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Items 1 to 35 of about 35
1. Goto T, Tomizawa N, Kobayashi E, Fujimura A: A comparative pharmacology study between the intracolonic and oral routes of 5-FU administration in a colon cancer-bearing Yoshida sarcoma rat model. J Pharmacol Sci; 2004 Jun;95(2):163-73
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comparative pharmacology study between the intracolonic and oral routes of 5-FU administration in a colon cancer-bearing Yoshida sarcoma rat model.
  • We prepared a colon cancer-bearing Yoshida sarcoma rat model to examine the dose-response relationship of antitumor activity of intracolonically or orally administered 5-fluorouracil (5-FU; 45, 30, 20, 13, and 8 mg/kg).
  • White blood cell count tended to decrease at high doses when 5-FU was administered intracolonically and showed a statistically significant decrease at doses of > or =30 mg/kg when 5-FU was administered orally.
  • Regarding the time-course of body weight, even the 5-FU highest dose (45 mg/kg) intracolonic administration group showed no inhibited body weight increase compared to the control group.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / therapeutic use. Colonic Neoplasms / drug therapy. Fluorouracil / administration & dosage. Fluorouracil / therapeutic use. Sarcoma, Yoshida / drug therapy
  • [MeSH-minor] Administration, Oral. Animals. Blood Cell Count. Body Weight / drug effects. Catheterization. Colon. Dose-Response Relationship, Drug. Hemoglobins / metabolism. Male. Neoplasm Transplantation. Rats

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  • (PMID = 15215640.001).
  • [ISSN] 1347-8613
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Hemoglobins; U3P01618RT / Fluorouracil
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2. Sadahiro S, Suzuki T, Ishikawa K, Nakamura T, Saguchi T, Kamijo A, Yasuda S, Makuuchi H, Murayama C: Preliminary study of the optimal dosing schedule for oral UFT/leucovorin chemotherapy. Anticancer Res; 2004 Mar-Apr;24(2B):625-30
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  • [Title] Preliminary study of the optimal dosing schedule for oral UFT/leucovorin chemotherapy.
  • BACKGROUND: We evaluated the optimal dosage schedule for combined oral chemotherapy using uracil/tegafur (UFT) and leucovorin (LV) in Yoshida sarcoma-bearing rats.
  • MATERIALS AND METHODS: The antitumor activity and survival effect were compared between two schedules, thrice daily administration on 5 days of the week followed by 2 drug-free days (schedule A) and twice daily on 7 days of the week (schedule B).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leucovorin / administration & dosage. Sarcoma, Yoshida / drug therapy. Tegafur / administration & dosage. Uracil / administration & dosage
  • [MeSH-minor] Animals. Body Weight / drug effects. Drug Administration Schedule. Eating / drug effects. Male. Rats

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  • (PMID = 15161004.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 1548R74NSZ / Tegafur; 56HH86ZVCT / Uracil; Q573I9DVLP / Leucovorin; 1-UFT protocol
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3. Hori K, Furumoto S, Kubota K: Tumor blood flow interruption after radiotherapy strongly inhibits tumor regrowth. Cancer Sci; 2008 Jul;99(7):1485-91
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  • To clarify the therapeutic significance of interrupting tumor blood flow after irradiation, we investigated X-irradiation-induced changes in hemodynamic parameters (blood flow, extravasation and washout of fluorescein isothiocyanate-dextran, and interstitial fluid pressure) in a variant of Yoshida sarcoma, LY80.
  • Tumors in anesthetized male Donryu rats received local irradiation (10 Gy).
  • At all times evaluated after irradiation, AC7700 completely stopped tumor blood flow.
  • This therapeutic combination and timing may have important benefits, even in tumors with low sensitivity to either treatment alone, because the effect was considerably greater than additive.
  • [MeSH-minor] Animals. Cell Proliferation / radiation effects. Combined Modality Therapy. Hemodynamics / radiation effects. Male. Rats. Regional Blood Flow / drug effects

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  • (PMID = 18452559.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC 7700; 452VLY9402 / Serine
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4. Metodiewa D, Skolimowski J, Kochman A, Koceva-Chyla A: The paradoxical apoptotic effects of novel nitroxide antioxidants on Yoshida sarcoma cells in vivo: a commentary. Anticancer Res; 2000 Jul-Aug;20(4):2593-9
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  • [Title] The paradoxical apoptotic effects of novel nitroxide antioxidants on Yoshida sarcoma cells in vivo: a commentary.
  • Here we show for the first time that the model nitroxide derivatives, free radical or its reduced piperidinium salt, suppressed cytotoxicity of ROS (O2 and H2O2) generated outside the cells (B14 line, model for neoplastic phenotype) in ***.
  • In the present study, we have also shown that a very substantial difference in the cell response occurred when the model rat tumor cells (Yoshida Sarcoma ascites) were treated in vivo with six novel synthesized nitroxide antioxidants.
  • Since the increase in the ROS generation followed by apoptotic changes of nuclei is the consistent recent finding in various experimental models of apoptosis, one fundamental question was raised: why nitroxide antioxidants paradoxically act as apoptosis inducers in vivo?
  • [MeSH-major] Antioxidants / pharmacology. Apoptosis / drug effects. Sarcoma, Yoshida / drug therapy
  • [MeSH-minor] Animals. Cricetinae. Dose-Response Relationship, Drug. Male. Rats. Reactive Oxygen Species / metabolism. Structure-Activity Relationship

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  • (PMID = 10953331.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] GREECE
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Reactive Oxygen Species
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5. Yoshida C, Takeuchi M: Histiocytic sarcoma: identification of its histiocytic origin using immunohistochemistry. Intern Med; 2008;47(3):165-9

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  • [Title] Histiocytic sarcoma: identification of its histiocytic origin using immunohistochemistry.
  • We describe a 56-year-old woman with histiocytic sarcoma involving the bone marrow.
  • Immunohistochemically, the neoplastic cells were positive for CD68, lysozyme, CD4 and CD163, but negative for B- and T-cell markers, S100 protein and epithelial markers.
  • The patient received multi-agent chemotherapy and is living at 22 months after diagnosis without recurrence.
  • Histiocytic sarcoma is an exceedingly rare hematopoietic neoplasm and the prognosis is poor due to its rapid progression, widespread disease and poor response to therapy.
  • [MeSH-major] Bone Marrow Neoplasms / diagnosis. Histiocytic Sarcoma / diagnosis

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  • (PMID = 18239326.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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6. Tachibana E, Saito K, Wakabayashi T, Nagasaka T, Furui T, Yoshida J: Sarcomatous transformation of a prolactinoma associated with development of a fatal internal carotid artery pseudoaneurysm--case report. Neurol Med Chir (Tokyo); 2000 Aug;40(8):427-31
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  • Administration of bromocriptine, radiotherapy, and chemotherapy were initiated.
  • In this case, prolactinoma underwent malignant change to sarcoma.
  • [MeSH-major] Aneurysm, False / complications. Carotid Artery Diseases / complications. Pituitary Neoplasms / complications. Pituitary Neoplasms / pathology. Prolactinoma / pathology. Sarcoma / pathology

