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1. Rothbarth J, Woutersen RA, Sparidans RW, van de Velde CJ, Mulder GJ: Melphalan antitumor efficacy and hepatotoxicity: the effect of variable infusion duration in the hepatic artery. J Pharmacol Exp Ther; 2003 Jun;305(3):1098-103
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  • [Title] Melphalan antitumor efficacy and hepatotoxicity: the effect of variable infusion duration in the hepatic artery.
  • The optimum conditions (duration and concentration) of a fixed dose, intra-arterial melphalan infusion in relation to its antitumor effect and toxicity in the liver were investigated in a rat colon tumor model (CC531) of liver metastases.
  • We studied the difference in tumor and liver uptake, as well as antitumor effect and hepatotoxicity after 5- and 20-min hepatic arterial infusion (HAI) of a fixed melphalan dose.
  • Melphalan content in perfusate, liver, and tumor tissue was analyzed by high-performance liquid chromatography.
  • The antitumor effect and hepatotoxicity in rats treated either systemically or with 5- and 20-min HAI, with a fixed dose melphalan (4.4 micromol), were assessed 2 weeks after treatment.
  • No difference in melphalan content of tumor/liver tissue or antitumor effect was observed between rats treated with 5- and 20-min HAI.
  • Rats treated with 5-min HAI weighed significantly less, and liver toxicity parameters were significantly increased compared with those of all other groups; eight of nine rats showed severe cholangiofibrosis.
  • Body weights and liver toxicity parameters of the rats treated with 20-min HAI were not statistically different from the control group.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Liver Neoplasms / drug therapy. Melphalan / therapeutic use
  • [MeSH-minor] Animals. Disease Models, Animal. Hepatic Artery / drug effects. Infusions, Intra-Arterial. Male. Neoplasm Transplantation. Rats. Treatment Outcome

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  • (PMID = 12606622.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; Q41OR9510P / Melphalan
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2. Jimenez RH, Boylan JM, Lee JS, Francesconi M, Castellani G, Sanders JA, Gruppuso PA: Rapamycin response in tumorigenic and non-tumorigenic hepatic cell lines. PLoS One; 2009 Oct 09;4(10):e7373
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  • [Title] Rapamycin response in tumorigenic and non-tumorigenic hepatic cell lines.
  • We hypothesized that hepatic cell lines with varying rapamycin responsiveness would show common characteristics accounting for resistance to the drug.
  • The non-tumorigenic rat liver epithelial cell line WB-F344 was highly sensitive while the tumorigenic WB311 cell line, originally derived from the WB-F344 line, was highly resistant.
  • CONCLUSIONS/SIGNIFICANCE: We conclude that the mechanisms of rapamycin resistance in hepatic cells involve alterations of signaling downstream from mTOR and that the mechanisms are highly heterogeneous, thus predicting that maintaining or promoting sensitivity will be highly challenging.

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  • (PMID = 19816606.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / F31 HD041893; United States / NCRR NIH HHS / RR / P20 RR017695; United States / NCRR NIH HHS / RR / P20RR017695; United States / NICHD NIH HHS / HD / R01 HD024455; United States / NICHD NIH HHS / HD / R01HD35831; United States / NICHD NIH HHS / HD / R01 HD035831; United States / NICHD NIH HHS / HD / R01HD24455
  • [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 / Antibiotics, Antineoplastic; 0 / Cyclin E; 0 / Intracellular Signaling Peptides and Proteins; 63231-63-0 / RNA; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, rat; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2756589
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3. Wu HP, Feng GS, Tian Y: Hepatic artery infusion of antisense oligodeoxynucleotide and lipiodol mixture transfect liver cancer in rats. World J Gastroenterol; 2005 Apr 28;11(16):2408-12
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  • [Title] Hepatic artery infusion of antisense oligodeoxynucleotide and lipiodol mixture transfect liver cancer in rats.
  • AIM: To study the distribution and stability of antisense oligodeoxynucleotide (ASODN) in Walker-256 cells and their distribution in liver, lung and kidney tissues after being infused alone or mixed with lipiodol via hepatic artery in a rat liver tumor model.
  • Its distribution in cells was observed by fluorescence microscope at different time points.
  • Walker-256 carcinosarcoma was transplanted into Wistar rat liver to establish a liver cancer model.
  • 5'-FITC-labeled VEGF ASODN mixed with (mixed group, n = 6) or without (TAI group, n = 6) ultra-fluid lipiodol was administrated via hepatic artery.
  • Frozen samples of liver, lung and kidney tissue were taken from rats after 1, 3 and 6 d, respectively.
  • In vivo experiment, on d 1 and 3 the fluorescence staining in liver was stronger in mixed group than in TAI group and more fluorescence could be detected in lung and kidney in TAI group than in mixed group.
  • ASODN could be seen in cancer cells and normal hepatic cells.
  • In mixed group, ASODN was mainly distributed in liver tumor tissues.
  • ASODN mixed with lipiodol infusion via hepatic artery can be used in the treatment of HCC.
  • [MeSH-major] Carcinoma 256, Walker / drug therapy. Contrast Media / pharmacokinetics. Iodized Oil / pharmacokinetics. Liver Neoplasms / drug therapy. Oligodeoxyribonucleotides, Antisense / pharmacokinetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Models, Animal. Fluorescein-5-isothiocyanate / pharmacokinetics. Fluorescent Dyes / pharmacokinetics. Hepatic Artery. Male. Neoplasm Transplantation. Rats. Rats, Wistar. Specific Pathogen-Free Organisms. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 15832409.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Fluorescent Dyes; 0 / Oligodeoxyribonucleotides, Antisense; 0 / Vascular Endothelial Growth Factor A; 8001-40-9 / Iodized Oil; I223NX31W9 / Fluorescein-5-isothiocyanate
  • [Other-IDs] NLM/ PMC4305626
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4. Zhu B, Liu GT, Wu RS, Strada SJ: Chemoprevention of bicyclol against hepatic preneoplastic lesions. Cancer Biol Ther; 2006 Dec;5(12):1665-73
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  • [Title] Chemoprevention of bicyclol against hepatic preneoplastic lesions.
  • Oral administration of 100 and 200 mg/kg body weight/day of 4,4-dimethoxy-5,6,5', 6'-dimethylene-dioxy-2-hydroxymethyl-2'-carbonyl biphenyl, Bicyclol, inhibited rat hepatic preneoplastic lesions induced by diethylnitrosamine (DEN).
  • With increases of total microsomal P450 and specific CYP2B1 activities in normal rat liver, Bicyclol enhanced particularly the denitrosation of DEN, a low toxic pathway of metabolism.
  • Such hypothesis was validated by the observation that Bicyclol inhibited DEN-induced unscheduled DNA synthesis, a DNA damage index, in primary cultured rat hepatocytes.
  • These data demonstrate that Bicyclol prevents carcinogens-induced animal neoplasm and cell malignant transformation via mechanisms at stages of initiation and promotion.
  • It substantiates those evidences that Bicyclol would be used as potential a chemopreventive agent for hepatocarcinogenesis along with its major therapy against chronic anti-hepatitis.
  • [MeSH-major] Biphenyl Compounds / therapeutic use. Gene Expression Regulation / drug effects. Liver Neoplasms / prevention & control. Precancerous Conditions / prevention & control
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Transformation, Neoplastic. Chemoprevention. Diethylnitrosamine. Disease Models, Animal. Genes, myc. Genes, ras. Male. RNA, Messenger / genetics. Rats. Rats, Wistar

