
  • CONCLUSIONS: These results highlight the particular gene expression profile of OSM-treated osteosarcoma cells and BMSCs, suggesting either a osteocytic or a glial-like phenotype.
  • Together with the implication of PKCdelta, ERK1/2, and STAT3, these results offer new lines of investigations for neural cell transplantation and osteosarcoma therapy.
  • [MeSH-minor] Alkaline Phosphatase / metabolism. Animals. Anthraquinones / pharmacology. Blotting, Western. Bone Marrow Cells / cytology. Bone and Bones / metabolism. Butadienes / pharmacology. Cell Cycle Proteins / metabolism. Cell Differentiation. Cell Line, Tumor. Cell Proliferation. Cyclin-Dependent Kinase Inhibitor p21. DNA / metabolism. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Immunohistochemistry. Inflammation. Integrin-Binding Sialoprotein. Interleukin-6 / metabolism. Mesoderm / cytology. Microscopy, Confocal. Microscopy, Electron. Models, Biological. Nitriles / pharmacology. Osteocalcin / metabolism. Osteosarcoma / metabolism. Protein Kinase C-delta. RNA, Messenger / metabolism. Rats. Regeneration. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor. Sialoglycoproteins / metabolism. Signal Transduction. Stem Cells / cytology. Thymidine / chemistry. Time Factors. Transfection

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  • (PMID = 15476586.001).
  • [ISSN] 0884-0431
  • [Journal-full-title] Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • [ISO-abbreviation] J. Bone Miner. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthraquinones; 0 / Butadienes; 0 / Cdkn1a protein, rat; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Glial Fibrillary Acidic Protein; 0 / Ibsp protein, rat; 0 / Integrin-Binding Sialoprotein; 0 / Interleukin-6; 0 / Nitriles; 0 / RNA, Messenger; 0 / STAT3 Transcription Factor; 0 / Sialoglycoproteins; 0 / Stat3 protein, rat; 0 / Trans-Activators; 0 / U 0126; 104982-03-8 / Osteocalcin; 3F3AT0Q12H / Alizarin Red S; 9007-49-2 / DNA; EC 2.7.1.- / Prkcd protein, rat; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C-delta; EC 3.1.3.1 / Alkaline Phosphatase; VC2W18DGKR / Thymidine
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9. Heymann D, Ory B, Blanchard F, Heymann MF, Coipeau P, Charrier C, Couillaud S, Thiery JP, Gouin F, Redini F: Enhanced tumor regression and tissue repair when zoledronic acid is combined with ifosfamide in rat osteosarcoma. Bone; 2005 Jul;37(1):74-86
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  • [Title] Enhanced tumor regression and tissue repair when zoledronic acid is combined with ifosfamide in rat osteosarcoma.
  • The efficacy of zoledronic acid (ZOL), with or without the anticancer drug ifosfamide (IFO), was tested on primary bone tumor growth using a rat-transplantable model of osteosarcoma.
  • The effects on bone remodeling and tumor growth were analyzed by radiography, micro-computed tomography (micro-CT), and histological staining.
  • The in vitro effects of ZOL were studied by proliferation, apoptosis, and cell cycle analyses on the osteosarcoma cells OSRGA compared to rat primary osteoblasts.
  • Treatment with ZOL was effective in preventing the formation of osteolytic lesions that developed in bone sites and in reducing the local tumor growth, as compared to the untreated rats.
  • The combination of ZOL and IFO was more effective than each agent alone in preventing tumor recurrence, improving tissue repair, and increasing bone formation as revealed by the analysis of trabecular architecture.
  • In situ cell death was determined by TUNEL staining on tumor tissue sections.