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  • (PMID = 10979267.001).
  • [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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7. Hori K, Saito S, Kubota K: A novel combretastatin A-4 derivative, AC7700, strongly stanches tumour blood flow and inhibits growth of tumours developing in various tissues and organs. Br J Cancer; 2002 May 20;86(10):1604-14
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  • [Title] A novel combretastatin A-4 derivative, AC7700, strongly stanches tumour blood flow and inhibits growth of tumours developing in various tissues and organs.
  • In a previous study, we used subcutaneous LY80 tumours (a subline of Yoshida sarcoma), Sato lung carcinoma, and methylcholanthrene-induced primary tumours, to demonstrate that a novel water-soluble combretastatin A-4 derivative, AC7700, abruptly and irreversibly stopped tumour blood flow.
  • In a model of cancer chemotherapy against metastases, LY80 cells (2x10(6)) were injected into the lateral tail vein, and AC7700 at 10 mg x kg(-1) was injected i.v. five times at intervals of 2 days, starting on day 7 after tumour cell injection.
  • The change in tumour blood flow and the therapeutic effect of AC7700 on microtumours were observed directly by using Sato lung carcinoma implanted in a rat transparent chamber.
  • AC7700 caused a marked decrease in the tumour blood flow of all LY80 tumours developing in various tissues and organs and growth of all tumours including lymph node metastases and microtumours was inhibited.
  • These results demonstrate that AC7700 is effective for tumours growing in various tissues and organs and for metastases.
  • We conclude that tumour blood flow stanching induced by AC7700 may become an effective therapeutic strategy for all cancers, including refractory cancers because the therapeutic effect is independent of tumour site and specific type of cancer.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Carcinoma / drug therapy. Lung Neoplasms / drug therapy. Prodrugs / therapeutic use. Sarcoma, Yoshida / drug therapy. Serine / analogs & derivatives. Serine / therapeutic use. Vasoconstrictor Agents / therapeutic use
  • [MeSH-minor] Animals. Drug Screening Assays, Antitumor. Heart Neoplasms / blood supply. Heart Neoplasms / drug therapy. Kidney Neoplasms / blood supply. Kidney Neoplasms / drug therapy. Liver Neoplasms, Experimental / blood supply. Liver Neoplasms, Experimental / drug therapy. Lymphatic Metastasis. Male. Neoplasm Transplantation. Organ Specificity. Rats. Regional Blood Flow / drug effects. Skin Window Technique. Stomach Neoplasms / blood supply. Stomach Neoplasms / drug therapy. Tumor Cells, Cultured / transplantation

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  • [Copyright] comCopyright 2002 Cancer Research UK
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  • (PMID = 12085211.001).
  • [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] Scotland
  • [Chemical-registry-number] 0 / AC 7700; 0 / Antineoplastic Agents, Phytogenic; 0 / Prodrugs; 0 / Vasoconstrictor Agents; 452VLY9402 / Serine
  • [Other-IDs] NLM/ PMC2746587
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8. Koceva-Chyła A, Kochman A, Głebska J, Gwoździnski K, Jóźwiak Z, Metodiewa D: Tempicol-3, a novel piperidine-N-oxide stable radical and antioxidant, with low toxicity acts as apoptosis inducer and cell proliferation modifier of Yoshida Sarcoma cells in vivo. Anticancer Res; 2000 Nov-Dec;20(6B):4611-8
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  • [Title] Tempicol-3, a novel piperidine-N-oxide stable radical and antioxidant, with low toxicity acts as apoptosis inducer and cell proliferation modifier of Yoshida Sarcoma cells in vivo.
  • The ability of Tempicol-3 to act as an antitumor agent in vivo was also investigated in a pharmacological test, using rats bearing 3-day old Yoshida Sarcoma (promotion phase of the disease).
  • We have also observed that lowtoxic Tempicol-3, at m.e.d. (minimal effective dose) suppressed tumorigenesis, acting as a cell proliferation modifier and apoptosis inducer in vivo.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antioxidants / pharmacology. Apoptosis / drug effects. Cell Division / drug effects. Sarcoma, Yoshida / drug therapy
  • [MeSH-minor] 3T3 Cells / drug effects. Animals. Ascites / drug therapy. Ascites / pathology. Cyclic N-Oxides / chemistry. Cyclic N-Oxides / pharmacology. Drug Screening Assays, Antitumor. Mice. Piperidines / pharmacology. Rats. Rats, Inbred BUF. Structure-Activity Relationship

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  • (PMID = 11205311.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antioxidants; 0 / Cyclic N-Oxides; 0 / Piperidines; 0 / tempicol 3; 14691-89-5 / tempace; VQN7359ICQ / TEMPO
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9. Araki H, Fukushima M, Kamiyama Y, Shirasaka T: Effect of consecutive lower-dose cisplatin in enhancement of 5-fluorouracil cytotoxicity in experimental tumor cells in vivo. Cancer Lett; 2000 Nov 28;160(2):185-91
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  • When CDDP (1 mg/kg) was administered i.p. to ascitic Yoshida sarcoma-bearing rats for 4 consecutive days, both the reduced folate levels and methionine synthase activity in the cells significantly increased, as the same as a single 5 mg/kg dose of CDDP.
  • Furthermore, when Yoshida sarcoma-bearing rats were pre-treated with 1 mg/kg CDDP for 5 consecutive days, [14C]L-methionine incorporation into the isolated ascitic cells was significantly inhibited as compared to that in non-treated cells, suggesting that consecutive administration of lower-dose CDDP is capable of inducing the intracellular modulation of reduced folate levels and methionine synthase activity via inhibition of cellular uptake of methionine.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / toxicity. Cisplatin / pharmacology. Fluorouracil / toxicity. Sarcoma, Yoshida / drug therapy
  • [MeSH-minor] 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase / biosynthesis. 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase / metabolism. Animals. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Combinations. Drug Synergism. Enzyme Induction / drug effects. Folic Acid / metabolism. Male. Methionine / pharmacokinetics. Mice. Neoplasm Transplantation. Oxonic Acid / administration & dosage. Pyridines / administration & dosage. Rats. Tegafur / administration & dosage

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  • (PMID = 11053648.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] IRELAND
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Pyridines; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; 935E97BOY8 / Folic Acid; AE28F7PNPL / Methionine; EC 2.1.1.13 / 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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10. Kurzidem M, Seidensticker P, Rassweiler J: Renal chemoembolization with mitomycin c/Ethibloc: pharmacokinetics and efficacy in an animal model. J Endourol; 2002 Sep;16(7):515-8
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  • BACKGROUND AND PURPOSE: Arterial embolization can be an alternative treatment for kidney malignancy.
  • MATERIALS AND METHODS: In 32 rats with implanted Yoshida sarcoma, nephrectomy was carried out 15, 30, 60, or 90 minutes after chemoembolization (1 mg v 2 mg of MMC/mL of Ethibloc) or chemoperfusion (1 mg of MMC/mL of NaCl) of the tumor-bearing kidney.
  • The MMC tissue concentration was measured in the kidney specimens.
  • We compared the survival time of rats with Yoshida sarcoma after chemoembolization (N = 15), chemoperfusion (N = 18), embolization (N = 18), nephrectomy (N = 21), and no treatment (N = 25).
  • RESULTS: The MMC tissue concentration in the rat model was much higher after chemoembolization than after chemoperfusion for at least 1.5 hours.
  • CONCLUSION: Chemoembolization produces persistently high tissue concentrations of MMC and avoids toxic peak serum levels.