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  • [CommentIn] Cancer Biol Ther. 2006 Dec;5(12):1674-6 [17421070.001]
  • (PMID = 17106253.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biphenyl Compounds; 0 / RNA, Messenger; 0 / bicyclol; 3IQ78TTX1A / Diethylnitrosamine
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5. Okimoto T, Yahata H, Itou H, Shinozaki K, Tanji H, Sakaguchi T, Asahara T: Safety and growth suppressive effect of intra-hepatic arterial injection of AdCMV-p53 combined with CDDP to rat liver metastatic tumors. J Exp Clin Cancer Res; 2003 Sep;22(3):399-406
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  • [Title] Safety and growth suppressive effect of intra-hepatic arterial injection of AdCMV-p53 combined with CDDP to rat liver metastatic tumors.
  • Surgical resection is thought to be the best treatment for liver carcinoma, including hepatocellular carcinoma and metastatic liver carcinoma if there are a small number of tumors.
  • Liver carcinoma is one of the main causes of death from cancer worldwide.
  • The prognosis of liver carcinoma is still poor.
  • Mutation of p53, which is well known as a tumor suppressor gene, is observed in many cases of advanced liver carcinoma.
  • Cancer gene therapy using p53, which transduces the wild-type p53 gene in the tumor, is a promising new strategy for treating liver carcinoma.
  • Selective and less invasive gene delivery to the liver tumor is necessary for clinical liver tumor gene therapy.
  • The first purpose of the current study was to determine the best way to deliver the gene of interest to the liver tumor selectively.
  • We injected AdCMV-LacZ via hepatic arteries of rats bearing RCN-9 colon cancer metastasis in the liver.
  • Injection via the hepatic artery resulted in more successful gene transduction to the liver tumor in a tumor-selective manner than did injection via the portal vein.
  • At 48 hrs after arterial injection of AdCMV-p53, CDDP (3 mg/kg) was administered in the peritoneal cavity of each rat.
  • The use of CDDP with arterial injection of AdCMV-p53 resulted in more extensive apoptosis in the rat liver tumors without any deterioration in liver function.
  • In conclusion, hepatic arterial injection of an adenovirus vector is better than portal vein injection for gene transduction efficiency, and causes no liver function disorder even when the injection is combined with CDDP.
  • [MeSH-major] Adenoviridae / genetics. Antineoplastic Agents / therapeutic use. Genetic Therapy / methods. Liver Neoplasms / drug therapy. Liver Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / therapeutic use
  • [MeSH-minor] Animals. Colonic Neoplasms / pathology. Cytomegalovirus / genetics. Disease Progression. Injections, Intra-Arterial. Male. Neoplasm Metastasis. Rats. Rats, Inbred F344

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  • (PMID = 14582698.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Suppressor Protein p53
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6. Gong LS, Zhang YD, Liu S: Target distribution of magnetic albumin nanoparticles containing adriamycin in transplanted rat liver cancer model. Hepatobiliary Pancreat Dis Int; 2004 Aug;3(3):365-8
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  • [Title] Target distribution of magnetic albumin nanoparticles containing adriamycin in transplanted rat liver cancer model.
  • BACKGROUND: Liver cancer is one of the most common diseases around the world.
  • The aim of this study was to verify the effect of magnetic field application on target distribution of nanoparticles in transplanted rat liver cancer model and to find out a new method for the treatment of malignant liver tumor.
  • METHODS: Seven days after the establishment of the model, the abdomen of the rat was exposed through a midline abdominal incision.
  • In the experimental group (12 rats), the tumor tissue was exposed to the magnetic field for 30 minutes.
  • Magnetic albumin nanoparticles containing adriamycin or at an equal dose of free adriamycin (0.5 mg/kg) were injected into the hepatic artery.
  • After the magnetic field was removed, the rat was immediately sacrificed.
  • Tissues of tumor, nontargeted sites of the liver, heart, kidney, lung, spleen, stomach and small intestine were analyzed for gamma-counts and examined histologically.
  • RESULTS: In the experimental group, the radioactivity of tumor tissue was 8.7 times that of liver tissue.
  • In the control group, the radioactivity of tumor tissue was 2.8 times that of normal liver tissue.
  • And over 80% of the injected nanoparticles distributed in the liver.
  • CONCLUSIONS: In the presence of magnetic field, magnetic albumin nanoparticles may accumulate in tumor tissues, of which the radioactivity can increase to 8.7 times that of normal liver.
  • Even if the magnetic field is not applied, magnetic albumin nanoparticles in tumor tissues still increase to 2.8 times that of normal liver tissues.
  • These findings indicate that normal organs in the presence of magnetic field are less exposed to chemotherapeutic drugs.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacokinetics. Carcinoma 256, Walker / drug therapy. Carcinoma, Hepatocellular / drug therapy. Doxorubicin / pharmacokinetics. Liver Neoplasms / drug therapy
  • [MeSH-minor] Albumins / pharmacokinetics. Animals. Disease Models, Animal. Electromagnetic Fields. Hepatic Artery. Magnetics. Male. Neoplasm Transplantation. Particle Size. Rats. Rats, Wistar