  • This is the first report of the anti-bone resorption and antitumoral activities of zoledronic acid in a rat model of osteosarcoma, and its beneficial association with an antitumoral chemotherapeutic drug in preventing tumor recurrence.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Osteosarcoma / drug therapy
  • [MeSH-minor] Animals. Bone Remodeling / drug effects. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Diphosphonates / administration & dosage. Fibrosis. Ifosfamide / administration & dosage. Imidazoles / administration & dosage. Male. Necrosis. Neoplasm Metastasis / drug therapy. Neoplasm Recurrence, Local / drug therapy. Osteoblasts / metabolism. Osteogenesis / drug effects. Rats. Rats, Sprague-Dawley. S Phase / drug effects. Survival Rate. Tibia / pathology. Tibia / radiography. Time Factors. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 15894525.001).
  • [ISSN] 8756-3282
  • [Journal-full-title] Bone
  • [ISO-abbreviation] Bone
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid; EC 3.4.22.- / Caspases; UM20QQM95Y / Ifosfamide
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10. Chen J, Gu CL, Wan SL, Fan SW: [Enhancement effect of caffeine on chemotherapy of osteosarcoma in Fischer 344/N rats]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2005 Sep;34(5):390-4
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  • [Title] [Enhancement effect of caffeine on chemotherapy of osteosarcoma in Fischer 344/N rats].
  • OBJECTIVE: To determine the enhancement effects of caffeine on chemotherapy of transplanted osteosarcoma in Fischer 344/N rats.
  • METHODS: Osteosarcoma-bearing Fischer 344/N rats were treated with cisplatin 2.5 mg/kg (Group DDP), caffeine 90 mg/kg x 2 d (Group caffeine), and cisplatin 2.5 mg/kg plus caffeine 90 mg/kg x 2 d (Group DDP+caffeine), and the control group was treated with normal saline in the same volume.
  • All drugs were given by intra-peritoneum injection with micro-pump, in the rate of 0.5 ml/h.
  • The tumor growth inhibition rate, PCNA index and apoptosis index were calculated, and the survival time were recorded.
  • And the survival time was (33.63 +/-4.63)d in control group, (52.13 +/-11.74)d in Group DDP, (35.63 +/-5.15)d in Group caffeine, and (55.13 +/-16.23)d in Group DDP+caffeine (P <0.01).
  • CONCLUSION: Caffeine could enhance the anti-tumor effect of cisplatin in rat osteosarcoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Caffeine / therapeutic use. Cisplatin / therapeutic use. Osteosarcoma / drug therapy
  • [MeSH-minor] Animals. Drug Synergism. Neoplasm Transplantation. Rats. Rats, Inbred F344

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  • (PMID = 16216047.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 3G6A5W338E / Caffeine; Q20Q21Q62J / Cisplatin
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11. Fujimoto T, Finnegan M: The effect of gadodiamide on cancer cell lines. Exp Oncol; 2009 Sep;31(3):185-7
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  • Human myeloma cell lines have demonstrated stimulated cell proliferation by the gadolinium cation through this receptor, and osteosarcoma cell lines possess the same cation receptor.
  • Although enhanced MRI is a very useful diagnostic tool for the treatment of sarcoma in the orthopedic area, incorporating the use of MRI contrast agents based on gadolinium raises the possibility of the stimulation of cancer cell growth.
  • METHODS: Human myeloma (RPMI 8226), osteosarcoma (Saos-2) and rat osteosarcoma (UMR-106) cell lines were exposed to various concentrations of common MRI contrast agent gadodiamide Omniscan (5 microM, 50 microM, 500 microM, 5 mM, 50 mM) in a culture medium.
  • RESULTS: Treatment with 5 microM to 5 mM gadodiamide did not stimulate cell proliferation; only cells exposed to 50 mM gadodiamide showed suppressed proliferation rates.
  • CONCLUSIONS: Since intravenously injected gadodiamide is diluted from 500 microM to 1 mM by patient blood flow at enhanced MRI examinations, the results of the present study suggest that gadodiamide has not effect on these types of cancer cells.
