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1. Erguvan-Onal R, Onal C, Gürlek A, Alkan A, Erkal HS, Mizrak B: Metastatic fibrosarcoma of the brain: transformation from conventional to epithelioid form--case report. Neurol Med Chir (Tokyo); 2004 Sep;44(9):497-501
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  • [Title] Metastatic fibrosarcoma of the brain: transformation from conventional to epithelioid form--case report.
  • A 45-year-old woman presented with an extremely rare metastatic fibrosarcoma of the brain manifesting as persistent headache.
  • She had undergone surgery for a fibrosarcoma of the soft tissue of the thigh 2 months earlier.
  • Computed tomography and scintigraphy showed multiple metastatic lesions of the lung.
  • She refused radiotherapy or chemotherapy.
  • Follow-up computed tomography showed multiple intracranial metastases.
  • [MeSH-major] Brain Neoplasms / secondary. Fibrosarcoma / secondary. Frontal Lobe / pathology
  • [MeSH-minor] Fatal Outcome. Female. Humans. Lung Neoplasms / secondary. Lung Neoplasms / surgery. Middle Aged. Neurosurgical Procedures / methods. Soft Tissue Neoplasms / pathology. Soft Tissue Neoplasms / surgery. Tomography, X-Ray Computed

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  • (PMID = 15600287.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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2. Choi GS, Lee MH, Kim SK, Kim CS, Lee HS, Im MW, Kil HY, Seong DH, Lee JR, Kim WC, Lee MG, Song SU: Combined treatment of an intratumoral injection of dendritic cells and systemic chemotherapy (Paclitaxel) for murine fibrosarcoma. Yonsei Med J; 2005 Dec 31;46(6):835-42
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  • [Title] Combined treatment of an intratumoral injection of dendritic cells and systemic chemotherapy (Paclitaxel) for murine fibrosarcoma.
  • A novel combined treatment of conventional chemotherapy with an intratumoral injection of syngeneic dendritic cells (DCs) has emerged as a potent cancer treatment strategy.
  • In this study, we evaluated the synergistic effect of an intraperitoneal (i.p.) injection of a chemotherapeutic drug, paclitaxel, and an intratumoral (i.t.) injection of syngeneic bone marrow-derived DCs for the treatment of pre-existing fibrosarcoma.
  • Subcutaneous tumors were established using MCA102 fibrosarcoma cells in syngeneic C57BL/6 mice.
  • The results demonstrated that the combined treatment of paclitaxel chemotherapy and the injection of DCs led to complete tumor regression, in contrast to only partial eradication of the tumors with chemotherapy or DCs alone.
  • Furthermore, the tumor-free mice were able to resist a repeat challenge with the same type of tumor.
  • These findings suggest that a combination therapy of systemic chemotherapy along with the intratumoral administration of DCs is a potent treatment strategy for fibrosarcoma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Dendritic Cells / transplantation. Fibrosarcoma / therapy. Paclitaxel / therapeutic use
  • [MeSH-minor] Animals. Bone Marrow Cells / cytology. Cell Line, Tumor. Cells, Cultured. Combined Modality Therapy. Immunologic Memory. Injections, Intraperitoneal. Mice. Phenotype. Transplantation, Isogeneic. Treatment Outcome

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  • (PMID = 16385661.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC2810599
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3. Ren W, Korchin B, Zhu QS, Wei C, Dicker A, Heymach J, Lazar A, Pollock RE, Lev D: Epidermal growth factor receptor blockade in combination with conventional chemotherapy inhibits soft tissue sarcoma cell growth in vitro and in vivo. Clin Cancer Res; 2008 May 1;14(9):2785-95
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  • [Title] Epidermal growth factor receptor blockade in combination with conventional chemotherapy inhibits soft tissue sarcoma cell growth in vitro and in vivo.
  • PURPOSE: The epidermal growth factor receptor (EGFR) is highly expressed in many human soft tissue sarcomas (STS).
  • However, EGFR blockade has not apparently been used for human STS therapy; therefore, we examined the in vitro and in vivo effects and the underlying mechanisms before considering EGFR blockade as a therapy for STS patients.
  • EXPERIMENTAL DESIGN: Human STS tissues and cell lines were used to study EGFR expression and activation.
  • An in vivo study (HT1080 human fibrosarcoma cell line in nude/nude mice: Iressa, doxorubicin, Iressa + doxorubicin, vehicle) was used to examine tumor growth; pEGFR, proliferating cell nuclear antigen, and terminal deoxyribonucleotide transferase-mediated nick-end labeling staining helped assess the effect of therapy in vivo on STS EGFR activation, proliferation, and apoptosis.
  • CONCLUSION: EGFR blockade combined with conventional chemotherapy results in anti-human STS activity in vitro and in vivo, suggesting the possibility that combining these synergistic treatments will improve anti-STS therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Doxorubicin / therapeutic use. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Sarcoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Synergism. Humans. Mice. Mice, Nude