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  • (PMID = 15313670.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Albumins; 0 / Antimetabolites, Antineoplastic; 80168379AG / Doxorubicin
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7. Hanada M, Baba A, Tsutsumishita Y, Noguchi T, Yamaoka T, Chiba N, Nishikaku F: Intra-hepatic arterial administration with miriplatin suspended in an oily lymphographic agent inhibits the growth of tumors implanted in rat livers by inducing platinum-DNA adducts to form and massive apoptosis. Cancer Chemother Pharmacol; 2009 Aug;64(3):473-83
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  • [Title] Intra-hepatic arterial administration with miriplatin suspended in an oily lymphographic agent inhibits the growth of tumors implanted in rat livers by inducing platinum-DNA adducts to form and massive apoptosis.
  • BACKGROUND: Miriplatin (formerly SM-11355), a novel lipophilic platinum complex developed to treat hepatocellular carcinoma, is administered into the hepatic artery using an oily lymphographic agent (Lipiodol Ultra-Fluide) as a carrier.
  • Platinum concentrations in tissues and DNA were assessed.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Chemoembolization, Therapeutic / methods. Iodized Oil / administration & dosage. Liver Neoplasms, Experimental / drug therapy. Organoplatinum Compounds / pharmacology
  • [MeSH-minor] Animals. Cisplatin / pharmacology. DNA Adducts / metabolism. Delayed-Action Preparations. Drug Carriers / administration & dosage. Drug Screening Assays, Antitumor. Hepatic Artery. Infusions, Intra-Arterial. Lymphography. Male. Neoplasm Transplantation. Rats

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  • (PMID = 19104812.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA Adducts; 0 / Delayed-Action Preparations; 0 / Drug Carriers; 0 / Organoplatinum Compounds; 780F0P8N4I / miriplatin; 8001-40-9 / Iodized Oil; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2691803
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8. Hanada M, Baba A, Tsutsumishita Y, Noguchi T, Yamaoka T: Intra-hepatic arterial administration with miriplatin suspended in an oily lymphographic agent inhibits the growth of human hepatoma cells orthotopically implanted in nude rats. Cancer Sci; 2009 Jan;100(1):189-94
Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

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  • [Title] Intra-hepatic arterial administration with miriplatin suspended in an oily lymphographic agent inhibits the growth of human hepatoma cells orthotopically implanted in nude rats.
  • In order to examine in vivo the antitumor activities of miriplatin suspended in an oily lymphographic agent (Lipiodol Ultra-Fluide, LPD) against human hepatocellular carcinoma (HCC) after the intra-hepatic arterial administration, we have developed a novel orthotopic model of HCC in which the human hepatoma cell line Li-7 was successively implanted and maintained in the liver of nude rats.
  • Li-7 tumors established in nude rat livers displayed a trabecular structure similar to their original morphology, and were exclusively supplied by the hepatic artery, suggesting that they exhibited in part the conditions of human HCC.
  • Miriplatin suspended in LPD (miriplatin/LPD) administered into the hepatic artery of this model dose-dependently inhibited the growth of Li-7 tumors without markedly enhancing body weight loss and caused a significant reduction in the growth rate at a dose of 400 microg/head compared to LPD alone.
  • In addition, at the therapeutic dose, miriplatin/LPD as well as cisplatin suspended in LPD (400 microg/head) was shown to be more active than zinostatin stimalamer suspended in LPD (20 microg/head) against Li-7 tumors after a single intra-hepatic arterial administration.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Iodized Oil / administration & dosage. Liver Neoplasms, Experimental / drug therapy. Organoplatinum Compounds / administration & dosage
  • [MeSH-minor] Animals. Cisplatin / administration & dosage. DNA Adducts / analysis. Hepatic Artery. Humans. Infusions, Intra-Arterial. Lymphography. Neoplasm Transplantation. Rats. Rats, Nude. Transplantation, Heterologous

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  • (PMID = 19037997.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA Adducts; 0 / Organoplatinum Compounds; 780F0P8N4I / miriplatin; 8001-40-9 / Iodized Oil; Q20Q21Q62J / Cisplatin
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9. Treshchalina EM, Andronova NV, Kobliakov VA, Raĭkhlin NT: [New models of experimental chemotherapy of tumors]. Vopr Onkol; 2001;47(6):701-5
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  • [Title] [New models of experimental chemotherapy of tumors].
  • New neoplastic models such as orthotopic solitary hepatic tumor (cholangiocellular cancer PC-1) as well as different strains of malignant pleuritis (hemoblastosis and ascitic tumors) have been evolved by transplanting tumor cell suspension to rat liver or murine pleural cavity.
  • Orthotopic hepatic tumor PC-1 may be used for evaluating systemic and regional therapy.
  • Models of tumorous pleuritis described with respect to their response to chemotherapy, may have an application in screening and preclinical examination of newly-developed antitumor drugs.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Ehrlich Tumor / drug therapy. Drug Evaluation, Preclinical. Leukemia, Experimental / drug therapy. Liver Neoplasms, Experimental / drug therapy
  • [MeSH-minor] Animals. Liver / pathology. Mice. Neoplasm Transplantation. Rats. Time Factors

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  • (PMID = 11826492.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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10. Brunstein F, Eggermont AM, de Wiel-Ambagtsheer Ga, van Tiel ST, Rens J, ten Hagen TL: Synergistic antitumor effects of histamine plus melphalan in isolated hepatic perfusion for liver metastases. Ann Surg Oncol; 2007 Feb;14(2):795-801
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  • [Title] Synergistic antitumor effects of histamine plus melphalan in isolated hepatic perfusion for liver metastases.
  • BACKGROUND: Nonresectable primary and metastatic liver tumors remain an important clinical problem.
  • Melphalan-based isolated hepatic perfusion (M-IHP) leads to more than 70% objective responses in selective groups of patients with nonresectable metastases confined to the liver.
  • METHODS: Our experimental rat IHP model is used for the treatment of soft tissue sarcoma liver metastases.
  • Blood samples are collected for monitoring liver enzymes.
  • Livers are excised 72 h and 7 days after treatment for histologic evaluation.
  • Hepatotoxicity peaked within 24 h after IHP, independent of the treatment administered, recovered in 48 h, and was related mainly to the elevation of transaminases (grade 3 ASAT and grade 1 ALAT for control group and grades 3 and 4, respectively, for all other treatments).
  • Histology of the liver showed no serious damage.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Histamine / administration & dosage. Liver Neoplasms, Experimental / drug therapy. Melphalan / administration & dosage. Sarcoma / drug therapy
  • [MeSH-minor] Animals. Chemotherapy, Cancer, Regional Perfusion. Disease Models, Animal. Drug Synergism. Male. Neoplasm Transplantation. Rats