  • [MeSH-major] Bone Neoplasms / drug therapy. Cell Proliferation / drug effects. Contrast Media / pharmacology. Gadolinium DTPA / pharmacology. Multiple Myeloma / drug therapy. Osteosarcoma / drug therapy

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  • (PMID = 19783960.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Contrast Media; 0 / DNA, Neoplasm; 84F6U3J2R6 / gadodiamide; K2I13DR72L / Gadolinium DTPA
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12. Wang H, Ng TB, Ooi VE, Liu WK: Effects of lectins with different carbohydrate-binding specificities on hepatoma, choriocarcinoma, melanoma and osteosarcoma cell lines. Int J Biochem Cell Biol; 2000 Mar;32(3):365-72
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  • [Title] Effects of lectins with different carbohydrate-binding specificities on hepatoma, choriocarcinoma, melanoma and osteosarcoma cell lines.
  • The effects of lectins with different carbohydrate-binding specificities on human hepatoma (H3B), human choriocarcinoma (JAr), mouse melanoma (B16) and rat osteosarcoma (ROS) cell lines were investigated.
  • [MeSH-major] Carbohydrate Metabolism. Lectins / metabolism. Lectins / pharmacology. Neoplasms / drug therapy. Neoplasms / metabolism
  • [MeSH-minor] Animals. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Division / drug effects. Cell Survival / drug effects. Choriocarcinoma / drug therapy. Choriocarcinoma / metabolism. Choriocarcinoma / pathology. Female. Humans. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Melanoma, Experimental / drug therapy. Melanoma, Experimental / metabolism. Melanoma, Experimental / pathology. Mice. Osteosarcoma / drug therapy. Osteosarcoma / metabolism. Osteosarcoma / pathology. Pregnancy. Rats. Tumor Cells, Cultured. Uterine Neoplasms / drug therapy. Uterine Neoplasms / metabolism. Uterine Neoplasms / pathology. Wheat Germ Agglutinins / metabolism. Wheat Germ Agglutinins / pharmacology

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  • (PMID = 10716633.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Lectins; 0 / Wheat Germ Agglutinins
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13. Rivera-Bermúdez MA, Bertics PJ, Albrecht RM, Mosavin R, Mellon WS: 1,25-Dihydroxyvitamin D3 selectively translocates PKCalpha to nuclei in ROS 17/2.8 cells. Mol Cell Endocrinol; 2002 Feb 25;188(1-2):227-39
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  • We have investigated protein kinase C (PKC) regulation by 1,25-(OH)2D3 in the rat osteosarcoma cell line ROS 17/2.8 since previous reports have implicated PKC in the 1,25-(OH)2D3-mediated regulation of osteocalcin gene expression (J. Biol. Chem.
  • Here we report that 1,25-(OH)2D3 increased PKCalpha, but not PKCbetaI, epsilon or zeta, levels in the nuclear fraction in a time-dependent manner.
  • Treatment with 20 nM 1,25-(OH)2D3 for 15 min, 30 min, 1 h and 24 h increased PKCalpha levels in the nuclear fraction by 2.3- to 2.6-fold.
  • 332 (1996) 142) was inhibited with bisindolylmaleimide treatment, suggesting that PKCalpha may be involved in the 1,25-(OH)2D3-mediated regulation of osteocalcin gene expression.
