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1. Wang SS, Zhang T, Wang XL, Hong L, Qi QH: Effect of arsenic trioxide on rat hepatocellular carcinoma and its renal cytotoxity. World J Gastroenterol; 2003 May;9(5):930-5
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  • [Title] Effect of arsenic trioxide on rat hepatocellular carcinoma and its renal cytotoxity.
  • AIM: To study the effect of arsenic trioxide (As(2)O(3)) on rat experimental hepatocellular carcinoma and its renal cytotoxicity.
  • METHODS: The hepatocellular carcinoma model was established by diethaylnitrosamine perfusion in stomach of 120 Wistar rats, and the treatment began at the end of 20 weeks.
  • Before the treatment, the rat models were randomly divided into 5 groups.
  • In the treatment groups, three doses of As(2)O(3) were injected into rat abdominal cavity; the total time of drug administration was 4 weeks.
  • Cisplatin control or the blank group was injected into abdominal cavity with equal amount of cisplatin or saline at the same time, respectively.
  • On the 7th, 14th and 28th day after the treatment, the hepatocellular carcinoma nodules were obtained and the morphologic changes of hepatocellular carcinoma cells were observed under light and electron microscopes; Immunohistochemistry (S-P methods) was employed to detect the expression of bcl-2, bax and PCNA in hepatocellular carcinoma tissues; flow cytometry (TUNEL assay) was used to detect the apoptosis of liver cancer cells and the change of cytokinetics.
  • On the 28th day, the renal was obtained and its histologic change was observed under light microscope, and immunohistochemistry (SP stain) was also employed to detect the expression of bcl-2 and PCNA.
  • RESULTS: As(2)O(3) could induce the apoptosis of rat liver cancer cells and exhibited typical morphologic changes.
  • The incidence of apoptosis of hapatocellular carcinoma cells was elevated (P=0.001).
  • Under the light microscope, the rat kidney in the cisplatin group exhibited tubular epithelium swelling and degeneration, protein casts in collecting tubules; While all arsenic groups didn't show the significant changes (P=0.013).
  • In the arsenic groups, the expression of bcl-2 in the renal tubular epithelium was increased (P=0.005), no obvious changes happened to PCNA LI.
  • CONCLUSION: As(2)O(3) can induce apoptosis of rat hepatocellular carcinoma cells.
  • As(2)O(3) can restrain the proliferation of rat hepatocellular carcinoma cells, in a dose-time dependent manner; Compared with cisplatin, As(2)O(3) didn't show obvious renal toxicity, which was related to the increasing expression of bcl-2 in renal tubular epithelium, the inhibition of apoptosis and the anti-oxidation effects.
  • [MeSH-major] Arsenicals / therapeutic use. Kidney / drug effects. Liver Neoplasms, Experimental / drug therapy. Oxides / therapeutic use. Oxides / toxicity
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Antineoplastic Agents / toxicity. Apoptosis / drug effects. Cell Division / drug effects. Cisplatin / therapeutic use. Cisplatin / toxicity. Female. Immunohistochemistry. Male. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Rats. Rats, Wistar