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  • (PMID = 12396445.001).
  • [ISSN] 0892-7790
  • [Journal-full-title] Journal of endourology
  • [ISO-abbreviation] J. Endourol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Drug Combinations; 0 / Fatty Acids; 0 / Propylene Glycols; 0 / Sclerosing Solutions; 117-96-4 / Diatrizoate; 50SG953SK6 / Mitomycin; 9010-66-6 / Zein; 91196-33-7 / alcoholic prolamine solution
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11. Yoshida S, Kaibara A, Ishibashi N, Shirouzu K: Glutamine supplementation in cancer patients. Nutrition; 2001 Sep;17(9):766-8
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  • OBJECTIVES: Three series of studies investigated whether 1) glutamine deficiency occurs in tumor-bearing rats, 2) glutamine supplementation improves protein metabolism during chemotherapy in tumor-bearing rats, and 3) oral glutamine supplement improves systemic immune and gut-barrier function in patients with esophageal cancer receiving radiochemotherapy.
  • METHODS: In the animal studies, AH109A hepatoma cells or Yoshida sarcoma cells were inoculated into male Donryu rats to induce tumors.
  • Glutamine-supplemented total parenteral nutrition reduced whole-body protein breakdown rate during chemotherapy in tumor-bearing rats.
  • CONCLUSIONS: Glutamine depletion in host tissues occurs in tumor-bearing rats.
  • [MeSH-major] Cachexia / therapy. Esophageal Neoplasms / therapy. Glutamine / administration & dosage. Glutamine / metabolism. Proteins / metabolism
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carbon Isotopes. Case-Control Studies. Combined Modality Therapy. Dietary Supplements. Disease Models, Animal. Humans. Male. Parenteral Nutrition, Total. Rats

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  • (PMID = 11527675.001).
  • [ISSN] 0899-9007
  • [Journal-full-title] Nutrition (Burbank, Los Angeles County, Calif.)
  • [ISO-abbreviation] Nutrition
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbon Isotopes; 0 / Proteins; 0RH81L854J / Glutamine
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12. Luboldt W, Pinkert J, Matzky C, Wunderlich G, Kotzerke J: Radiopharmaceutical tracking of particles injected into tumors: a model to study clearance kinetics. Curr Drug Deliv; 2009 Jul;6(3):255-60
Hazardous Substances Data Bank. Sulfur, Elemental .

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  • OBJECTIVES: Success of selective drug therapies depends on the drug's depot time in the target to treat.
  • Depot time is currently being prolonged, using drug-eluting beads or microspheres for selective internal radiation therapy.
  • The purpose of this study was to establish a model for investigating the depot time of particles injected into tumors in relation to tumor vascularization and particle size.
  • MATERIALS AND METHODS: An animal model with two different vascularized tumors (Walker Carcinoma 256 (hypervascularized) and Yoshida Sarcoma (hypovascularized)) was used.
  • Measurements were adjusted for decay times and then compared.
  • CONCLUSIONS: Particle stay time, biodistribution, and stability can be easily monitored as shown in this animal model.
  • Prolonged retention is independent of vascularization and particle size and appears to be sufficient for therapy.
  • [MeSH-minor] Animals. Carcinoma 256, Walker / blood supply. Carcinoma 256, Walker / metabolism. Epinephrine / pharmacology. Female. Humans. Injections, Intralesional. Kidney / metabolism. Liver / metabolism. Lung / metabolism. Radioisotopes / chemistry. Rats. Rats, Wistar. Rhenium / chemistry. Sarcoma, Yoshida / blood supply. Sarcoma, Yoshida / metabolism. Serum Albumin / chemistry. Spleen / metabolism. Sulfur / chemistry. Tissue Distribution / drug effects

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  • (PMID = 19604139.001).
  • [ISSN] 1567-2018
  • [Journal-full-title] Current drug delivery
  • [ISO-abbreviation] Curr Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Radioisotopes; 0 / Radiopharmaceuticals; 0 / Serum Albumin; 0 / rhenium sulfur colloid; 70FD1KFU70 / Sulfur; 7440-15-5 / Rhenium; YKH834O4BH / Epinephrine
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13. Metodiewa D, Kochman A, Gebicka L, Skolimowski J: Evidence for peroxidative oxidation of substituted piperidine nitroxides, acting as apoptosis inducers in Yoshida Sarcoma cells in vivo. Anticancer Res; 2000 Jul-Aug;20(4):2421-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence for peroxidative oxidation of substituted piperidine nitroxides, acting as apoptosis inducers in Yoshida Sarcoma cells in vivo.
  • Based on these considerations we hypothesize that the administration of oxidizable free radical nitroxide compounds--antioxidants may be a useful strategy in the treatment and investigations of cancer diseases.
  • An in vivo study ("Screening test of chemicals employing Yoshida Sarcoma animals") was carried out to verify whether the structure and/or the chain length of substituent of oxidizable nitroxide derivatives--antioxidants could influence their apoptotic activity.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Piperidines / pharmacology. Sarcoma, Yoshida / drug therapy

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  • (PMID = 10953305.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] GREECE
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Piperidines
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14. Rassweiler J, Prager P, Haferkamp A, Alken P, Kauffmann GW, Richter G: Transarterial nephrectomy: the current status of experimental and clinical studies. J Endourol; 2008 Apr;22(4):767-82
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  • For several years, minimally invasive alternatives have been developed such as laparoscopic nephrectomy or transarterial renal ablation.
  • MATERIALS AND METHODS: Based on own in vitro studies, the principle of capillary embolization with occlusion of the entire arterial system up to the capillaries by a precipitating corn protein (Ethibloc) has been developed in animal studies (i.e., rat and canine kidney model).
  • Further studies using the model of unilateral transarterial implantation of Yoshida-sarcoma cells compared capillary chemoembolization using Ethibloc/mitomycin C (MMC) versus chemoperfusion and capillary embolization.
  • RESULTS: Capillary embolization proved to be significantly superior to a central (i.e., ligation of renal artery) or peripheral type of occlusion resulting in complete coagulation necrosis of the normal rat and canine kidney with reduction of the elevated blood pressure, similar to nephrectomy in the model of renal hypertension.
  • In the highly aggressive Yoshida-sarcoma model, capillary chemoembolization yielded an 80% complete response rate compared to only 75% after capillary embolization and 70% after chemoperfusion.
  • Clinical studies included 68 preoperatively as well as 62 palliatively embolized patients with renal cell carcinoma.
  • The procedure was relatively well tolerated and usually associated with a mild postembolization syndrome.
  • Because of the local ablative efficiency, it may still represent a minimally invasive option in advanced stages of renal carcinoma (i.e., in combination with immunochemotherapy or targeted therapy).

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  • (PMID = 18366320.001).
  • [ISSN] 0892-7790
  • [Journal-full-title] Journal of endourology
  • [ISO-abbreviation] J. Endourol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Fatty Acids; 0 / Propylene Glycols; 0 / Sclerosing Solutions; 117-96-4 / Diatrizoate; 9010-66-6 / Zein; 91196-33-7 / alcoholic prolamine solution; M43H21IO8R / Dimethylnitrosamine
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15. Sato H, Hori K, Sugiyama K, Tanda S, Sato Y: [Tumor microcirculation and selective enhancement of drug delivery--clinical applications based on pathophysiological experiments]. Gan To Kagaku Ryoho; 2000 Jul;27(8):1191-200
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  • [Title] [Tumor microcirculation and selective enhancement of drug delivery--clinical applications based on pathophysiological experiments].
  • Tumor tissue is composed of cancer cells (parenchyma) and tumor vessels (interstitium).
  • This would be a certain cause of insufficient drug delivery to tumor tissues.
  • Among the experimental evidence using Yoshida Sarcoma and Ascites Hepatomas, functional differences in microcirculation between tumor and normal tissues were found by Suzuki et al. (1977).
  • Under hypertensive state induced by the continuous infusion of angiotensin II, tumor blood flow increased remarkably, while there was no change or decrease in blood flow in normal tissues such as the brain, bone marrow, liver and kidney.
  • Augmentation of the anti-tumor effects of angiotensin II-induced hypertension chemotherapy (IHC) for advanced gastric carcinoma was revealed in two randomized controlled trials (RCT-1 & 2) of collaborative study groups in Japan.
  • It is very important for exact evaluation after chemotherapy to understand or estimate the pathohistological changes in the tumor and its degenerated or repaired tissues, which present various clinical images.
  • IHC with smaller DI could lead to a reduction in the accumulation of toxicities of anti-cancer drugs in the host.
  • In conclusion, IHC might be applied to all kinds of tumors to enhance the chemotherapeutic effects through selective increase of drug delivery to tumors.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Delivery Systems / methods. Sarcoma, Yoshida / blood supply. Sarcoma, Yoshida / drug therapy. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Blood Pressure / drug effects. Doxorubicin / administration & dosage. Drug Administration Schedule. Fluorouracil / administration & dosage. Humans. Microcirculation. Mitomycin / administration & dosage. Rats