  • [MeSH-major] Bone Neoplasms / drug therapy. Calcitriol / pharmacology. Calcium Channel Agonists / pharmacology. Isoenzymes / metabolism. Osteosarcoma / drug therapy. Protein Kinase C / metabolism
  • [MeSH-minor] Blotting, Northern. Cell Nucleus / enzymology. Dactinomycin / pharmacology. Fluorescent Antibody Technique. Gene Expression. Humans. Immunoblotting. Osteocalcin / genetics. Osteocalcin / metabolism. Protein Kinase C-alpha. RNA, Messenger / metabolism. Subcellular Fractions. Tetradecanoylphorbol Acetate / pharmacology. Time Factors. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / enzymology

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  • (PMID = 11911960.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Calcium Channel Agonists; 0 / Isoenzymes; 0 / RNA, Messenger; 104982-03-8 / Osteocalcin; 1CC1JFE158 / Dactinomycin; EC 2.7.11.13 / PRKCA protein, human; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C-alpha; FXC9231JVH / Calcitriol; NI40JAQ945 / Tetradecanoylphorbol Acetate
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14. Reddy GS, Robinson M, Wang G, Palmore GT, Gennaro L, Vouros P, De Clercq P, Vandewalle M, Young W, Ling S, Verstuyf A, Bouillon R: Removal of C-ring from the CD-ring skeleton of 1alpha,25-dihydroxyvitamin D3 does not alter its target tissue metabolism significantly. Arch Biochem Biophys; 2007 Apr 15;460(2):254-61
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  • [Title] Removal of C-ring from the CD-ring skeleton of 1alpha,25-dihydroxyvitamin D3 does not alter its target tissue metabolism significantly.
  • It is now well established that 1alpha,25(OH)2D3 is metabolized in its target tissues through the modifications of both side chain and A-ring.
  • During the past two decades, a great number of vitamin D analogs were synthesized by altering the structure of both side chain and A-ring of 1alpha,25(OH)2D3 with the aim to generate novel vitamin D compounds that inhibit proliferation and induce differentiation of various types of normal and cancer cells without causing significant hypercalcemia.
  • Previously, we used some of these analogs as molecular probes to examine how changes in 1alpha,25(OH)2D3 structure would affect its target tissue metabolism.
  • Presently, it is unknown how the removal of C-ring from the CD-ring skeleton of 1alpha,25(OH)2D3 would affect its target tissue metabolism.
  • In the present study, we compared the metabolic fate of SL 117 and WU 515 with that of 1alpha,25(OH)2D3 in both the isolated perfused rat kidney, which expresses only the C-24 oxidation pathway and rat osteosarcoma cells (UMR 106), which express both the C-24 oxidation and C-3 epimerization pathways.
  • The results of our present study indicate that SL 117 is metabolized like 1alpha,25(OH)2D3, into polar metabolites via the C-24 oxidation pathway in both rat kidney and UMR 106 cells.
  • Unlike in rat kidney, both SL 117 and WU 515 are also metabolized into less polar metabolites in UMR 106 cells.
  • In summary, we report that removal of the C-ring from the CD-ring skeleton of 1alpha,25(OH)2D3 does not alter its target tissue metabolism significantly.
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Hypercalcemia / drug therapy. Hypercalcemia / metabolism. Kidney / metabolism. Male. Neoplasms / drug therapy. Neoplasms / metabolism. Oxidation-Reduction. Rats. Rats, Sprague-Dawley

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  • (PMID = 17196157.001).
  • [ISSN] 0003-9861
  • [Journal-full-title] Archives of biochemistry and biophysics
  • [ISO-abbreviation] Arch. Biochem. Biophys.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK52488
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vitamins; FXC9231JVH / Calcitriol
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15. Ek ET, Dass CR, Contreras KG, Choong PF: Pigment epithelium-derived factor overexpression inhibits orthotopic osteosarcoma growth, angiogenesis and metastasis. Cancer Gene Ther; 2007 Jul;14(7):616-26
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  • [Title] Pigment epithelium-derived factor overexpression inhibits orthotopic osteosarcoma growth, angiogenesis and metastasis.
  • Despite significant improvements, the current management of primary osteosarcoma is still limited by the development of metastatic disease, which occurs in approximately 30% of patients despite aggressive multiagent chemotherapy and tumor-ablative surgery.
  • In this study we report, for the first time, the multitargeted role of PEDF in the inhibition of growth, angiogenesis and metastasis of two orthotopic models of osteosarcoma (rat UMR 106-01 and human SaOS-2).
  • Through stable plasmid-mediated gene transfer of full-length human PEDF, we show that PEDF overexpression significantly reduced tumor cell proliferation (P<0.05) and Matrigel invasion (UMR(PEDF), P<0.001; SaOS(PEDF), P<0.05) and increased adhesion to collagen type-1 (P<0.01), in vitro.