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  • (PMID = 17096052.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 820484N8I3 / Histamine; Q41OR9510P / Melphalan
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11. Li FR, Yan WH, Guo YH, Qi H, Zhou HX: Preparation of carboplatin-Fe@C-loaded chitosan nanoparticles and study on hyperthermia combined with pharmacotherapy for liver cancer. Int J Hyperthermia; 2009 Aug;25(5):383-91
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  • [Title] Preparation of carboplatin-Fe@C-loaded chitosan nanoparticles and study on hyperthermia combined with pharmacotherapy for liver cancer.
  • It is suitable to various types of tumors.
  • The purpose of this study was to prepare carboplatin-Fe@C-loaded chitosan nanoparticles with Fe@C as a magnetic core and to investigate efficacy of hyperthermia combined with chemotherapy for transplanted liver cancer in rats.
  • The shape, size, drug-loading rate, and in vitro cumulative release of the nanoparticles were observed and heat product under high frequency alternating electromagnetic field in vitro was explored.
  • Eighty rats with transplanted liver cancer were randomly divided into 4 groups (group A: control group, group B: free carboplatin group, group C: nanoparticles with static magnetic field group, and group D: nanoparticles with static field and alternating magnetic field).
  • Drug was injected into the hepatic artery.
  • The therapeutic effect of hyperthermia combined with chemotherapy for tumor, toxicity and rat survival time were observed.
  • The drug-loading rate of the nanoparticles was 11.0 +/- 1.1%.
  • The cumulative release percentage of carboplatin-Fe@C-loaded chitosan nanoparticles in vitro at different point time phase of 24 h, 48 h, 72 h, 96 h and 120 h were 51%, 68%, 80%, 87% and 91%, respectively.
  • In vivo experiments showed that after particle injection, tumor temperature reached 42.6 degrees +/- 0.2 degrees C within 10 min in the alternating magnetic field; and the temperatures in the right hepatic lobes and the rectum were significantly lower than in the tumor and the constant temperature could last up to 30 min.
  • The inhibition ratio of tumor weight in group D was significantly enhanced, no obviously toxic and side-effect occurred and survival time was prolonged.
  • They can target liver cancer tissue by static magnetic field, and with the application of alternating magnetic field, effectively raise tumor tissue temperature and facilitate tumor apoptosis.
  • The combination of chemotherapy and magnetic materials into nanoparticles as described herein demonstrates promising efficacy.
  • [MeSH-major] Carboplatin / therapeutic use. Chitosan / therapeutic use. Ferric Compounds / therapeutic use. Liver Neoplasms / therapy. Nanoparticles / therapeutic use
  • [MeSH-minor] Animals. Combined Modality Therapy. Hyperthermia, Induced / methods. Magnetics. Neoplasm Transplantation. Rats

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  • (PMID = 19391033.001).
  • [ISSN] 1464-5157
  • [Journal-full-title] International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • [ISO-abbreviation] Int J Hyperthermia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ferric Compounds; 9012-76-4 / Chitosan; BG3F62OND5 / Carboplatin
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12. Seelig MH, Leible M, Sänger J, Berger MR: Chemoembolization of rat liver metastasis with microspheres and gemcitabine followed by evaluation of tumor cell load by chemiluminescence. Oncol Rep; 2004 May;11(5):1107-13
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  • [Title] Chemoembolization of rat liver metastasis with microspheres and gemcitabine followed by evaluation of tumor cell load by chemiluminescence.
  • An orthotopic, isogenic rat model was used to determine the potential of chemoembolization (CHE) for reducing the tumor cell load of a diffusely metastatic liver.
  • Seven days after injecting CC531-lac-Z cells intraportally to male WAG/Rij rats, tumor positive animals were treated by injection into the hepatic artery with solvent (n=17), degradable starch microspheres (DSM, 30 mg/kg; n=16), DSM plus 5-fluorouracil (5-FU, dosages: 90, 60, and 40 mg/kg) or DSM plus gemcitabine (Gem, dosages: 100, 80, 50, and 10 mg/kg).
  • After 3 more weeks the experiment was terminated, the livers were weighted and the number of CC531-lac-Z cells per liver was determined.
  • In summary, the comparison of CHE with 5-FU or Gem shows that the efficacy of Gem in reducing the hepatic tumor cell load was significantly higher and its therapeutic ratio was greater than that of 5-FU.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Chemoembolization, Therapeutic. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary
  • [MeSH-minor] Animals. Cell Line, Tumor. Colonic Neoplasms / drug therapy. Colonic Neoplasms / pathology. Disease Models, Animal. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Fluorouracil / therapeutic use. Male. Microspheres. Neoplasm Transplantation. Organ Size. Rats. Rats, Inbred Strains. Tumor Burden