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  • (PMID = 10945016.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin; 80168379AG / Doxorubicin; U3P01618RT / Fluorouracil; FAM protocol
  • [Number-of-references] 77
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16. Wakahashi K, Shimoyama M, Katayama Y, Minagawa K, Yoshida K, Sasaki R, Nakayama S, Yokozaki H, Yanagita E, Itoh T, Hayashi Y, Matsui T: Histiocytic sarcoma with two immunohistopathologically distinct populations. Int J Hematol; 2010 Nov;92(4):642-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histiocytic sarcoma with two immunohistopathologically distinct populations.
  • This report is a case of histiocytic sarcoma (HS), in which tumor cells consist of two immunohistopathologically distinct populations (A) oval CD68+lysozyme+CD163- cells and (B) abundant cytoplasm or spindle-shaped CD68+lysozyme-CD163+ cells.
  • Cervical lymph node was infiltrated mainly by population (A), where chemotherapy was quite effective.
  • It is also notable that CD163-negative stage of HS may exist and still be reactive for the treatment.
  • [MeSH-major] Histiocytic Sarcoma / immunology. Histiocytic Sarcoma / pathology
  • [MeSH-minor] Aged. Antigens, CD / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Cell Shape. Fatal Outcome. Humans. Lymph Nodes / chemistry. Lymph Nodes / metabolism. Lymph Nodes / pathology. Male. Muramidase / analysis. Receptors, Cell Surface / analysis

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  • (PMID = 20924729.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD163 antigen; 0 / CD68 antigen, human; 0 / Receptors, Cell Surface; EC 3.2.1.17 / Muramidase
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17. Meijsing B, Carbó N, López-Soriano FJ, Argilés JM: Effects of the phosphodiesterase-IV inhibitor EMD 95832/3 on tumour growth and cachexia in rats bearing the Yoshida AH-130 ascites hepatoma. Cancer Lett; 2002 Dec 15;188(1-2):53-8
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  • [Title] Effects of the phosphodiesterase-IV inhibitor EMD 95832/3 on tumour growth and cachexia in rats bearing the Yoshida AH-130 ascites hepatoma.
  • Administration of the phosphodiesterase-IV inhibitor EMD 95832/3 (Merck KGaA, Darmstadt, Germany) to rats bearing the ascites hepatoma Yoshida AH-130, a highly cachectic tumour, could not prevent either the anorexia nor the massive weight loss (affecting both adipose and skeletal muscle tissues) present in the tumour-bearing animals.
  • This compound did not have any effects on the fractional rates of protein turnover in skeletal muscle, and did not affect circulating triacylglycerols or lipoprotein lipase activity in adipose tissue.
  • It is concluded that the drug is unable to reverse the cachectic state in this particular experimental tumour model.
  • [MeSH-major] 3',5'-Cyclic-AMP Phosphodiesterases / antagonists & inhibitors. Cachexia / drug therapy. Liver Neoplasms, Experimental / pathology. Phosphodiesterase Inhibitors / therapeutic use. Sarcoma, Yoshida / pathology
  • [MeSH-minor] Adipose Tissue / anatomy & histology. Adipose Tissue / drug effects. Alanine / blood. Animals. Blood Glucose / drug effects. Cell Cycle / drug effects. Cell Division / drug effects. Cyclic Nucleotide Phosphodiesterases, Type 4. Lactic Acid / blood. Lipoprotein Lipase / metabolism. Male. Organ Size / drug effects. Rats. Rats, Wistar. Triglycerides / blood. Tumor Necrosis Factor-alpha / metabolism. Weight Loss / drug effects

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  • (PMID = 12406548.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Phosphodiesterase Inhibitors; 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; 33X04XA5AT / Lactic Acid; EC 3.1.1.34 / Lipoprotein Lipase; EC 3.1.4.17 / 3',5'-Cyclic-AMP Phosphodiesterases; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 4; OF5P57N2ZX / Alanine
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18. Yoshida K, Kusuzaki K, Matsubara T, Matsumine A, Kumamoto T, Komada Y, Naka N, Uchida A: Periosteal Ewing's sarcoma treated by photodynamic therapy with acridine orange. Oncol Rep; 2005 Feb;13(2):279-82
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  • [Title] Periosteal Ewing's sarcoma treated by photodynamic therapy with acridine orange.
  • We recently encountered a very rare case of periosteal Ewing's sarcoma (PES), which was treated by surgery followed by photodynamic therapy using acridine orange with radiodynamic therapy.
  • Histopathological examination of biopsy specimens revealed a small round cell sarcoma suggestive of Ewing's sarcoma or PNET, and immunohistochemistry showed positive staining for MIC2.
  • Therefore, we administered preoperative chemotherapy, as a result of which the tumor shrank to 48% of its original volume.
  • With a view to preserve excellent shoulder and upper limb function, we attempted intralesional tumor resection supported by photodynamic therapy using acridine orange with radiodynamic therapy.
  • After surgery followed by postoperative chemotherapy, the patient has, until the time of writing, had no local tumor recurrence and no evidence of metastatic disease, and can move his shoulder fully and throw a ball well.
  • Since it has been reported that PES has a better prognosis and responsiveness to chemotherapy than intramedullary Ewing's sarcoma, we believe that such reduction surgery with photodynamic therapy might be the strategy of choice to obtain satisfactory limb function in cases of PES.
  • [MeSH-major] Bone Neoplasms / drug therapy. Humerus. Periosteum. Photochemotherapy / methods. Sarcoma, Ewing / drug therapy

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  • (PMID = 15643511.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] F30N4O6XVV / Acridine Orange
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19. Shinoda H, Yoshida A, Teruya-Feldstein J: Malignant histiocytoses/disseminated histiocytic sarcoma with hemophagocytic syndrome in a patient with mediastinal germ cell tumor. Appl Immunohistochem Mol Morphol; 2009 Jul;17(4):338-44
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  • [Title] Malignant histiocytoses/disseminated histiocytic sarcoma with hemophagocytic syndrome in a patient with mediastinal germ cell tumor.
  • We describe a case of a 24-year-old man with a large anterior mediastinal mass showing a nonseminomatous germ cell tumor then subsequently developed hemophagocytic syndrome involving the bone marrow and liver.
  • During the course of chemotherapy, he developed profound thrombocytopenia, eccymoses, and bleeding.
  • He had moderate splenomegaly and splenectomy was performed to restore adequate hematologic reserve to permit further chemotherapy.
  • The patient was refractory to therapy and ultimately died 5 months after diagnosis.