  • In vivo, PEDF overexpression dramatically suppressed orthotopic osteosarcoma growth (P<0.05) and the development of spontaneous pulmonary metastases (UMR(PEDF), P<0.05; SaOS(PEDF), P<0.001).
  • Therefore, together these results suggest that PEDF may be a new and promising approach for the treatment of osteosarcoma.
  • [MeSH-major] Bone Neoplasms / pathology. Eye Proteins / genetics. Gene Expression Regulation. Neoplasm Metastasis / prevention & control. Neovascularization, Pathologic / prevention & control. Nerve Growth Factors / genetics. Osteosarcoma / pathology. Serpins / genetics

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  • (PMID = 17479108.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Eye Proteins; 0 / Nerve Growth Factors; 0 / Serpins; 0 / pigment epithelium-derived factor; 63231-63-0 / RNA
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16. Hsieh CL, Gardner TA, Miao L, Balian G, Chung LW: Cotargeting tumor and stroma in a novel chimeric tumor model involving the growth of both human prostate cancer and bone stromal cells. Cancer Gene Ther; 2004 Feb;11(2):148-55
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  • We have established in vitro coculture and in vivo chimeric tumor models to evaluate the roles of stromal cells isolated from either osteosarcoma or normal bone, a site where prostate cancer cells frequently metastasize, in contributing to the growth and survival of human prostate cancer cells.
  • We have evaluated extensively the effects of toxic gene therapy using luciferase-tagged chimeric human prostate cancer models both in vitro and in vivo.
  • (1) The rate of human prostate cancer cell growth in vitro is accelerated by coculturing with human and rat osteosarcoma or normal mouse bone marrow stromal cell lines.
  • No growth stimulation was noted when cocultured with a human prostate epithelial cell line. (2) Disabling the growth of normal bone stromal cells using transgenic targeting with a bystander gene, herpes simplex virus thymidine kinase (hsv-TK), plus the pro-drug ganciclovir (GCV) or acyclovir markedly depressed the growth of cocultured human prostate cancer cells in vitro and human prostate cancer-mouse normal bone stroma chimeric tumors in vivo. (3) By cotargeting both human prostate cancer and normal mouse bone stromal cells in vitro with an adenoviral construct, Ad-hOC-TK (a replication-defective Ad5 vector with the bystander transgene hsv-TK under the control of a human osteocalcin (hOC) promoter) plus GCV4, we observed greater inhibition of tumor cell growth than by targeting a single cell compartment with Ad-PSA-TK (a vector construct similar to Ad-hOC-TK except that the transgene expression is under regulation by a full-length human PSA promoter).
  • These results, taken together, established a basic principle that cotargeting both tumor and its supporting stroma is more efficacious than targeting a single cell compartment in the treatment of human prostate cancer bone metastasis.
  • [MeSH-major] Bone Marrow Cells / physiology. Disease Models, Animal. Genetic Therapy. Prostatic Neoplasms / therapy. Stromal Cells / physiology


17. Tsushima N, Yabuki M, Harada H, Katsumata T, Kanamaru H, Nakatsuka I, Yamamoto M, Nakatsuka M: Tissue distribution and pharmacological potential of SM-16896, a novel oestrogen-bisphosphonate hybrid compound. J Pharm Pharmacol; 2000 Jan;52(1):27-37
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  • [Title] Tissue distribution and pharmacological potential of SM-16896, a novel oestrogen-bisphosphonate hybrid compound.
  • The tissue distribution pattern and pharmacological potential are reported.
  • SM-16896 (1 microM) induced a 4.5-fold transcriptional activity in rat osteosarcoma UMR-106 cells compared with vehicle-treated control, when we used the expression vector for human oestrogen receptor and a CAT reporter plasmid containing an oestrogen-responsive element.