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4. Hirahara N, Nio Y, Sasaki S, Minari Y, Takamura M, Iguchi C, Dong M, Yamasawa K, Tamura K: Inoculation of human interleukin-17 gene-transfected Meth-A fibrosarcoma cells induces T cell-dependent tumor-specific immunity in mice. Oncology; 2001;61(1):79-89
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  • [Title] Inoculation of human interleukin-17 gene-transfected Meth-A fibrosarcoma cells induces T cell-dependent tumor-specific immunity in mice.
  • Murine Meth-A fibrosarcoma cells were transfected with the hIL-17 gene using the lipofectin method.
  • Challenge with tumor cells in conventional BALB/c mice, however, resulted in the rejection of Meth-A/IL-17 cells, but the other two lines did grow.
  • Injecting the anti-thy 1,2 (CD90), anti-CD4 or anti-CD8 monoclonal antibody into conventional BALB/c mice resulted in the resumption of in vivo growth of Meth-A/IL-17 cells, but injecting the anti-asialo GM1 antibody did not.
  • [MeSH-major] Antigens, Neoplasm / immunology. Fibrosarcoma / therapy. Genetic Therapy / methods. Immunotherapy / methods. Interleukin-17 / genetics. Interleukin-17 / immunology. T-Lymphocytes / drug effects
  • [MeSH-minor] Animals. Blotting, Northern. Cell Division. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunity, Cellular. Immunohistochemistry. Killer Cells, Natural / drug effects. Mice. Mice, Inbred BALB C. Mice, Nude. Plasmids / genetics. Polymerase Chain Reaction. Transfection. Tumor Cells, Cultured

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  • [Copyright] Copyright 2001 S. Karger AG, Basel
  • (PMID = 11474253.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Interleukin-17; 0 / Meth A sarcoma-associated rejection antigen, mouse
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5. Sengupta S, Tyagi P, Chandra S, Kochupillai V, Gupta SK: Encapsulation in cationic liposomes enhances antitumour efficacy and reduces the toxicity of etoposide, a topo-isomerase II inhibitor. Pharmacology; 2001;62(3):163-71
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  • The present study was thus designed to encapsulate etoposide in cationic liposomes and to evaluate its antitumour efficacy and systemic toxicity in comparison with a conventional parenteral formulation.
  • Fibrosarcoma was induced in mice by subcutaneous administration of 20-methylcholanthrene.
  • Chemotherapy was started when the tumour reached 200 mm(3) in volume.
  • The median time of death was calculated to be 19.5, 26.25 and 56 days in vehicle-treated controls, non-liposomal-etoposide- and liposomal-etoposide-treated groups, respectively.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Etoposide / administration & dosage. Etoposide / therapeutic use. Fibrosarcoma / drug therapy. Liposomes
  • [MeSH-minor] Animals. Blood Platelets / drug effects. Body Weight. Capsules. Leukocytes / drug effects. Male. Mice. Random Allocation

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  • [Copyright] Copyright 2001 S. Karger AG, Basel
  • (PMID = 11287818.001).
  • [ISSN] 0031-7012
  • [Journal-full-title] Pharmacology
  • [ISO-abbreviation] Pharmacology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Capsules; 0 / Liposomes; 6PLQ3CP4P3 / Etoposide
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6. Ferrario A, Von Tiehl K, Wong S, Luna M, Gomer CJ: Cyclooxygenase-2 inhibitor treatment enhances photodynamic therapy-mediated tumor response. Cancer Res; 2002 Jul 15;62(14):3956-61
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  • [Title] Cyclooxygenase-2 inhibitor treatment enhances photodynamic therapy-mediated tumor response.
  • Photodynamic therapy (PDT) continues to be used in the treatment of solid tumors.
  • Clinical results are promising, but the therapy has not been optimized, and tumor recurrences can occur.
  • Recently, it has been shown that inhibitors of cyclooxygenase (COX)-2 can be effective in combination with conventional chemotherapy and radiation therapy.
  • COX-2 was also elevated in radiation-induced fibrosarcoma (RIF) tumors after treatment with PDT.
  • Additionally, we demonstrated that NS-398 enhanced PDT responsiveness in RIF tumors without increasing toxicity to normal tissue.
  • These results provide strong evidence that combination procedures involving selective COX-2 inhibitors may improve the therapeutic effectiveness of PDT.
  • [MeSH-major] Cyclooxygenase Inhibitors / pharmacology. Fibrosarcoma / enzymology. Mammary Neoplasms, Experimental / enzymology. Nitrobenzenes / pharmacology. Photochemotherapy / methods. Sulfonamides / pharmacology
  • [MeSH-minor] Animals. Cyclooxygenase 1. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Enzyme Induction / drug effects. Female. Isoenzymes / antagonists & inhibitors. Isoenzymes / biosynthesis. Isoenzymes / metabolism. Membrane Proteins. Mice. Mice, Inbred C3H. Prostaglandin-Endoperoxide Synthases / biosynthesis. Prostaglandin-Endoperoxide Synthases / metabolism. Tumor Cells, Cultured

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  • (PMID = 12124326.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R0-1 CA-31230
  • [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 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Nitrobenzenes; 0 / Sulfonamides; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.14.99.1 / Ptgs1 protein, mouse
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7. Murai R, Yoshida Y, Muraguchi T, Nishimoto E, Morioka Y, Kitayama H, Kondoh S, Kawazoe Y, Hiraoka M, Uesugi M, Noda M: A novel screen using the Reck tumor suppressor gene promoter detects both conventional and metastasis-suppressing anticancer drugs. Oncotarget; 2010 Aug;1(4):252-64
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  • [Title] A novel screen using the Reck tumor suppressor gene promoter detects both conventional and metastasis-suppressing anticancer drugs.
  • The membrane-anchored matrix metalloproteinase-regulator RECK is often downregulated in various types of cancers; the levels of residual RECK in resected tumors often correlate with better prognosis.
  • RECK is therefore a promising marker for benignancy and a potential effector in cancer therapy.
  • Our pilot experiments with 880 known bioactive compounds detected 34 compounds that activate RECK promoter; among these, 10 were authentic anticancer drugs.
  • The top-ranking compound, disulfiram, strongly suppressed spontaneous lung-metastasis of human fibrosarcoma cells in nude mice.
  • Our data demonstrate the value of this screen in discovering effective cancer therapeutics.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Screening Assays, Antitumor / methods. GPI-Linked Proteins / genetics. Promoter Regions, Genetic
  • [MeSH-minor] Alkaline Phosphatase / genetics. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Disulfiram / pharmacology. Doxycycline / pharmacology. Drug Discovery. Gene Expression Regulation, Neoplastic. Humans. Immunoblotting. Mice. Neoplasm Metastasis. Prognosis. Proto-Oncogene Proteins p21(ras) / genetics. Rats