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  • (PMID = 18987551.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / S100 Proteins
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20. Dubin M, Fernandez Villamil SH, Stoppani AO: [Cytotoxicity of beta-lapachone, an naphthoquinone with possible therapeutic use]. Medicina (B Aires); 2001;61(3):343-50
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  • [Title] [Cytotoxicity of beta-lapachone, an naphthoquinone with possible therapeutic use].
  • [Transliterated title] Citotoxicidad de la beta-lapachona: una o-naftoquinona con posibles usos terapéuticos.
  • Initial observations proved its capability for inhibiting growth of Yoshida tumor and Walker 256 carcinosarcoma. beta-Lap redox-cycling in the presence of reductants and oxygen yields "reactive oxygen species" (ROS: O2-, OH and H2O2) which cytotoxicity led to assume its role in beta-lap activity in cells. beta-Lap inhibited DNA synthesis in Trypanosoma cruzi as well as topoisomerases I and II, poly(ADP-ribose) polymerase (PARP) in different cells.
  • These enzymes are essential for maintaining DNA structure. beta-Lap inhibited growth of a large variety of tumor cells including epidermoid laringeal cancer, prostate, colon, ovary and breast cancer and also different types of leukemia cells.
  • Advances in knowledge of apoptosis ("programmed cell death") and necrosis provided useful information for understanding the mechanism of beta-lap cytotoxicity.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Naphthoquinones / pharmacology. Neoplasms / drug therapy. Poly(ADP-ribose) Polymerases / metabolism. Reactive Oxygen Species / physiology
  • [MeSH-minor] Animals. Carcinoma 256, Walker / drug therapy. Carcinoma 256, Walker / enzymology. Humans. Sarcoma, Yoshida / drug therapy. Sarcoma, Yoshida / enzymology. Topoisomerase I Inhibitors

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  • (PMID = 11474885.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Naphthoquinones; 0 / Reactive Oxygen Species; 0 / Topoisomerase I Inhibitors; 4707-32-8 / beta-lapachone; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
  • [Number-of-references] 58
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21. Busquets S, Fuster G, Ametller E, Olivan M, Figueras M, Costelli P, Carbó N, Argilés JM, López-Soriano FJ: Resveratrol does not ameliorate muscle wasting in different types of cancer cachexia models. Clin Nutr; 2007 Apr;26(2):239-44
Hazardous Substances Data Bank. RESVERATROL .

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  • [Title] Resveratrol does not ameliorate muscle wasting in different types of cancer cachexia models.
  • However, administration of resveratrol in vivo to both rats bearing the Yoshida AH-130 ascites hepatoma (at the dose of 1 mg/kg body weight) and mice bearing the Lewis lung carcinoma (at two different doses, 5 and 25 mg/kg body weight) had no effect on skeletal muscle mass or body weight in tumour-bearing rodents.
  • CONCLUSIONS: It is therefore concluded from this study that resveratrol is unable to influence muscle mass in vivo and has no potential role as anticachectic agent for the treatment of muscle wasting associated with tumour growth.
  • [MeSH-major] Cachexia / drug therapy. Muscle Proteins / metabolism. Muscle, Skeletal / drug effects. Neoplasms, Experimental / metabolism. Stilbenes / pharmacology
  • [MeSH-minor] Animals. Body Weight / drug effects. Body Weight / physiology. Carcinoma, Lewis Lung. Disease Models, Animal. Energy Intake / drug effects. Energy Intake / physiology. Fish Oils. Male. Mice. Mice, Inbred C57BL. NF-kappa B / antagonists & inhibitors. Organ Size / drug effects. Random Allocation. Rats. Rats, Wistar. Sarcoma, Yoshida

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  • (PMID = 17261345.001).
  • [ISSN] 0261-5614
  • [Journal-full-title] Clinical nutrition (Edinburgh, Scotland)
  • [ISO-abbreviation] Clin Nutr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fish Oils; 0 / Muscle Proteins; 0 / NF-kappa B; 0 / Stilbenes; Q369O8926L / resveratrol
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22. Fahrig R, Heinrich JC, Nickel B, Wilfert F, Leisser C, Krupitza G, Praha C, Sonntag D, Fiedler B, Scherthan H, Ernst H: Inhibition of induced chemoresistance by cotreatment with (E)-5-(2-bromovinyl)-2'-deoxyuridine (RP101). Cancer Res; 2003 Sep 15;63(18):5745-53
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  • Although several drugs are in development that circumvent or decrease existing chemoresistance, none has the potential to prevent or reduce its induction.
  • Here, we present data from a drug that could perhaps fill this gap.
  • Cotreatment of chemotherapy with (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU, RP101) prevented the decrease of apoptotic effects during the course of chemotherapy and reduced nonspecific toxicity.
  • During recovery, when treatment was with BVDU only, microfilamental proteins were up-regulated, and proteins involved in ATP generation or cell survival (STAT3 and JUN-D) were down-regulated.
  • That way, in three different rat tumor models, the antitumor efficiency of chemotherapy was optimized, and toxic side effects were reduced.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Bromodeoxyuridine / analogs & derivatives. Bromodeoxyuridine / pharmacology. Vinblastine / analogs & derivatives
  • [MeSH-minor] Animals. Cisplatin / administration & dosage. DNA-Binding Proteins / metabolism. Doxorubicin / administration & dosage. Drug Resistance, Neoplasm. Drug Synergism. Electrophoresis, Gel, Two-Dimensional. Fibroblasts / drug effects. Ifosfamide / administration & dosage. Methotrexate / administration & dosage. Methotrexate / pharmacology. Mice. Mitomycin / administration & dosage. Mitoxantrone / administration & dosage. NAD(P)H Dehydrogenase (Quinone) / metabolism. Rats. Rats, Sprague-Dawley. STAT3 Transcription Factor. Sarcoma, Yoshida / drug therapy. Sarcoma, Yoshida / metabolism. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Trans-Activators / metabolism. Tumor Cells, Cultured

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  • (PMID = 14522895.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, mouse; 0 / Stat3 protein, rat; 0 / Trans-Activators; 2M3055079H / brivudine; 50SG953SK6 / Mitomycin; 5V9KLZ54CY / Vinblastine; 80168379AG / Doxorubicin; BZ114NVM5P / Mitoxantrone; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; G34N38R2N1 / Bromodeoxyuridine; Q20Q21Q62J / Cisplatin; Q6C979R91Y / vinorelbine; UM20QQM95Y / Ifosfamide; YL5FZ2Y5U1 / Methotrexate
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23. Bacher G, Nickel B, Emig P, Vanhoefer U, Seeber S, Shandra A, Klenner T, Beckers T: D-24851, a novel synthetic microtubule inhibitor, exerts curative antitumoral activity in vivo, shows efficacy toward multidrug-resistant tumor cells, and lacks neurotoxicity. Cancer Res; 2001 Jan 01;61(1):392-9
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  • N-(pyridin-4-yl)-[1-(4-chlorbenzyl)-indol-3-yl]-glyoxyl-amid (D-24851) is a novel synthetic compound that was identified in a cell-based screening assay to discover cytotoxic drugs.
  • D-24851 destabilizes microtubules and blocks cell cycle transition specifically at G2-M phase.
  • The binding site of D-24851 does not overlap with the tubulin binding sites of known microtubule-destabilizing agents like vincristine or colchicine.
  • In vitro, D-24851 has potent cytotoxic activity toward a panel of established human tumor cell lines including SKOV3 ovarian cancer, U87 glioblastoma, and ASPC-1 pancreatic cancer cells.
  • In vivo, oral D-24851 treatment induced complete tumor regressions (cures) in rats bearing Yoshida AH13 sarcomas.
  • Interestingly, multidrug-resistant cell lines generated by vincristine-driven selection or transfection with the Mr 170,000 P-glycoprotein encoding cDNA were rendered resistant toward paclitaxel, vincristine, or doxorubicin but not towards D-24851 when compared with the parental cells.
  • Because of its synthetic nature, its oral applicability, its potent in vitro and in vivo antitumoral activity, its efficacy against multidrug-resistant tumors, and the lack of neurotoxicity, D-24851 may have significant potential for the treatment of various malignancies.
  • [MeSH-minor] ATP-Binding Cassette Transporters / metabolism. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Animals. Binding Sites. Binding, Competitive. Cell Cycle / drug effects. Cell Division / drug effects. Colchicine / metabolism. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Female. Humans. Microtubules / drug effects. Motor Activity / drug effects. Multidrug Resistance-Associated Proteins. Nervous System Diseases / chemically induced. Neural Conduction / drug effects. Rats. Rats, Sprague-Dawley. Rats, Wistar. Sarcoma, Yoshida / drug therapy. Tubulin / metabolism. Tumor Cells, Cultured / drug effects. Vincristine / metabolism