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  • (PMID = 15069554.001).
  • [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 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
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13. Rodenbach M, Eyol E, Seelig MH, Berger MR: Combination treatment of CC531-lac-Z rat liver metastases by chemoembolization with pemetrexed disodium and gemcitabine. J Cancer Res Clin Oncol; 2005 May;131(5):289-99
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  • [Title] Combination treatment of CC531-lac-Z rat liver metastases by chemoembolization with pemetrexed disodium and gemcitabine.
  • PURPOSE: The aim of this study was to evaluate the combination effect of pemetrexed disodium (MTA; Alimta; LY 231514) and gemcitabine (GEM) administered by hepatic artery and portal vein chemoembolization (HACE and PVCE) in a colorectal cancer rat liver metastasis model.
  • MATERIALS AND METHODS: Proliferation studies on CC531-lac-Z rat colon cancer cells were performed using the MTT assay to obtain the optimal combination schedule of the two antineoplastic agents.
  • To generate diffuse liver metastasis, 4 x 10(6) tumor cells were implanted into the portal vein of male WAG/Rij rats.
  • GEM (50 mg/kg) was also given locoregionally by hepatic artery chemoembolization (HACE) as well as systemically.
  • Efficacy of treatment in terms of liver metastases burden was determined at the end of the experiment by measuring the beta-galactosidase activity of CC531-lac-Z cells with a chemoluminescence assay.
  • Simultaneous drug exposure showed less than additive combination effects (O/E ratios > or = 1.25).
  • In vivo, locoregional administration by HACE with GEM was significantly more effective than systemic intravenous bolus treatment (P = 0.03).
  • Repeated systemic treatment with MTA yielded a slight reduction in tumor cell load that was significant versus control at the medium and high doses (60 mg/kg, P = 0.009; 90 mg/kg, P = 0.046) but not versus intraportal chemoembolization.
  • The combination treatment of systemic (60 and 90 mg/kg) or locoregional (60 mg/kg) MTA with HACE using GEM (50 mg/kg) resulted in more than 80% tumor growth inhibition; this antineoplastic combination effect was maximally additive.
  • CONCLUSION: A regimen-dependent synergistic combination effect of both drugs was found in vitro.
  • In animals, hepatic artery chemoembolization with GEM was superior to systemic intravenous bolus treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Deoxycytidine / analogs & derivatives. Glutamates / therapeutic use. Guanine / analogs & derivatives. Liver Neoplasms / secondary. Liver Neoplasms / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Chemoembolization, Therapeutic. Colorectal Neoplasms. Combined Modality Therapy. Death. Disease Models, Animal. Male. Neoplasm Metastasis. Pemetrexed. Rats. Rats, Inbred Strains

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  • (PMID = 15657768.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glutamates; 04Q9AIZ7NO / Pemetrexed; 0W860991D6 / Deoxycytidine; 5Z93L87A1R / Guanine; B76N6SBZ8R / gemcitabine
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14. Moran DM, Mayes N, Koniaris LG, Cahill PA, McKillop IH: Interleukin-6 inhibits cell proliferation in a rat model of hepatocellular carcinoma. Liver Int; 2005 Apr;25(2):445-57
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  • [Title] Interleukin-6 inhibits cell proliferation in a rat model of hepatocellular carcinoma.
  • BACKGROUND: Interleukin-6 (IL-6) plays a critical role in normal hepatic growth and liver regeneration.
  • METHODS: An in vivo rat HCC model was established and IL-6 receptor (IL-6R) and downstream signaling pathway expression and activity were determined in HCC and normal liver specimens.
  • RESULTS: HCC specimens demonstrated decreased IL-6Ralpha/gp130 expression as compared with the normal liver.
  • IL-6 treatment of HCC cells inhibits serum-stimulated mitogenesis, possibly via differences in activation profiles of intracellular signaling pathways and their effect on CDK inhibitor expression/activity.
  • [MeSH-major] Cell Proliferation / drug effects. DNA-Binding Proteins / metabolism. Hepatocytes / cytology. Interleukin-6 / metabolism. Receptors, Interleukin-6 / metabolism. Trans-Activators / metabolism
  • [MeSH-minor] Animals. Base Sequence. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / pathology. Cell Line, Tumor. Disease Models, Animal. Liver Neoplasms, Experimental. Male. Mitogen-Activated Protein Kinase 3 / metabolism. Molecular Sequence Data. Probability. RNA, Neoplasm / analysis. Random Allocation. Rats. Rats, Inbred ACI. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor. Sensitivity and Specificity. Signal Transduction

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  • [Copyright] Copyright Blackwell Munksgaard 2005
  • [CommentIn] Liver Int. 2006 Oct;26(8):1018-9 [16953844.001]
  • (PMID = 15780071.001).
  • [ISSN] 1478-3223
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA90895
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Interleukin-6; 0 / RNA, Neoplasm; 0 / Receptors, Interleukin-6; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, rat; 0 / Trans-Activators; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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15. van Duijnhoven FH, Tollenaar RA, Terpstra OT, Kuppen PJ: Locoregional therapies of liver metastases in a rat CC531 coloncarcinoma model results in increased resistance to tumour rechallenge. Clin Exp Metastasis; 2005;22(3):247-53
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  • [Title] Locoregional therapies of liver metastases in a rat CC531 coloncarcinoma model results in increased resistance to tumour rechallenge.
  • BACKGROUND: Locoregional treatments like photodynamic therapy (PDT), radiofrequency ablation (RFA) or hepatic artery infusion (HAI) of chemotherapeutics may be applied for unresectable colorectal liver metastases.
  • We evaluated the effect of these treatments on the immune response in a rat colon tumour liver metastases model.
  • METHOD: Wag/Rij rats were inoculated at day 0 with CC531 tumour cells at two sites in the liver.
  • At day 15, one of two tumours was treated with RFA or PDT, or the liver was treated by HAI.
  • Twelve days later (day 27), rats were rechallenged locally with CC531 cells in the liver or systemically with CC531 cells in the femoral vein.
  • At day 42, tumour growth in liver and lungs was determined.
  • RESULTS: RFA, PDT and HAI were very effective in liver tumour eradication, but following RFA or PDT there was no inhibitory effect on untreated nearby liver tumours.
  • Outgrowth after local rechallenge was, however, significantly inhibited in RFA-, PDT- and HAI-treated rats, whereas all control rats showed outgrowth of a third liver tumour.
  • After systemic rechallenge, control rats developed lung metastases whereas treated rats did not, but this difference was not statistically significant.
  • [MeSH-major] Catheter Ablation. Colonic Neoplasms / drug therapy. Liver Neoplasms / drug therapy. Photochemotherapy
  • [MeSH-minor] Animals. Antibodies / immunology. Disease Models, Animal. Disease Progression. Infusion Pumps, Implantable. Male. Melphalan / therapeutic use. Neoplasm Metastasis. Porphyrins / therapeutic use. Rats. Rats, Inbred Strains