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  • (PMID = 21304177.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GPI-Linked Proteins; 0 / RECK protein, human; EC 3.1.3.1 / Alkaline Phosphatase; EC 3.6.5.2 / HRAS protein, human; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); N12000U13O / Doxycycline; TR3MLJ1UAI / Disulfiram
  • [Other-IDs] NLM/ PMC3248105
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8. Cook JL, Miura TA, Iklé DN, Lewis AM Jr, Routes JM: E1A oncogene-induced sensitization of human tumor cells to innate immune defenses and chemotherapy-induced apoptosis in vitro and in vivo. Cancer Res; 2003 Jun 15;63(12):3435-43
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  • [Title] E1A oncogene-induced sensitization of human tumor cells to innate immune defenses and chemotherapy-induced apoptosis in vitro and in vivo.
  • Expression of the adenoviral E1A oncogene induces susceptibility of neoplastic cells from different species to both immune-mediated and chemotherapy-induced cell death.
  • However, conventional in vivo assays of tumor development lack similar precision for measurement of oncogene-induced changes in tumor cell traits.
  • These results were confirmed in studies of E1A-expressing human fibrosarcoma cells.
  • This experimental approach should be useful for studies of the effects of other oncogene-related tumor cell traits on tumorigenicity and could be used for preclinical studies of different treatment strategies for human tumors.
  • [MeSH-major] Adenovirus E1A Proteins / physiology. Apoptosis / physiology. Bone Neoplasms / pathology. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Drug Resistance, Neoplasm / physiology. Osteosarcoma / pathology
  • [MeSH-minor] Adenoviruses, Human / genetics. Adenoviruses, Human / physiology. Animals. Antineoplastic Agents / therapeutic use. Cell Line / transplantation. Cytotoxicity, Immunologic. Etoposide / therapeutic use. Female. Fibrosarcoma / immunology. Fibrosarcoma / pathology. Genes, p53. Humans. Immunologic Surveillance. Kidney. Killer Cells, Natural / immunology. Mice. Mice, Nude. Oncogenes. Rats. Rats, Nude. Time Factors. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / immunology. Tumor Suppressor Protein p53 / deficiency. Xenograft Model Antitumor Assays

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  • (PMID = 12810682.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA76491; United States / NCI NIH HHS / CA / CA86727
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenovirus E1A Proteins; 0 / Antineoplastic Agents; 0 / Tumor Suppressor Protein p53; 6PLQ3CP4P3 / Etoposide
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9. Van de Putte M, Wang H, Chen F, de Witte PA, Ni Y: Hypericin as a marker for determination of tissue viability after intratumoral ethanol injection in a murine liver tumor model. Acad Radiol; 2008 Jan;15(1):107-13
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  • [Title] Hypericin as a marker for determination of tissue viability after intratumoral ethanol injection in a murine liver tumor model.
  • RATIONALE AND OBJECTIVES: In this preclinical proof-of-principle study, the necrosis avid agent hypericin was investigated as a potential early indicator for therapeutic response after ethanol-mediated chemical ablation in murine liver tumors.
  • MATERIALS AND METHODS: Seven mice bearing intrahepatic radiation-induced fibrosarcoma-1 tumors were intravenously injected with hypericin 1 hour before (n = 3) or 24 hours after (n = 4) intratumoral ethanol injection.
  • Mice were euthanized 24 hours after hypericin injection and, taking advantage of the fluorescent property of the compound, the excised livers were investigated qualitatively and quantitatively by means of fluoromacroscopic and fluoromicroscopic examinations, colocalized with conventional histomorphology.
  • RESULTS: Significant differences in hypericin fluorescence were found in necrosis, viable tumor and normal liver tissue in decreasing order (P < .05) (ie, in necrosis, mean fluorescence densities were about 4.5 times higher than in viable tumor and approximately 14 times higher than in normal liver).
  • When hypericin was injected 1 hour before, maximal blood concentrations were achieved at the time of ethanol treatment, so that on ablation an outstanding extravasation took place in the entire necrotic area in comparison with accumulation of hypericin only at the peripheral zone of necrosis when it was injected 24 hours after ablation.
  • CONCLUSIONS: Hypericin specifically enhanced the imaging contrast between necrotic and viable tissues and nonspecifically distinguished viable tumor from normal liver.
  • [MeSH-major] Antineoplastic Agents. Ethanol / administration & dosage. Fibrosarcoma / drug therapy. Liver Neoplasms / drug therapy. Perylene / analogs & derivatives