  • Daily subcutaneous administration of 0.5 mgkg(-1) SM-16896 for 12 weeks (five times per week) to 13-week-old ovariectomized rats suppressed the ovariectomized-induced reduction in bone mineral density.
  • In the same experiment, the implantation of a 17beta-oestradiol time-release pellet (0.25 mg/pellet/90 days) almost completely suppressed the reduction of both the bone mineral density and uterine tissue weight.
  • Thus, bisphosphonate-conjugated oestrogens have the potential to improve patient compliance in oestrogen therapy by minimizing adverse effects and reducing the frequency of medication.
  • [MeSH-minor] Animals. Body Weight / drug effects. Bone Density / drug effects. Female. Humans. Molecular Structure. Organ Size / drug effects. Ovariectomy. Rats. Rats, Sprague-Dawley. Rats, Wistar. Tissue Distribution. Uterus / drug effects. Uterus / metabolism

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  • (PMID = 10716600.001).
  • [ISSN] 0022-3573
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Receptors, Estrogen; 0 / SM 16896
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18. Liebau C, Roesel C, Schmidt S, Karreman C, Prisack JB, Bojar H, Merk H, Wolfram N, Baltzer AW: Immunotherapy by gene transfer with plasmids encoding IL-12/IL-18 is superior to IL-23/IL-18 gene transfer in a rat osteosarcoma model. Anticancer Res; 2004 Sep-Oct;24(5A):2861-7
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  • [Title] Immunotherapy by gene transfer with plasmids encoding IL-12/IL-18 is superior to IL-23/IL-18 gene transfer in a rat osteosarcoma model.
  • Despite dramatic therapeutic advances, namely neo-adjuvant and adjuvant chemotherapy, progress is at a plateau.
  • Cytokine-mediated gene therapy might represent a further advance in the therapy of the osteosarcoma.
  • MATERIALS AND METHODS: We transfected UMR 108 osteosarcoma cells with different plasmids encoding IL-12, IL-23, proIL-18 and ICE (Interleukin-converting enzyme).
  • CONCLUSION: IL-23 seems to be a less effective immuno-therapeutic for adjuvant treatment of osteosarcomas than IL-12 and IL-18, when taking only IFN-gamma induction into consideration.
  • [MeSH-major] Bone Neoplasms / therapy. Genetic Therapy / methods. Immunotherapy / methods. Interleukins / genetics. Interleukins / immunology. Osteosarcoma / therapy

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  • (PMID = 15517889.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Il23a protein, rat; 0 / Interleukin-18; 0 / Interleukin-23; 0 / Interleukin-23 Subunit p19; 0 / Interleukins; 0 / RNA, Messenger; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma; EC 3.4.22.36 / Caspase 1
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19. van der Veen AH, ten Hagen TL, Seynhaeve AL, Eggermont AM: Lack of cell-cycle specific effects of tumor necrosis factor-alpha on tumor cells in vitro: implications for combination tumor therapy with doxorubicin. Cancer Invest; 2002;20(4):499-508
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  • [Title] Lack of cell-cycle specific effects of tumor necrosis factor-alpha on tumor cells in vitro: implications for combination tumor therapy with doxorubicin.
  • Addition of tumor necrosis factor-alpha (TNF-alpha) to chemotherapy enhances tumor response in several treatment modalities.
  • However, it has been shown that TNF-alpha, and several other cytokines, exert inhibitory effects on cell-cycle progression and by doing so may attenuate sensitivity of these cells to cell-cycle dependent cytotoxic drugs (e.g., doxorubicin).
  • The rat cell lines were prepared from tumors, which were used previously in animal studies, in which synergy was shown between TNF-alpha and the cytotoxic drugs.
  • Results demonstrate that the addition of TNF-alpha to doxorubicin or melphalan in vitro had no attenuating effect on the cytotoxic drugs.
  • Depending on the cell type used, addition of TNF-alpha induced no or only an additive cytotoxic effect.