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  • (PMID = 16158252.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 5,10,15,20-tetrakis(m-hydroxyphenyl)bacteriochlorin; 0 / Antibodies; 0 / Porphyrins; Q41OR9510P / Melphalan
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16. Badgwell BD, Valentino DJ, Jeffes EB, Dieffenbach K, Dulkanchainun SB, Yamamoto RS, Granger GA, Jakowatz JG, Carson WE: Intra-arterial administration of TNF-alpha followed by arterial ablation is an effective therapy for a regionally confined TNF-resistant rat mammary adenocarcinoma. Cancer Immunol Immunother; 2003 Jan;52(1):10-6
eScholarship, California Digital Library, University of California. Full text from University of California eScholarship .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intra-arterial administration of TNF-alpha followed by arterial ablation is an effective therapy for a regionally confined TNF-resistant rat mammary adenocarcinoma.
  • The intra-arterial (IA) administration of TNF-alpha to patients with liver metastases represents one such approach, and recent work suggests that subsequent ablation of the tumor's arterial supply via embolization may enhance the efficacy of intra-arterial treatments (hepatic chemoembolization).
  • The present study was undertaken to test the hypothesis that IA administration of TNF-alpha is superior to the intravenous (IV) route for inhibition of tumor growth in a regionally confined rat mammary adenocarcinoma model that provides for ablation of the arterial supply to the tumor following cytokine therapy.
  • Control animals received either no treatment or IA infusion of 2% normal rat serum (NRS) followed by ipsilateral CFA ligation.
  • Tumor size was measured every other day after treatment.
  • Tumor growth inhibition occurred in the first 5 to 10 days after treatment.
  • IA administration of TNF-alpha resulted in statistically significant diminution of tumor size as compared to untreated controls and animals receiving IA 2% normal rat serum (NRS; P<0.05 at days 6, 8 and 10), regardless of the dose employed.
  • IA administration of biologic response modifiers like TNF-alpha may therefore be a useful approach for the hepatic chemoembolization of breast adenocarcinomas metastatic to the liver.
  • [MeSH-major] Adenocarcinoma / drug therapy. Femoral Artery / surgery. Immunologic Factors / therapeutic use. Mammary Neoplasms, Experimental / drug therapy. Tumor Necrosis Factor-alpha / therapeutic use
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Female. Hindlimb. Infusions, Intravenous. Injections, Intra-Arterial. L Cells (Cell Line) / drug effects. Ligation. Mice. Neoplasm Transplantation. Rats. Rats, Inbred F344. Recombinant Proteins / therapeutic use. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / transplantation

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  • (PMID = 12536235.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA86016; United States / NCI NIH HHS / CA / P30 CA16058
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha
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17. Hribaschek A, Ridwelski K, Pross M, Meyer F, Kuhn R, Halangk W, Boltze C, Lippert H: Intraperitoneal treatment using taxol is effective for experimental peritoneal carcinomatosis in a rat model. Oncol Rep; 2003 Nov-Dec;10(6):1793-8
Hazardous Substances Data Bank. TAXOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intraperitoneal treatment using taxol is effective for experimental peritoneal carcinomatosis in a rat model.
  • Currently, there are no established protocols for the treatment or prevention of peritoneal carcinomatosis.
  • as late intraperitoneal (i.p.) chemotherapy (15, 20, 25 days following surgery; aiming for reduction of a manifest peritoneal carcinomatosis; group C) into the abdominal cavity.
  • Tumor growth was quantified by tumor weight of the greater omentum and the mesenteric site, number of detectable tumor lesions, occurrence of hepatic and pulmonary metastases and the amount of ascites.
  • Taxol was highly effective in preventing or reducing i.p. tumor spread when the drug was given directly or within a short time interval after tumor cell implantation (groups A and B), whereas no significant antineoplastic potential was found in the treatment of an established peritoneal carcinomatosis.
  • [MeSH-major] Carcinoma / drug therapy. Paclitaxel / therapeutic use. Peritoneal Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / pathology. Animals. Antineoplastic Agents, Phytogenic / therapeutic use. Cell Division. Cell Line, Tumor. Colonic Neoplasms / drug therapy. Disease Models, Animal. Humans. Infusions, Parenteral. Lung / pathology. Neoplasm Metastasis. Neoplasm Transplantation. Rats

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  • (PMID = 14534698.001).
  • [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, Phytogenic; P88XT4IS4D / Paclitaxel
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18. Xia R, Chen X: Effects of Danshen injection on the malignant obstructive jaundice in the SD rat model. J Huazhong Univ Sci Technolog Med Sci; 2006;26(6):686-9
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  • [Title] Effects of Danshen injection on the malignant obstructive jaundice in the SD rat model.
  • To observe the effects of Danshen on the growth of hepatocellular carcinoma in the SD rats, a model of malignant obstructive jaundice was established by inoculation of transplanted tumor into the hepatic portal with the walker-256 hepatocarcinoma line, which resulted in the obstruction by the infiltration and metastasis of hepatocellular carcinoma.
  • The liver function, morphological changes and the expressions of PCNA, VEGF and ICAM-1 in carcinoma foci, peri-carcinoma tissues, adjacent lobe (left-internal lobe) and lung tissues were observed after the treatment with the 4 agents.
  • Our results showed that the protective effect of Danshen on liver function was significantly better than that of NS and 5-FU (P<0.01).
  • Danshen also provided protective effect on the morphological damage of liver caused by obstructive jaundice.
  • The expressions of PCNA,VEGF and ICAM-1 PCNA, VEGF and ICAM-1 in carcinoma foci, peri-carcinoma tissues, adjacent lobe (left-internal lobe) and lung tissues were lower than those in control group and InV group, with the differences being significant (P<0.01).
  • It is concluded that Danshen injection not only has protective effects on liver injury caused by obstructive jaundice, but can inhibit the proliferation and growth of hepatocarcinoma, interfere with the vascularization of tumors, prevent recurrence and metastasis of hepatocarcinoma.
  • [MeSH-major] Drugs, Chinese Herbal / therapeutic use. Jaundice, Obstructive / drug therapy. Phenanthrolines / therapeutic use
  • [MeSH-minor] Animals. Carcinoma, Hepatocellular / complications. Disease Models, Animal. Intercellular Adhesion Molecule-1 / metabolism. Liver / pathology. Liver Neoplasms / complications. Male. Neoplasm Metastasis. Proliferating Cell Nuclear Antigen / metabolism. Rats. Rats, Wistar. Vascular Endothelial Growth Factor A / metabolism