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  • (PMID = 18078913.001).
  • [ISSN] 1076-6332
  • [Journal-full-title] Academic radiology
  • [ISO-abbreviation] Acad Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 3K9958V90M / Ethanol; 5QD5427UN7 / Perylene; 7V2F1075HD / hypericin
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10. Wacnik PW, Kehl LJ, Trempe TM, Ramnaraine ML, Beitz AJ, Wilcox GL: Tumor implantation in mouse humerus evokes movement-related hyperalgesia exceeding that evoked by intramuscular carrageenan. Pain; 2003 Jan;101(1-2):175-86
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  • In this paper we compare two innovative models of movement-related pain: tumor-induced nociception following implantation of fibrosarcoma cells into bone and muscle inflammation-induced nociception following injection of the irritant carrageenan into muscle.
  • Movement-related hyperalgesia, known clinically as a specific type of 'breakthrough pain', is a common feature of bone cancer and is thought to be a predictor of poor response to conventional analgesic pharmacotherapy (Bruera et al., 1995, J.
  • Control groups receiving implants of vehicle or no treatment at all did not manifest this forelimb hyperalgesia.
  • B6C3/F1 mice implanted with non-lysis-inducing G3.26 melanoma cells or vehicle did not manifest significant hyperalgesia when compared to B6C3/F1 mice receiving fibrosarcoma cells, indicating a dependence on bone involvement for induction of hyperalgesia in this model.
  • Tumor-implanted mice with a level of hyperalgesia comparable to that induced by carrageenan required almost three times more morphine (ED(50) 18.5mg/kg) for equivalent attenuation of forelimb hyperalgesia.
  • Importantly, they may also aid in predicting differences in analgesic efficacy in different types of musculoskeletal pain.
  • [MeSH-major] Bone Neoplasms / complications. Fibrosarcoma / complications. Hyperalgesia / physiopathology. Movement

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  • (PMID = 12507712.001).
  • [ISSN] 0304-3959
  • [Journal-full-title] Pain
  • [ISO-abbreviation] Pain
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01-CA84233-01A2; United States / NIDCR NIH HHS / DE / 5T 32-DEO 7288-02
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Analgesics, Opioid; 76I7G6D29C / Morphine; 9000-07-1 / Carrageenan
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11. Kawaguchi K: Robotic radiosurgery for severe recurrent and primary head and neck cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e17038

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  • Here we describe our aim to improve local control and to obtain organ preservation by using the non-surgical outpatient procedure the CyberKnife frameless radiosurgery (CK).
  • METHODS: Between March 2006 and January 2008, 22 patients with severe recurrent, previously treated with conventional methods, and 14 patients with primary lesions were treated with CK in the management of head and neck cancer.
  • All the patients had biopsy confirmation of disease prior to radiation therapy; rT2 (3 patients), rT3 (8), rT4 (9), T2 (5), T3 (3), T4 (6), N1 (4), N2b (3), M1 (1), tongue (11), mandibule (11), maxilla (6), maxillary sinus (4), soft palate (2), with sq. cell ca.(34), adenoid cystic ca.(1), fibrosarcoma (1).
  • The treatment plan was set up based on CT, MRI and PET-CT in Yokohama CyberKnife Center.
  • Between the 4-6 month follow-up, 4 cases were performed additional CK treatment for the recurrent lesions, however, 3 patients with T4 tongue cancer were not cured.
  • Finally, the total control rate of the primary cases was 10/14 (71.4%), however, 8/9 (88.9%) primary cases except tongue cancer has been controlled treated by CK with chemotherapy.
  • There have been no seriously complications of treatment caused by CK except severe osteoradionecrosis of the 4 patients irradiated with maximum dose.
  • CONCLUSIONS: It is now possible with the development of CyberKnife Radiosurgery to improve our treatments of the local control in head and neck cancer.