  • Only the tested rat osteosarcoma tumor cells demonstrated a cell arrest in the G2 phase, which did not result in attenuation of the cytotoxicity of doxorubicin towards these cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Cycle / drug effects. Doxorubicin / pharmacology. Melphalan / pharmacology. Tumor Cells, Cultured / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Drug Resistance, Neoplasm. Drug Synergism. Drug Therapy, Combination. G2 Phase / drug effects. Humans. In Vitro Techniques. Mice. Rats

  • Hazardous Substances Data Bank. MELPHALAN .
  • Hazardous Substances Data Bank. DOXORUBICIN .
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  • (PMID = 12094545.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Necrosis Factor-alpha; 80168379AG / Doxorubicin; Q41OR9510P / Melphalan
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20. Vaisman DN, McCarthy AD, Cortizo AM: Bone-specific alkaline phosphatase activity is inhibited by bisphosphonates: role of divalent cations. Biol Trace Elem Res; 2005 May;104(2):131-40
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bisphosphonates (BPs) are drugs widely used in the treatment of various bone diseases.
  • In this study, we investigated the possible direct effect of three N-containing BPs (alendronate, pamidronate, and zoledronate) on the specific activity of bone ALP obtained from an extract of UMR106 rat osteosarcoma cells.
  • Enzymatic activity was measured by spectrophotometric detection of p-nitrophenol product and by in situ visualization of ALP bands after an electrophoresis on cellulose acetate gels.
  • [MeSH-minor] Alendronate / pharmacology. Animals. Bone Resorption / drug therapy. Imidazoles / pharmacology. Isoenzymes / antagonists & inhibitors. Isoenzymes / isolation & purification. Osteoblasts / enzymology. Osteosarcoma / enzymology. Rats. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. Alendronic acid .
  • Hazardous Substances Data Bank. MAGNESIUM, ELEMENTAL .
  • Hazardous Substances Data Bank. ZINC, ELEMENTAL .
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  • (PMID = 15894813.001).
  • [ISSN] 0163-4984
  • [Journal-full-title] Biological trace element research
  • [ISO-abbreviation] Biol Trace Elem Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cations, Divalent; 0 / Diphosphonates; 0 / Imidazoles; 0 / Isoenzymes; 6XC1PAD3KF / zoledronic acid; EC 3.1.3.1 / Alkaline Phosphatase; I38ZP9992A / Magnesium; J41CSQ7QDS / Zinc; OYY3447OMC / pamidronate; X1J18R4W8P / Alendronate
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21. Kuijpers G, Schneider B, Stadel B, Colman E: Recombinant human parathyroid hormone. Preclinical data on rat osteosarcoma were not dismissed. BMJ; 2002 May 18;324(7347):1218; author reply 1218
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recombinant human parathyroid hormone. Preclinical data on rat osteosarcoma were not dismissed.
  • [MeSH-major] Bone Neoplasms / chemically induced. Osteosarcoma / chemically induced. Teriparatide / adverse effects
  • [MeSH-minor] Animals. Drug Evaluation, Preclinical. Models, Animal. Osteoporosis / drug therapy. Rats. Recombinant Proteins / adverse effects. Recombinant Proteins / therapeutic use

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • Hazardous Substances Data Bank. TERIPARATIDE .
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  • [Cites] Bone. 2001 Dec;29(6):517-22 [11728921.001]
  • [Cites] BMJ. 2002 Feb 23;324(7335):435-6 [11859030.001]
  • [Cites] J Bone Miner Res. 2002 Apr;17(4):716-24 [11918229.001]
  • [CommentOn] BMJ. 2002 Feb 23;324(7335):435-6 [11859030.001]
  • [ErratumIn] BMJ 2002 Jun 8;324(7350):1398
  • (PMID = 12016199.001).
  • [ISSN] 1756-1833
  • [Journal-full-title] BMJ (Clinical research ed.)
  • [ISO-abbreviation] BMJ
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Proteins; 10T9CSU89I / Teriparatide
  • [Other-IDs] NLM/ PMC1123174
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