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  • (PMID = 11196193.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Acetamides; 0 / Antineoplastic Agents; 0 / Indoles; 0 / Multidrug Resistance-Associated Proteins; 0 / Tubulin; 5J49Q6B70F / Vincristine; 80K4H2RB8P / indibulin; SML2Y3J35T / Colchicine
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24. Yoshida Y, Osaka S, Tokuhashi Y: Analysis of limb function after various reconstruction methods according to tumor location following resection of pediatric malignant bone tumors. World J Surg Oncol; 2010;8:39
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  • PATIENTS AND METHODS: We classified the tumors according to their location into 3 types by preoperative MRI, and evaluated reconstruction methods after wide resection, paying attention to whether the joint function could be preserved.
  • The mean age of the patients was 10.6 years, Osteosarcoma was observed in 26 patients, Ewing's sarcoma in 3, and PNET(primitive neuroectodermal tumor) and chondrosarcoma (grade 1) in 1 each.
  • RESULTS: Type I were those located in the diaphysis, and reconstruction was performed using a vascularized fibular graft(vascularized fibular graft).
  • Type 2 were those located in contact with the epiphyseal line or within 1 cm from this line, and VFG was performed in 1, and distraction osteogenesis in 1.
  • Type III were those extending from the diaphysis to the epiphysis beyond the epiphyseal line, and a Growing Kotz was mainly used in 10 patients.
  • The mean functional assessment score was the highest for Type I (96%: n = 4) according to the type and for VFG (99%) according to the reconstruction method.
  • CONCLUSION: The final functional results were the most satisfactory for Types I and II according to tumor location.
  • Therefore, considering the function of the affected limb, a limb reconstruction method allowing the maximal preservation of joint function should be selected after careful evaluation of the effects of chemotherapy and the location of the tumor.
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chondrosarcoma / pathology. Chondrosarcoma / surgery. Female. Follow-Up Studies. Humans. Male. Neuroectodermal Tumors, Primitive, Peripheral / pathology. Neuroectodermal Tumors, Primitive, Peripheral / surgery. Osteosarcoma / pathology. Osteosarcoma / surgery. Sarcoma, Ewing / pathology. Sarcoma, Ewing / surgery. Surgical Flaps. Survival Rate. Treatment Outcome

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  • (PMID = 20482815.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2881919
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25. Endo K, Kuratate I, Watanabe M, Yoshida H, Teshima R, Osaki M, Ito H: Wild-type p53 gene transfection in human cultured sarcomas: effect of CDDP. Oncol Rep; 2001 May-Jun;8(3):637-42
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  • [Title] Wild-type p53 gene transfection in human cultured sarcomas: effect of CDDP.
  • We examined the susceptibility of five human bone and soft tissue sarcoma cell lines to transfection with recombinant p53 adenovirus vector (AxCA-p53).
  • Transfection efficiency was more than 90% at 72 h with AxCA-lacZ at a multiplicity of infection (MOI) of 50 in all the cell lines, except for MG-63 (p53 gene mutated) cells.
  • Western blot analysis showed overexpression of both P21/Waf1 and Bax protein in all the cell lines, implying sufficient and successful p53 gene transfection.
  • The two apoptosis-induced cell lines showed a gradual increase in Bax expression up to 72 h and non-detectable expression of Bcl-XL from 48 h, suggesting the involvement of an apoptosis-inducing mechanism.
  • Pre-treatment with cis-diamminedichloroplatinum (II) (CDDP) at 0.1 microg/ml significantly suppressed tumor cell viability in NY and HuO-3N1 (mutated), but not in the other three lines including HT-1080 carrying the wild-type p53 gene, implying the existence of different mechanisms for the tumor suppressive effect of p53 gene transfection and CDDP.
  • These results indicate that wild-type p53 gene transfection with CDDP is a promising therapy for some, but not all, non-resectable bone-and soft tissue sarcomas, regardless of intrinsic p53 gene status.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bone Neoplasms / drug therapy. Cisplatin / pharmacology. Genes, p53 / genetics. Proto-Oncogene Proteins c-bcl-2. Sarcoma / drug therapy. Soft Tissue Neoplasms / drug therapy. Transfection. Tumor Cells, Cultured / drug effects
  • [MeSH-minor] Adenoviruses, Human / genetics. Apoptosis / drug effects. Blotting, Western. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / metabolism. Flow Cytometry. Gene Expression. Humans. Lac Operon / physiology. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins / metabolism. bcl-2-Associated X Protein

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  • (PMID = 11295094.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; Q20Q21Q62J / Cisplatin
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26. Yoshida A, Edgar MA, Garcia J, Meyers PA, Morris CD, Panicek DM: Primary desmoplastic small round cell tumor of the femur. Skeletal Radiol; 2008 Sep;37(9):857-62
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  • [Title] Primary desmoplastic small round cell tumor of the femur.
  • Desmoplastic small round cell tumor (DSRCT) is a rare malignant neoplasm typically involving the abdominal cavity of a young male.
  • The patient presented with knee pain, and radiological findings were strongly suggestive of osteogenic sarcoma.
  • Despite chemotherapy and complete tumor excision, the patient developed progressive lung and bone metastases and died 3 years after initial presentation.
  • [MeSH-major] Diagnostic Imaging. Femoral Neoplasms / diagnosis. Sarcoma, Small Cell / diagnosis

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  • [ISSN] 0364-2348
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  • [ISO-abbreviation] Skeletal Radiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
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27. Fukushima M: [Antitumor activity and function of S-1, a new oral tegafur-based formulation]. Gan To Kagaku Ryoho; 2006 Jun;33 Suppl 1:19-26
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  • TS-1 (S-1), developed by the scientific theory of both potentiating antitumor activity of 5-fluorouracil (5-FU) and reducing gastrointestinal toxicity induced by 5-FU, is a new oral formulation consisting of 1 M tegafur, 0.4 M gimeracil and 1 M oteracil potassium.
  • We investigated the antitumor efficacy of S-1 alone and in combination with other cytotoxic anticancer drugs using subcutaneously or orthotopically implanted murine and human tumors in rodents.
  • In combination with other anticancer drugs such as CPT-11 and taxanes, S-1 exercised synergistic antitumor efficacy not only on 5-FU-sensitive tumors with low expression levels of thymidylate synthase (TS) but also on 5-FU-resistant tumors with originally higher and/or elevated levels of TS expression.
  • Throughout our preclinical antitumor studies of S-1, alone and/or in combination with other anticancer drugs, it would be expected to contribute greatly to the treatment of cancer patients.
  • [MeSH-major] Antimetabolites, Antineoplastic. Neoplasms / drug therapy. Oxonic Acid / pharmacology. Tegafur / pharmacology
  • [MeSH-minor] Administration, Oral. Animals. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Drug Administration Schedule. Drug Combinations. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Humans. Mice. Neoplasm Transplantation. Pharmaceutical Preparations. Rats. Sarcoma, Yoshida / drug therapy. Uracil / administration & dosage