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  • (PMID = 27961782.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Patterson AV, Williams KJ, Cowen RL, Jaffar M, Telfer BA, Saunders M, Airley R, Honess D, van der Kogel AJ, Wolf CR, Stratford IJ: Oxygen-sensitive enzyme-prodrug gene therapy for the eradication of radiation-resistant solid tumours. Gene Ther; 2002 Jul;9(14):946-54
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  • [Title] Oxygen-sensitive enzyme-prodrug gene therapy for the eradication of radiation-resistant solid tumours.
  • Overwhelming clinical and experimental data demonstrate that tumour hypoxia is associated with aggressive disease and poor treatment outcome as hypoxic cells are refractive to radiotherapy and some forms of chemotherapy.
  • However, hypoxia is rare in physiologically normal tissues representing a tumour-specific condition.
  • To selectively target this therapeutically refractive cell population, we have combined bioreductive chemotherapy with hypoxia-directed gene therapy.
  • We have transfected the human fibrosarcoma cell line, HT1080, with a hypoxia-regulated expression vector encoding the human flavoprotein cytochrome c P450 reductase (HRE-P450R).
  • Xenografts of both the HRE-P450R and empty vector transfectants had comparable hypoxic fractions and were refractive to single dose radiotherapy of up to 15 Gy.
  • However, combining a prodrug of RSU1069 with a reduced radiotherapy dose of 10 Gy represents a curative regimen (50% tumour-free survival; day 100) in the HRE-P450R xenografts.
  • Thus, an oxygen-sensitive gene-directed enzyme prodrug therapy approach may have utility when incorporated into conventional radiotherapy and/or chemotherapy protocols for loco-regional disease in any tissue where hypoxia is a contra-indication to treatment success. doi:10.1038/sj.gt.3301702
  • [MeSH-major] Fibrosarcoma / therapy. Genetic Therapy / methods. NADPH-Ferrihemoprotein Reductase / genetics. Nitroimidazoles / therapeutic use. Prodrugs / therapeutic use
  • [MeSH-minor] Animals. Combined Modality Therapy. Female. Genetic Vectors / genetics. Genetic Vectors / pharmacology. Humans. Hypoxia. Mice. Mice, Nude. Misonidazole / analogs & derivatives. Misonidazole / metabolism. Neoplasm Transplantation. Radiation Tolerance. Radiation-Sensitizing Agents / metabolism. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 12085243.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500366
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nitroimidazoles; 0 / Prodrugs; 0 / Radiation-Sensitizing Agents; 122178-49-8 / RB 6145; 88876-88-4 / 1-(2-nitro-1-imidazolyl)-3-aziridino-2-propanol; 8FE7LTN8XE / Misonidazole; EC 1.6.2.4 / NADPH-Ferrihemoprotein Reductase
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13. Davidsen ML, Würtz SØ, Rømer MU, Sørensen NM, Johansen SK, Christensen IJ, Larsen JK, Offenberg H, Brünner N, Lademann U: TIMP-1 gene deficiency increases tumour cell sensitivity to chemotherapy-induced apoptosis. Br J Cancer; 2006 Oct 23;95(8):1114-20
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  • [Title] TIMP-1 gene deficiency increases tumour cell sensitivity to chemotherapy-induced apoptosis.
  • Tissue inhibitor of metalloproteinases-1 (TIMP-1) is one of four inhibitors of the matrix metalloproteinases, which are capable of degrading most components of the extracellular matrix.
  • In this regard, several studies have demonstrated an antiapoptotic effect of TIMP-1 in a number of different cell types.
  • Since chemotherapy works by inducing apoptosis in cancer cells, we raised the hypothesis that TIMP-1 promotes resistance against chemotherapeutic drugs.
  • In order to investigate this hypothesis, we have established TIMP-1 gene-deficient and TIMP-1 wild-type fibrosarcoma cells from mouse lung tissue.
  • We have characterised these cells with regard to TIMP-1 genotype, TIMP-1 expression, malignant transformation and sensitivity to chemotherapy-induced apoptosis.
  • We show that TIMP-1 gene deficiency increases the response to chemotherapy considerably, confirming that TIMP-1 protects the cells from apoptosis.
  • This is to our knowledge the first study investigating TIMP-1 and chemotherapy-induced apoptosis employing a powerful model system comprising TIMP-1 gene-deficient cells and their genetically identical wild-type controls.
  • For future studies, this cell system can be used to uncover the mechanisms and signalling pathways involved in the TIMP-1-mediated inhibition of apoptosis as well as to investigate the possibility of using TIMP-1 inhibitors to optimise the effect of conventional chemotherapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Tissue Inhibitor of Metalloproteinase-1 / genetics
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Division / genetics. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / genetics. Cell Transformation, Neoplastic / genetics. Cells, Cultured. Cytarabine / pharmacology. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Etoposide / pharmacology. Female. Gene Expression / genetics. Genotype. Male. Mice. Mice, Inbred BALB C. Mice, Knockout. Mice, Transgenic. Time Factors. Vincristine / pharmacology

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  • (PMID = 17047657.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tissue Inhibitor of Metalloproteinase-1; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide
  • [Other-IDs] NLM/ PMC2360707
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14. Charalabopoulos K, Karkabounas S, Charalabopoulos AK, Papalimneou V, Ioachim E, Giannakopoulos X: Inhibition of benzo(a)pyrene-induced carcinogenesis by vitamin C alone and by vitamin C/vitamin E and selenium/glutathione. Biol Trace Elem Res; 2003;93(1-3):201-12
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  • By calculating the carcinogenic potency of benzo(a)pyrene and the anticarcinogenic potency of substances used as well as histological examination of developed tumors and survival time of treated animals, it was found that vitamin C exerts a significant anticarcinogenic effect of 8.3 units and that the combination of the two anticarcinogens used produced a significant prolongation of the animals survival time with anticarcinogenic potency of 22.1 and 22.2 units, respectively.
  • The question of an additional supportive administration of such agents complementary to the conventional cancer chemotherapy in humans is raised.
  • [MeSH-minor] Animals. Drug Synergism. Female. Fibrosarcoma / chemically induced. Fibrosarcoma / prevention & control. Rats. Rats, Wistar. Survival Analysis

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  • (PMID = 12835502.001).
  • [ISSN] 0163-4984
  • [Journal-full-title] Biological trace element research
  • [ISO-abbreviation] Biol Trace Elem Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzopyrenes; 1406-18-4 / Vitamin E; GAN16C9B8O / Glutathione; H6241UJ22B / Selenium; PQ6CK8PD0R / Ascorbic Acid
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15. Nascimento AF, Bertoni F, Fletcher CD: Epithelioid variant of myxofibrosarcoma: expanding the clinicomorphologic spectrum of myxofibrosarcoma in a series of 17 cases. Am J Surg Pathol; 2007 Jan;31(1):99-105
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  • Myxofibrosarcoma (MFS) is one of the most common soft tissue sarcomas of elderly patients and has a predilection for the limbs.
  • In 10 cases, the tumor was located in subcutaneous tissue and in 6 cases it was subfascial.
  • Twelve patients were treated by surgery followed by chemotherapy and/or radiation (8 cases).
  • One patient received chemotherapy after an incisional biopsy and 1 patient was treated by surgery alone.
  • Ten patients (71.4%) developed local recurrences.
  • Seven patients (50%) developed metastases to lungs or retroperitoneum.
  • The epithelioid areas were generally multifocal with admixed areas of conventional MFS.
  • [MeSH-major] Epithelioid Cells / pathology. Fibrosarcoma / secondary. Sarcoma / secondary. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Carcinoma / diagnosis. Combined Modality Therapy. Diagnosis, Differential. Extremities. Fatal Outcome. Female. Humans. Immunoenzyme Techniques. Liposarcoma / diagnosis. Male. Melanoma / diagnosis. Middle Aged. Myoepithelioma / diagnosis. Rhabdomyosarcoma / diagnosis