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  • [Cites] Ai Zheng. 2003 Dec;22(12):1363-6 [14693071.001]
  • (PMID = 17357489.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Phenanthrolines; 0 / Proliferating Cell Nuclear Antigen; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, rat; 126547-89-5 / Intercellular Adhesion Molecule-1; 79483-68-4 / dan-shen root extract
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19. Li X, Feng GS, Zheng CS, Zhuo CK, Liu X: Influence of transarterial chemoembolization on angiogenesis and expression of vascular endothelial growth factor and basic fibroblast growth factor in rat with Walker-256 transplanted hepatoma: an experimental study. World J Gastroenterol; 2003 Nov;9(11):2445-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of transarterial chemoembolization on angiogenesis and expression of vascular endothelial growth factor and basic fibroblast growth factor in rat with Walker-256 transplanted hepatoma: an experimental study.
  • METHODS: Male Wistar rats were inoculated with Walker-256 tumor in the left lobe of liver.
  • Normal saline, 5-Fu, 5-Fu and lipiodol were infused through hepatic artery respectively.
  • MVD of the control group, chemotherapy group and chemoemoblization group was 80.84+/-24.24, 83.05+/-20.29 and 85.20+/-23.91 (F=0.193, P=0.873), respectively.
  • CONCLUSION: There has been little influence of lipiodol chemoembolization on the formation of tumor angiogenesis, but the development of neovascularization and expression of VEGF play important roles in establishment of collateral circulation and reconstruction of blood supply of residual cancer tissue.
  • [MeSH-major] Carcinoma 256, Walker / physiopathology. Chemoembolization, Therapeutic. Fibroblast Growth Factor 2 / metabolism. Liver Neoplasms, Experimental / physiopathology. Neovascularization, Pathologic / therapy. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Animals. Immunohistochemistry. Male. Microcirculation. Neoplasm Transplantation. Rats. Rats, Wistar

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  • (PMID = 14606073.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2
  • [Other-IDs] NLM/ PMC4656518
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20. Levi M, DeRemer SJ, Dou C, Ensminger WD, Smith DE: Disposition of WR-1065 in the liver of tumor-bearing rats following regional vs systemic administration of amifostine. Biopharm Drug Dispos; 2004 Jan;25(1):27-35
Hazardous Substances Data Bank. AMIFOSTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disposition of WR-1065 in the liver of tumor-bearing rats following regional vs systemic administration of amifostine.
  • PURPOSE: Amifostine is a prodrug in which selectivity is largely determined by the preferential formation and uptake of its cytoprotective metabolite, WR-1065, in normal tissues as a result of differences in membrane-bound alkaline phosphatase activity.
  • It was hypothesized that amifostine may be a good candidate for regional drug delivery to the liver because of its large hepatic extraction and total body clearance.
  • METHODS: Rat livers were implanted with Walker-256 tumors.
  • WR-1065 concentrations in the blood, liver and tumor were measured at various times.
  • The portal dosing WR-1065 liver AUC15-60 was 60% higher than the values for systemic dosing.
  • The liver/tumor concentration ratios of WR-1065 following portal dosing were up to 8-fold higher than the ratio following systemic administration.
  • CONCLUSIONS: Amifostine may provide increased liver protection and decreased tumor protection from radio- or chemotherapy when administered by the portal vein.
  • [MeSH-major] Amifostine / administration & dosage. Amifostine / metabolism. Drug Delivery Systems / methods. Liver Neoplasms, Experimental / drug therapy. Mercaptoethylamines / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / metabolism. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Carcinoma 256, Walker / blood supply. Carcinoma 256, Walker / surgery. Disease Models, Animal. Drug Screening Assays, Antitumor. Femoral Vein / drug effects. Infusions, Intravenous. Male. Neoplasm Transplantation / methods. Portal Vein / drug effects. Prodrugs / administration & dosage. Prodrugs / metabolism. Rats. Rats, Sprague-Dawley

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  • [Copyright] Copyright 2004 John Wiley & Sons, Ltd.
  • (PMID = 14716750.001).
  • [ISSN] 0142-2782
  • [Journal-full-title] Biopharmaceutics & drug disposition
  • [ISO-abbreviation] Biopharm Drug Dispos
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA098502
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Mercaptoethylamines; 0 / Prodrugs; 31098-42-7 / WR 1065; M487QF2F4V / Amifostine
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21. Jäger W, Salamon A, Szekeres T: Metabolism of the novel IMP dehydrogenase inhibitor benzamide riboside. Curr Med Chem; 2002 Apr;9(7):781-6
Hazardous Substances Data Bank. RIBAVIRIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A recent study demonstrates enzymatic deamination of BR to non-cytotoxic benzene carboxylic acid (BR-COOH) as the main hepatic BR biotransformation product in rat liver.
  • As the IMPDH inhibitors tiazofurin and ribavirin exhibit predominant accumulation and biotransformation in liver, hepatic metabolism may be an important factor also for BR activation and inactivation and should be considered in human liver during cancer therapy when BR is used as a single drug or in combination with other anticancer agents.
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Forecasting. Humans. Isoenzymes / antagonists & inhibitors. K562 Cells. Liver / drug effects. Rats. Ribavirin / analogs & derivatives. Ribavirin / pharmacology