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  • (PMID = 16897968.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0 / Pharmaceutical Preparations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 56HH86ZVCT / Uracil; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; 1-UFT protocol
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28. Combaret L, Tilignac T, Claustre A, Voisin L, Taillandier D, Obled C, Tanaka K, Attaix D: Torbafylline (HWA 448) inhibits enhanced skeletal muscle ubiquitin-proteasome-dependent proteolysis in cancer and septic rats. Biochem J; 2002 Jan 15;361(Pt 2):185-92
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  • The development of new pharmacological approaches for preventing muscle wasting in cancer is an important goal because cachectic patients display a reduced response to chemotherapy and radiotherapy.
  • In cancer rats, the drug blocked the lipopolysaccharide-induced hyperproduction of TNF and prevented muscle wasting.
  • The drug also normalized the enhanced muscle expression of Ub, which prevails in the atrophying muscles from cancer rats.
  • Finally, the drug also prevented muscle wasting in septic rats (which exhibit increased TNF production), and was much more potent than pentoxifylline or other xanthine derivatives.
  • [MeSH-major] Cysteine Endopeptidases / metabolism. Multienzyme Complexes / metabolism. Muscle, Skeletal / drug effects. Pentoxifylline / analogs & derivatives. Pentoxifylline / pharmacology. Sarcoma, Yoshida / metabolism. Sepsis / metabolism. Ubiquitin / metabolism
  • [MeSH-minor] Animals. Down-Regulation / drug effects. Hydrolysis. Male. Proteasome Endopeptidase Complex. RNA, Messenger / genetics. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 11772390.001).
  • [ISSN] 0264-6021
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Multienzyme Complexes; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0 / Ubiquitin; 65O78F9T1W / torbafylline; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.25.1 / Proteasome Endopeptidase Complex; SD6QCT3TSU / Pentoxifylline
  • [Other-IDs] NLM/ PMC1222298
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29. Osaka S, Sugita H, Osaka E, Yoshida Y, Ryu J: Surgical management of malignant soft tissue tumours in patients aged 65 years or older. J Orthop Surg (Hong Kong); 2003 Jun;11(1):28-33
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  • [Title] Surgical management of malignant soft tissue tumours in patients aged 65 years or older.
  • OBJECTIVE: With the aim to determine the most effective treatment for primary malignant musculoskeletal tumours in patients aged 65 years or older, we reviewed cases of low- and high-grade neoplasms, surgical margins, surgical methods, and the prognoses of elderly and aged patients at our institution.
  • METHODS: Records of 25 patients aged 65 years or older who had malignant soft tissue tumours from December 1986 to February 1997 were reviewed.
  • As adjuvant therapy, radiotherapy was used in 5 cases and chemotherapy in 3.
  • [MeSH-major] Histiocytoma, Benign Fibrous / surgery. Neoplasm Recurrence, Local / surgery. Orthopedic Procedures. Sarcoma / surgery. Soft Tissue Neoplasms / surgery

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  • (PMID = 12810968.001).
  • [ISSN] 1022-5536
  • [Journal-full-title] Journal of orthopaedic surgery (Hong Kong)
  • [ISO-abbreviation] J Orthop Surg (Hong Kong)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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30. Arakawa K, Endo Y, Kimura M, Yoshida T, Kitaoka T, Inakazu T, Nonami Y, Abe M, Masuyama A, Nojima M, Sasaki T: Multifunctional anti-angiogenic activity of the cyclic peroxide ANO-2 with antitumor activity. Int J Cancer; 2002 Jul 10;100(2):220-7
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  • Our focus was to develop an anti-angiogenic drug possessing the inhibitory activity of urokinase-type plasminogen activator (u-PA) production.
  • 1-Phenyl-1, 4-epoxy-1H,4H-naphtho[1,8-de][1, 2]dioxepin (ANO-2) potently inhibited cathepsin B (IC(50) = 0.47 microM) as well as u-PA production.
  • Additionally, in vivo administration of ANO-2 inhibited angiogenesis induced by mouse Sarcoma-180 cells tested using the mouse dorsal air sac assay.
  • These in vitro and in vivo activities indicate that ANO-2 has considerable potential as a new and potent anti-angiogenic drug that inhibits both u-PA production and enzymatic activity of cathepsins, indicating that ANO-2 may be a multifunctional inhibitor of angiogenesis.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Antineoplastic Agents / pharmacology. Carcinoma, Lewis Lung / blood supply. Lung Neoplasms / blood supply. Naphthalenes / pharmacology. Neovascularization, Pathologic / drug therapy. Oxepins / pharmacology
  • [MeSH-minor] Air Sacs / blood supply. Animals. Cathepsin B / antagonists & inhibitors. Chick Embryo. Female. Humans. Mice. Mice, Inbred C57BL. Mice, Inbred ICR. RNA, Messenger / metabolism. Ribonuclease, Pancreatic / metabolism. Sarcoma / blood supply. Sarcoma / prevention & control. Umbilical Veins / cytology. Urokinase-Type Plasminogen Activator / antagonists & inhibitors. Urokinase-Type Plasminogen Activator / genetics. Urokinase-Type Plasminogen Activator / urine. Xenograft Model Antitumor Assays

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12115573.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-phenyl-1,4-epoxy-1H,4H-naphtho(1,8-de)(1,2)dioxepin; 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Naphthalenes; 0 / Oxepins; 0 / RNA, Messenger; EC 3.1.27.5 / Ribonuclease, Pancreatic; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; EC 3.4.22.1 / Cathepsin B
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31. Koga F, Kawano K, Honda M, Sumi S, Horimi H, Kondo S, Yoshida K: Sarcomatoid renal cell carcinoma with scant carcinomatous components. Int J Urol; 2000 Feb;7(2):58-60; discussion 61
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  • [Title] Sarcomatoid renal cell carcinoma with scant carcinomatous components.
  • At that time a diagnosis of rhabdomyosarcoma of the kidney was made.
  • However, further microscopic examination of another eight sections revealed small areas of clear cell-type renal cell carcinoma (RCC) which transited to sarcomatous components and led to a diagnosis of sarcomatoid RCC.
  • The patient underwent three cycles of adjuvant chemotherapy.
  • He has been free of the disease for 14 months after nephrectomy.
  • [MeSH-major] Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology
  • [MeSH-minor] Adult. Humans. Male. Sarcoma / pathology

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  • (PMID = 10710249.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] AUSTRALIA
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32. Busquets S, Figueras MT, Fuster G, Almendro V, Moore-Carrasco R, Ametller E, Argilés JM, López-Soriano FJ: Anticachectic effects of formoterol: a drug for potential treatment of muscle wasting. Cancer Res; 2004 Sep 15;64(18):6725-31
The Lens. Cited by Patents in .