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  • (PMID = 17197925.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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16. Chow LT, Kumta SM: Primary osteochondrorhabdomyosarcoma (malignant mesenchymoma) of the fibula: a rare tumour in an unusual site -- case report and review of the literature. APMIS; 2004 Sep;112(9):617-23
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  • Malignant mesenchymoma, defined by Stout as sarcomas comprising two or more unrelated differentiated tissue elements other than a fibrosarcoma component, is rare.
  • The clinical features of primary malignant mesenchymoma of bone thus resemble those of conventional osteosarcoma.
  • Moreover, our case illustrates that, with combination chemotherapy targeted for individual elements, the prognosis of this rare tumour might be much improved, as in osteosarcoma.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Child. Female. Humans. Immunohistochemistry

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  • (PMID = 15601312.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Denmark
  • [Number-of-references] 22
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17. Shahverdi AR, Saadat F, Khorramizadeh MR, Iranshahi M, Khoshayand MR: Two matrix metalloproteinases inhibitors from Ferula persica var. persica. Phytomedicine; 2006 Nov;13(9-10):712-7

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  • The influence of these extracts vs. a reference drug, diclofenac sodium, on MMP production by the fibrosarcoma cell line was investigated using an in vitro cytotoxicity assay, sodium dodecyl sulfate-polyacrylamide, and gelatin zymography.
  • Using conventional spectroscopy methods, the active fractions were identified as t-butyl 3-[(1-methylthiopropyl)dithio]-2-propenyl malonate (persicasulphide B) and umbelliprenin, previously isolated from F. persica var. latisecta.
  • Since inhibition of MMP activity has been employed in modality therapy in diseases such as cancer, this compound might be promising in the preparation of anti-MMP therapeutic derivatives.

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  • (PMID = 16487689.001).
  • [ISSN] 0944-7113
  • [Journal-full-title] Phytomedicine : international journal of phytotherapy and phytopharmacology
  • [ISO-abbreviation] Phytomedicine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Malonates; 0 / Matrix Metalloproteinase Inhibitors; 0 / Plant Extracts; 0 / Umbelliferones; 0 / persicasulfide B; MSD8N8A1LQ / umbelliprenin
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18. Deorukhkar AA, Chander R, Pandey R, Sainis KB: A novel N-alkylated prodigiosin analogue induced death in tumour cell through apoptosis or necrosis depending upon the cell type. Cancer Chemother Pharmacol; 2008 Mar;61(3):355-63
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  • [Title] A novel N-alkylated prodigiosin analogue induced death in tumour cell through apoptosis or necrosis depending upon the cell type.
  • RESULTS: MAMPDM inhibited the proliferation of murine fibrosarcoma, S-180 cells and induced cell death.
  • CONCLUSIONS: MAMPDM could induce cell death by either apoptosis or necrosis depending upon the cell type.
  • This would be of advantage in elimination of tumor cells defective in apoptotic pathway and therefore, refractory to the conventional therapies.
  • [MeSH-major] Alkenes / pharmacology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Prodigiosin / analogs & derivatives. Prodigiosin / pharmacology. Pyrroles / pharmacology
  • [MeSH-minor] Alkylation. Animals. Cell Line, Tumor. Cell Membrane Permeability / drug effects. Cell Survival / drug effects. DNA Fragmentation / drug effects. DNA, Neoplasm / biosynthesis. DNA, Neoplasm / genetics. Dactinomycin / pharmacology. Diploidy. Enzyme Inhibitors / pharmacology. Lymphoma, T-Cell / drug therapy. Lymphoma, T-Cell / pathology. Mice. Necrosis. Rats. Sarcoma 180 / drug therapy. Staurosporine / pharmacology. Tetrazolium Salts. Thiazoles

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  • (PMID = 17429627.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 2,2'-(3-methoxy-1'amyl-5'-methyl-4-(1-pyrryl)) dipyrryl-methene; 0 / Alkenes; 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / Pyrroles; 0 / Tetrazolium Salts; 0 / Thiazoles; 1CC1JFE158 / Dactinomycin; 298-93-1 / thiazolyl blue; H88EPA0A3N / Staurosporine; OL369FU7CJ / Prodigiosin
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19. Atobe K, Ishida T, Ishida E, Hashimoto K, Kobayashi H, Yasuda J, Aoki T, Obata K, Kikuchi H, Akita H, Asai T, Harashima H, Oku N, Kiwada H: In vitro efficacy of a sterically stabilized immunoliposomes targeted to membrane type 1 matrix metalloproteinase (MT1-MMP). Biol Pharm Bull; 2007 May;30(5):972-8
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  • [Title] In vitro efficacy of a sterically stabilized immunoliposomes targeted to membrane type 1 matrix metalloproteinase (MT1-MMP).
  • The poor selective cytotoxicity of anticancer drugs lead to dose-limiting adverse effects which compromise the clinical outcome.
  • Solid tumors recruit new blood vessels to support their growth, and epitopes that are uniquely expressed on tumor cells and tumor endothelial cells (ECs) can function as targets for immunoliposomal anticancer drugs.
  • Membrane type 1 matrix metalloproteinase (MT1-MMP), an important protein related to tumor growth and angiogenesis, is expressed on malignant tumor cells and is activated ECs.
  • The binding and intracellular distribution of SIL[anti-MT1-MMP(Fab')] and a non-targeted sterically stabilized liposomes (SL) were examined using human fibrosarcoma HT-1080 cells.
  • SIL[anti-MT1-MMP(Fab')] was taken up by the cells in a lipid concentration, temperature, and time dependent manner, ultimately accumulating in the lysosomes.
  • This strategy may have the potential for overcoming some major limitations in conventional chemotherapy in vivo.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antineoplastic Agents / administration & dosage. Endothelial Cells / drug effects. Immunoglobulin Fab Fragments / immunology. Matrix Metalloproteinase 14 / biosynthesis
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. Doxorubicin / administration & dosage. Doxorubicin / pharmacology. Drug Stability. Flow Cytometry. Humans. Liposomes. Microscopy, Confocal