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  • (PMID = 11966442.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 0 / Nucleosides; 138385-29-2 / 3-(1-deoxyribofuranosyl)benzamide; 49717AWG6K / Ribavirin; EC 1.1.1.205 / IMP Dehydrogenase; ULJ82834RE / tiazofurin
  • [Number-of-references] 30
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22. Lambert JD, Meyers RO, Timmermann BN, Dorr RT: tetra-O-methylnordihydroguaiaretic acid inhibits melanoma in vivo. Cancer Lett; 2001 Sep 28;171(1):47-56
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • tetra-O-methylnordihydroguaiaretic acid is a derivative of a naturally-occurring lignan, nordihydroguaiaretic acid, that has previously been shown to inhibit various cancer types in vitro and in vivo.
  • Additionally, nordihydroguaiaretic acid has been shown to have nephrotoxic effects in the rat.
  • Further, this compound inhibits the synthesis of DNA by melanoma cells and causes cell cycle arrest in G0/G1 and G2/M phases of the cell cycle. tetra-O-Methylnordihydroguaiaretic acid also inhibits the growth of both murine and human melanomas and human colon cancer in vivo without apparent hepatic or renal toxicity.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents, Phytogenic / therapeutic use. Colonic Neoplasms / drug therapy. Masoprocol / therapeutic use. Melanoma, Experimental / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Breast Neoplasms / pathology. Cell Cycle / drug effects. DNA Replication / drug effects. Female. Intracellular Membranes / drug effects. Kidney / drug effects. Liver / drug effects. Lung Neoplasms / pathology. Male. Melanoma / pathology. Membrane Potentials / drug effects. Mice. Mice, Inbred C57BL. Mice, SCID. Mitochondria / drug effects. Neoplasm Transplantation. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / transplantation. Xenograft Model Antitumor Assays

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  • (PMID = 11485827.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / FIC NIH HHS / TW / 401TW00316
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 53YET703F2 / terameprocol; 7BO8G1BYQU / Masoprocol
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23. Huang Z, Waxman DJ: Modulation of cyclophosphamide-based cytochrome P450 gene therapy using liver P450 inhibitors. Cancer Gene Ther; 2001 Jun;8(6):450-8
Hazardous Substances Data Bank. METYRAPONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modulation of cyclophosphamide-based cytochrome P450 gene therapy using liver P450 inhibitors.
  • This gene therapy strategy provides for intratumoral prodrug activation, but is also associated with a high level of hepatic prodrug activation, which reduces the extent of intratumoral prodrug activation and contributes to systemic drug toxicity.
  • To address this issue, five P450 inhibitors were tested for their ability to block liver CYP2C-catalyzed CPA activation selectively, i.e., without inhibiting the corresponding intratumoral activation of CPA catalyzed by a transduced CYP2B enzyme.
  • In vitro studies revealed that the P450 inhibitors 1-aminobenzotriazole and DDEP were preferentially inhibitory toward CYP2C-dependent liver microsomal CPA activation, whereas the P450 inhibitor SKF-525A inhibited CYP2C- and CYP2B-dependent CPA activation without P450 form selectivity.
  • Rat pharmacokinetic studies confirmed the inhibitory action of these compounds in vivo, with up to a 4-fold decrease in C(max) and a 7-fold increase in apparent half-life of the activated CPA metabolite, 4-hydroxy-CPA, seen in the case of 1-aminobenzotriazole.
  • Although the rate of hepatic CPA activation could thus be decreased substantially by P450 inhibitor treatment, the net extent of hepatic CPA activation was only modestly decreased, as judged by plasma area-under-the-curve values for 4-hydroxy-CPA.
  • Moreover, P450 inhibitor treatment did not decrease CPA's host toxicity and did not enhance the tumor growth delay response to CPA in rats bearing CYP2B1-transduced gliosarcomas.
  • These findings are discussed in the context of P450-based gene therapy strategies and ongoing efforts to enhance anticancer drug activity by increasing the exposure of P450-expressing tumors to the P450-activated prodrug CPA.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacokinetics. Cyclophosphamide / pharmacokinetics. Cytochrome P-450 Enzyme Inhibitors. Cytochrome P-450 Enzyme System / genetics. Genetic Therapy / methods. Liver / enzymology
  • [MeSH-minor] Animals. Body Weight / drug effects. Combined Modality Therapy. Dose-Response Relationship, Drug. Enzyme Activation. Male. Metyrapone / pharmacology. Neoplasm Transplantation. Neoplasms / drug therapy. Neoplasms, Experimental / drug therapy. Rats. Rats, Inbred F344. Time Factors

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  • (PMID = 11498765.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA49248
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Cytochrome P-450 Enzyme Inhibitors; 8N3DW7272P / Cyclophosphamide; 9035-51-2 / Cytochrome P-450 Enzyme System; ZS9KD92H6V / Metyrapone
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24. Gervaz P, Scholl B, Padrun V, Gillet M: Growth inhibition of liver metastases by the anti-angiogenic drug TNP-470. Liver; 2000 Apr;20(2):108-13
MedlinePlus Health Information. consumer health - Liver Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth inhibition of liver metastases by the anti-angiogenic drug TNP-470.
  • OBJECTIVE: This study was undertaken in order to assess the efficacy of a potent angiogenesis inhibitor, TNP-470, on tumor growth in a syngeneic rodent model of liver metastases from colorectal cancer.
  • However, the antitumor effect of this drug has not been studied in models reproducing a natural metastatic environment.
  • Since the liver provides an extensive vascular bed for secondary tumor growth, an anti-angiogenic strategy may therefore be less efficient for treating hepatic metastases than primary tumors.
  • METHODS: 10(7) DHD K12 colon carcinoma cells were injected intrasplenically into syngeneic BD IX rats to produce diffuse liver metastases.
  • In both the treatment and control groups (n=7), tumor volume was determined using a computerized analytical system, and tumor microvessel density was measured by immunostaining with anti-von Willebrand Factor monoclonal antibody.
  • Liver weight (15.2 g vs 11.7 g, p=0.01), and tumor volume (1218 mm3 vs 406 mm3, p=0.03) were significantly reduced in the TNP-470 group compared to the control group.
  • CONCLUSION: TNP-470 inhibits the growth of liver metastases in a syngeneic rat model of colorectal cancer.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Carcinoma / drug therapy. Colorectal Neoplasms / drug therapy. Liver Neoplasms / drug therapy. Neovascularization, Pathologic / drug therapy. Sesquiterpenes / therapeutic use
  • [MeSH-minor] Animals. Cell Division. Cell Survival / drug effects. Cyclohexanes. Injections, Subcutaneous. Liver / drug effects. Liver / pathology. Neoplasm Transplantation. Organ Size / drug effects. Rats. Tumor Cells, Cultured

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  • (PMID = 10847478.001).
  • [ISSN] 0106-9543
  • [Journal-full-title] Liver
  • [ISO-abbreviation] Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] DENMARK
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cyclohexanes; 0 / Sesquiterpenes; 129298-91-5 / O-(chloroacetylcarbamoyl)fumagillol
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