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  • [Title] Anticachectic effects of formoterol: a drug for potential treatment of muscle wasting.
  • The anti-wasting effects of the drug were based on both an activation of the rate of protein synthesis and an inhibition of the rate of muscle proteolysis.
  • Northern blot analysis revealed that formoterol treatment resulted in a decrease in the mRNA content of ubiquitin and proteasome subunits in gastrocnemius muscles; this, together with the decreased proteasome activity observed, suggest that the main anti-proteolytic action of the drug may be based on an inhibition of the ATP-ubiquitin-dependent proteolytic system.
  • The present results indicate that formoterol exerted a selective, powerful protective action on heart and skeletal muscle by antagonizing the enhanced protein degradation that characterizes cancer cachexia, and it could be revealed as a potential therapeutic tool in pathologic states wherein muscle protein hypercatabolism is a critical feature such as cancer cachexia or other wasting diseases.
  • [MeSH-major] Adrenergic beta-Agonists / pharmacology. Cachexia / drug therapy. Ethanolamines / pharmacology. Muscle, Skeletal / pathology. Neoplasms, Experimental / metabolism
  • [MeSH-minor] Animals. Carcinoma, Lewis Lung / metabolism. Carcinoma, Lewis Lung / pathology. Disease Models, Animal. Eating / drug effects. Formoterol Fumarate. Liver Neoplasms, Experimental / metabolism. Liver Neoplasms, Experimental / pathology. Male. Mice. Mice, Inbred C57BL. Muscle Proteins / metabolism. Rats. Rats, Wistar. Sarcoma, Yoshida / metabolism. Sarcoma, Yoshida / pathology

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  • (PMID = 15374990.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic beta-Agonists; 0 / Ethanolamines; 0 / Muscle Proteins; W34SHF8J2K / Formoterol Fumarate
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33. Carbó N, López-Soriano J, Costelli P, Busquets S, Alvarez B, Baccino FM, Quinn LS, López-Soriano FJ, Argilés JM: Interleukin-15 antagonizes muscle protein waste in tumour-bearing rats. Br J Cancer; 2000 Aug;83(4):526-31
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tissue protein hypercatabolism (TPH) is an important feature in cancer cachexia, particularly with regard to the skeletal muscle.
  • The Yoshida AH-130 rat ascites hepatoma is a model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle wasting, primarily due to TPH.
  • Indeed, IL-15 treatment partly inhibited skeletal muscle wasting in AH-130-bearing rats by decreasing (8-fold) protein degradative rates (as measured by 14C-bicarbonate pre-loading of muscle proteins) to values even lower than those observed in non-tumour-bearing animals.
  • The present data give new insights into the mechanisms by which IL-15 exerts its preventive effect on muscle protein wasting and seem to warrant the implementation of experimental protocols involving the use of the cytokine in the treatment of pathological states characterized by TPH, particularly in skeletal muscle, such as in the present model of cancer cachexia.
  • [MeSH-major] Cachexia / drug therapy. Interleukin-15 / pharmacology. Liver Neoplasms, Experimental / metabolism. Muscle Proteins / metabolism. Muscle, Skeletal / drug effects. Sarcoma, Yoshida / metabolism
  • [MeSH-minor] Animals. Male. Muscular Atrophy / drug therapy. Muscular Atrophy / etiology. Muscular Atrophy / metabolism. Neoplasm Transplantation. Rats. Rats, Wistar

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  • (PMID = 10945502.001).
  • [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] SCOTLAND
  • [Chemical-registry-number] 0 / Interleukin-15; 0 / Muscle Proteins
  • [Other-IDs] NLM/ PMC2374658
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34. Okamoto M, Gohda H, Ohe G, Yoshida H, Matsuno T, Saito M, Sato M: Cytokine-inducing activity and antitumor effect of a liposome-incorporated interferon-gamma-inducing molecule derived from OK-432, a streptococcal preparation. J Immunother; 2000 Jan;23(1):94-103
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • In the current study, the liposomes were used to improve the delivery of the agent (OK-PSA) to effector cells and to increase the therapeutic effect.
  • [MeSH-minor] Adenocarcinoma. Animals. Cells, Cultured. Cytokines. Cytotoxicity, Immunologic. Drug Carriers. G(M1) Ganglioside / immunology. Humans. Killer Cells, Lymphokine-Activated / immunology. Killer Cells, Natural / immunology. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / immunology. Liposomes. Mice. Mice, Inbred BALB C. Salivary Gland Neoplasms. Sarcoma, Experimental / drug therapy. Sarcoma, Experimental / physiopathology. Spleen / cytology. Spleen / immunology. Tumor Cells, Cultured

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  • (PMID = 10687142.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / Drug Carriers; 0 / Interleukin-1; 0 / Liposomes; 0 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha; 37758-47-7 / G(M1) Ganglioside; 39325-01-4 / Picibanil; 71012-19-6 / asialo GM1 ganglioside; 82115-62-6 / Interferon-gamma
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35. Yoshisue K, Masuda H, Matsushima E, Ikeda K, Nagayama S, Kawaguchi Y: Tissue distribution and biotransformation of potassium oxonate after oral administration of a novel antitumor agent (drug combination of tegafur, 5-chloro-2,4-dihydroxypyridine, and potassium oxonate) to rats. Drug Metab Dispos; 2000 Oct;28(10):1162-7
Hazardous Substances Data Bank. FLUOROURACIL .

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  • [Title] Tissue distribution and biotransformation of potassium oxonate after oral administration of a novel antitumor agent (drug combination of tegafur, 5-chloro-2,4-dihydroxypyridine, and potassium oxonate) to rats.
  • In this study, we investigated the tissue distribution and the metabolic fate of Oxo in rats after oral administration of S-1.
  • Oxo was mainly distributed to the intracellular sites of the small intestines in a much higher concentration than 5-FU, but little distributed to other tissues, including tumorous ones in which 5-FU was observed after oral administration of S-1.
  • Plasma concentration-time profiles of Oxo and its metabolites after i.v. and oral administration of S-1 revealed that Oxo was mainly converted to cyanuric acid in the GI tract.
  • Furthermore, the analysis of drug-related radioactivity in GI contents and in vitro studies suggested that Oxo was converted to cyanuric acid by two routes, the first being direct conversion by the gut flora in the cecum, and the second, conversion by xanthine oxidase or perhaps by aldehyde oxidase after degradation to 5-azauracil (5-AZU) by the gastric acid.
  • These results indicate that, although a part of the administered Oxo was degraded in the GI tract, Oxo was mainly distributed to the intracellular sites of the small intestines in a much higher concentration than 5-FU and that little was distributed to other tissues, including tumors.
  • [MeSH-minor] Administration, Oral. Allopurinol / pharmacology. Animals. Area Under Curve. Biotransformation. Carbon Radioisotopes. Chlorpromazine / pharmacology. Drug Combinations. Drugs, Chinese Herbal / pharmacology. Fluorouracil / blood. Fluorouracil / metabolism. Intestine, Small / metabolism. Male. Microsomes, Liver / drug effects. Microsomes, Liver / metabolism. Rats. Rats, Inbred Strains. Sarcoma, Yoshida / drug therapy. Sarcoma, Yoshida / metabolism. Tissue Distribution. Triazines / blood. Triazines / metabolism. Xanthine Oxidase / metabolism

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  • (PMID = 10997934.001).
  • [ISSN] 0090-9556
  • [Journal-full-title] Drug metabolism and disposition: the biological fate of chemicals
  • [ISO-abbreviation] Drug Metab. Dispos.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Carbon Radioisotopes; 0 / Drug Combinations; 0 / Drugs, Chinese Herbal; 0 / Pyridines; 0 / Triazines; 0 / shakuyaku-kanzoh-toh; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 56HH86ZVCT / Uracil; 5VT6420TIG / Oxonic Acid; 63CZ7GJN5I / Allopurinol; 71-33-0 / 5-azauracil; EC 1.17.3.2 / Xanthine Oxidase; H497R4QKTZ / cyanuric acid; U3P01618RT / Fluorouracil; U42B7VYA4P / Chlorpromazine
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