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  • (PMID = 17473445.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Immunoglobulin Fab Fragments; 0 / Liposomes; 80168379AG / Doxorubicin; EC 3.4.24.80 / Matrix Metalloproteinase 14
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20. Truman JP, García-Barros M, Kaag M, Hambardzumyan D, Stancevic B, Chan M, Fuks Z, Kolesnick R, Haimovitz-Friedman A: Endothelial membrane remodeling is obligate for anti-angiogenic radiosensitization during tumor radiosurgery. PLoS One; 2010;5(8):e12310
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  • BACKGROUND: While there is significant interest in combining anti-angiogenesis therapy with conventional anti-cancer treatment, clinical trials have as of yet yielded limited therapeutic gain, mainly because mechanisms of anti-angiogenic therapy remain to a large extent unknown.
  • Currently, anti-angiogenic tumor therapy is conceptualized to either "normalize" dysfunctional tumor vasculature, or to prevent recruitment of circulating endothelial precursors into the tumor.
  • In vivo, MCA/129 fibrosarcoma tumors were implanted in asmase(+/+) mice or asmase(-/-) littermates and irradiated in the presence or absence of anti-VEGFR2 DC101 or anti-VEGF G6-31 antibodies.
  • Anti-angiogenic radiosensitization was abrogated in tumors implanted in asmase(-/-) mice that provide apoptosis-resistant vasculature, or in wild-type littermates pre-treated with anti-ceramide antibody, indicating that ceramide is necessary for this effect.
  • CONCLUSIONS/SIGNIFICANCE: These studies show that angiogenic factors fail to suppress apoptosis if ceramide remains elevated while anti-angiogenic therapies fail without ceramide elevation, defining a ceramide rheostat that determines outcome of single dose radiotherapy.
  • Understanding the temporal sequencing of anti-angiogenic drugs and radiation enables optimized radiosensitization and design of innovative radiosurgery clinical trials.
  • [MeSH-major] Cell Membrane / drug effects. Endothelial Cells / pathology. Neoplasms / blood supply. Neoplasms / pathology. Neovascularization, Pathologic / drug therapy. Radiation-Sensitizing Agents / pharmacology. Radiosurgery
  • [MeSH-minor] Animals. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Apoptosis / drug effects. Apoptosis / radiation effects. Cell Death / drug effects. Cell Death / radiation effects. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / radiation effects. Ceramides / metabolism. Enzyme Activation / drug effects. Enzyme Activation / radiation effects. Fibroblast Growth Factor 2 / pharmacology. Humans. Mice. Radiotherapy Dosage. Signal Transduction / drug effects. Signal Transduction / radiation effects. Sphingomyelin Phosphodiesterase / metabolism. Time Factors. Vascular Endothelial Growth Factor A / immunology. Vascular Endothelial Growth Factor A / pharmacology

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  • [RepublishedIn] PLoS One. 2010;5(9). doi: 10.1371/annotation/6e222ad5-b175-4a00-9d04-4d120568a897 [20941382.001]
  • (PMID = 20808818.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA085704; United States / NCI NIH HHS / CA / R01 CA105125
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Ceramides; 0 / DC101 monoclonal antibody; 0 / Radiation-Sensitizing Agents; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; EC 3.1.4.12 / Sphingomyelin Phosphodiesterase
  • [Other-IDs] NLM/ PMC2924400
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21. El-Rayes BF, Ibrahim D, Shields AF, LoRusso PM, Zalupski MM, Philip PA: Phase I study of liposomal doxorubicin (Doxil) and cyclophosphamide in solid tumors. Invest New Drugs; 2005 Jan;23(1):57-62
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

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  • PATIENTS AND METHODS: Eligibility criteria included: a diagnosis of non-hematologic cancer with no conventional effective therapy, normal renal, liver and bone marrow function, and ECOG performance status of 0-2.
  • Both drugs were administered intravenously on day 1 of a 21-day cycle.
  • Three patients with adenocarcinoma of the stomach, fibrosarcoma of the stomach and renal cell carcinoma showed objective antitumor responses.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cyclophosphamide / administration & dosage. Dose-Response Relationship, Drug. Doxorubicin / administration & dosage. Drug Carriers. Female. Humans. Injections, Intravenous. Liposomes. Male. Maximum Tolerated Dose. Middle Aged

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  • (PMID = 15528981.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Carriers; 0 / Liposomes; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide
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22. Staals EL, Bacchini P, Mercuri M, Bertoni F: Dedifferentiated chondrosarcomas arising in preexisting osteochondromas. J Bone Joint Surg Am; 2007 May;89(5):987-93
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  • BACKGROUND: Dedifferentiated chondrosarcomas that arise in osteochondromas are extremely rare lesions for which very little information on treatment and outcome is available in the literature.
  • The purpose of the present study was to describe the specific clinical, radiographic, and histologic features of this lesion and to evaluate the oncologic outcome after different treatment strategies.
  • Radiographic studies, histologic slides, and clinical records were reviewed, the features of those studies were tabulated, and prognostic features and the results of treatment were identified.
  • Radiographically, ten lesions appeared as a conventional secondary chondrosarcoma arising in an exostosis, whereas eight showed typical signs of dedifferentiation.
  • The dedifferentiated component was considered to be an osteosarcoma in nine cases (including six cases in which it was osteoblastic and three in which it was fibroblastic), a malignant fibrous histiocytoma in eight, and a fibrosarcoma in one.
  • For the fifteen patients who were managed at the authors' institution, the two and five-year survival rates were 47% and 29%, respectively; the median survival time was fourteen months.
  • Patients who were managed with a combination of surgery and chemotherapy had a better overall survival rate than did those who were managed with surgery alone (p = 0.03).
  • In the present small series, overall survival was better when wide surgical resection was combined with adjuvant chemotherapy.

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  • (PMID = 17473135.001).
  • [ISSN] 0021-9355
  • [Journal-full-title] The Journal of bone and joint surgery. American volume
  • [ISO-abbreviation] J Bone Joint Surg Am
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Truman JP, García-Barros M, Kaag M, Hambardzumyan D, Stancevic B, Chan M, Fuks Z, Kolesnick R, Haimovitz-Friedman A: Endothelial membrane remodeling is obligate for anti-angiogenic radiosensitization during tumor radiosurgery. PLoS One; 2010 Sep 30;5(9)
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  • BACKGROUND: While there is significant interest in combining anti-angiogenesis therapy with conventional anti-cancer treatment, clinical trials have as of yet yielded limited therapeutic gain, mainly because mechanisms of anti-angiogenic therapy remain to a large extent unknown.
  • Currently, anti-angiogenic tumor therapy is conceptualized to either “normalize” dysfunctional tumor vasculature, or to prevent recruitment of circulating endothelial precursors into the tumor.
  • In vivo, MCA/129 fibrosarcoma tumors were implanted in asmase+/+ mice or asmase−/− littermates and irradiated in the presence or absence of anti-VEGFR2 DC101 or anti-VEGF G6-31 antibodies.
  • Anti-angiogenic radiosensitization was abrogated in tumors implanted in asmase−/− mice that provide apoptosis-resistant vasculature, or in wild-type littermates pre-treated with anti-ceramide antibody, indicating that ceramide is necessary for this effect.
  • CONCLUSIONS/SIGNIFICANCE: These studies show that angiogenic factors fail to suppress apoptosis if ceramide remains elevated while anti-angiogenic therapies fail without ceramide elevation, defining a ceramide rheostat that determines outcome of single dose radiotherapy.
  • Understanding the temporal sequencing of anti-angiogenic drugs and radiation enables optimized radiosensitization and design of innovative radiosurgery clinical trials.

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  • [RepublishedFrom] PLoS One. 2010;5(8):e12310 [20808818.001]
  • (PMID = 20941382.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA085704; United States / NCI NIH HHS / CA / R01 CA105125
  • [Publication-type] Corrected and Republished Article; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Ceramides; 0 / DC101 monoclonal antibody; 0 / Radiation-Sensitizing Agents; 0 / Vascular Endothelial Growth Factor A; 4201-58-5 / N-palmitoylsphingosine; EC 3.1.4.- / acid sphingomyelinase-1; EC 3.1.4.12 / Sphingomyelin Phosphodiesterase
  • [Other-IDs] NLM/ PMC2947950
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24. Mirshafiey A, Cuzzocrea S, Rehm BH, Matsuo H: M2000: a revolution in pharmacology. Med Sci Monit; 2005 Aug;11(8):PI53-63
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  • BACKGROUND: The tolerability and the anti-inflammatory and immunosuppressive properties of a novel designed non-steroidal anti-inflammatory drug, M2000 (beta-D-mannuronic acid), were investigated in various experimental models.
  • Its therapeutic potency on kidney diseases was studied using experimental models of nephrosis and immune complex glomerulonephritis (ICG).
  • Biocompatibility and pharmacotoxicology assessment of M2000 was carried out using a fibrosarcoma cell line, zymography, and serum and urine determinants.
  • Lymph node cell proliferation assay in EAE confirmed the immunosuppressive efficacy of the tested drug.
  • Moreover, this drug inhibited MMP-2 activity.
  • The pharmacotoxicology study showed that M2000 is the safest anti-inflammatory and immunosuppressive drug in comparison with dexamethasone and conventional NSAIDs tested.
  • CONCLUSIONS: M2000 is the first novel designed NSAID with the lowest molecular weight, no gastro-nephrotoxicity, and therapeutic effects in glomerulonephritis and nephrosis and could be strongly recommended on an extensive scale as the safest drug for decreasing anti-inflammatory reactions.
  • [MeSH-major] Arthritis, Rheumatoid / drug therapy. Glomerulonephritis / drug therapy. Hydrocarbons / pharmacology. Hydrocarbons / therapeutic use. Multiple Sclerosis / drug therapy
  • [MeSH-minor] Animals. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antibodies / immunology. Arthritis, Experimental / drug therapy. Arthritis, Experimental / pathology. Cattle. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Hindlimb / drug effects. Hindlimb / pathology. Immunosuppression. Interleukin-6 / biosynthesis. Interleukin-6 / metabolism. Lipids / blood. Male. Matrix Metalloproteinase 2 / metabolism. Mice. Neurons / drug effects. Neurons / pathology. Rats. Rats, Inbred Lew. Serum Albumin, Bovine / immunology

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  • (PMID = 16049391.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antibodies; 0 / Hydrocarbons; 0 / Interleukin-6; 0 / Lipids; 0 / Serum Albumin, Bovine; EC 3.4.24.24 / Matrix Metalloproteinase 2
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