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  • (PMID = 12717832.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; Q20Q21Q62J / Cisplatin; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC4611399
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2. Mertins SD, Myers TG, Holbeck SL, Medina-Perez W, Wang E, Kohlhagen G, Pommier Y, Bates SE: In vitro evaluation of dimethane sulfonate analogues with potential alkylating activity and selective renal cell carcinoma cytotoxicity. Mol Cancer Ther; 2004 Jul;3(7):849-60
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  • [Title] In vitro evaluation of dimethane sulfonate analogues with potential alkylating activity and selective renal cell carcinoma cytotoxicity.
  • We identified five structurally related dimethane sulfonates with putative selective cytotoxicity in renal cancer cell lines.
  • A COMPARE analysis with the National Cancer Institute Anticancer Drug Screen standard agent database found significant correlations between the IC50 of the test compounds and the IC50 of alkylating agents (e.g., r = 0.68, P < 0.00001 for chlorambucil).
  • In cytotoxicity studies, chlorambucil-resistant Walker rat carcinoma cells were 4- to 11-fold cross-resistant to the test compounds compared with 14-fold resistant to chlorambucil.
  • To determine effects on cell cycle progression, renal cell carcinoma (RCC) line 109 was labeled with bromodeoxyuridine prior to drug treatment.
  • Complete cell cycle arrest occurred in cells treated with an IC90 dose of NSC 268965. p53 protein levels increased as much as 5.7-fold in RCC line 109 and as much as 20.4-fold in breast cancer line MCF-7 following an 18-hour drug exposure.
  • [MeSH-major] Alkylating Agents / chemistry. Alkylating Agents / toxicity. Carcinoma, Renal Cell / drug therapy. Kidney Neoplasms / drug therapy. Mesylates / chemistry. Mesylates / toxicity
  • [MeSH-minor] Animals. Bromodeoxyuridine / analysis. Busulfan / analogs & derivatives. Carmustine / analogs & derivatives. Cell Cycle / drug effects. DNA Damage. Drug Evaluation, Preclinical. Drug Resistance, Neoplasm / drug effects. Humans. Inhibitory Concentration 50. Rats. Tumor Suppressor Protein p53 / analysis. Tumor Suppressor Protein p53 / metabolism. Yeasts / drug effects

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  • (PMID = 15252146.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Mesylates; 0 / Tumor Suppressor Protein p53; G1LN9045DK / Busulfan; G34N38R2N1 / Bromodeoxyuridine; U68WG3173Y / Carmustine
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3. Arcidiacono MV, Sato T, Alvarez-Hernandez D, Yang J, Tokumoto M, Gonzalez-Suarez I, Lu Y, Tominaga Y, Cannata-Andia J, Slatopolsky E, Dusso AS: EGFR activation increases parathyroid hyperplasia and calcitriol resistance in kidney disease. J Am Soc Nephrol; 2008 Feb;19(2):310-20
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  • [Title] EGFR activation increases parathyroid hyperplasia and calcitriol resistance in kidney disease.
  • In a rat model of SH, activation of the EGF receptor (EGFR) by TGF-alpha is required for the development of parathyroid hyperplasia, but the relationship between EGFR activation and reduced VDR content is unknown.
  • With the use of the same rat model, it was found that pharmacologic inhibition of EGFR activation with erlotinib prevented the upregulation of parathyroid TGF-alpha, the progression of growth, and the reduction of VDR.
  • Increased TGF-alpha/EGFR activation induced the synthesis of liver-enriched inhibitory protein, a potent mitogen and the dominant negative isoform of the transcription factor CCAAT enhancer binding protein-beta, in human hyperplastic parathyroid glands and in the human epidermoid carcinoma cell line A431, which mimics hyperplastic parathyroid cells.
  • Similarly, in nodular hyperplasia, which is the most severe form of SH and the most resistant to calcitriol therapy, higher TGF-alpha activation of the EGFR was associated with an 80% reduction in VDR mRNA levels.
  • Thus, in SH, EGFR activation is the cause of both hyperplastic growth and VDR reduction and therefore influences the efficacy of therapy with calcitriol.

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  • (PMID = 18216322.001).
  • [ISSN] 1533-3450
  • [Journal-full-title] Journal of the American Society of Nephrology : JASN
  • [ISO-abbreviation] J. Am. Soc. Nephrol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK062713; United States / NIDDK NIH HHS / DK / DK062713
  • [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 / CCAAT-Enhancer-Binding Protein-beta; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / Receptors, Calcitriol; 0 / Transforming Growth Factor alpha; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; FXC9231JVH / Calcitriol
  • [Other-IDs] NLM/ PMC2396751
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4. Esquis P, Consolo D, Magnin G, Pointaire P, Moretto P, Ynsa MD, Beltramo JL, Drogoul C, Simonet M, Benoit L, Rat P, Chauffert B: High intra-abdominal pressure enhances the penetration and antitumor effect of intraperitoneal cisplatin on experimental peritoneal carcinomatosis. Ann Surg; 2006 Jul;244(1):106-12
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  • Platinum tissue concentration was measured by atomic absorption spectroscopy (AAS), and platinum distribution into the tumor nodules was assessed by the particular-induced x-ray emission (PIXE) method.
  • Consequently, IAP treatment induced an extended survival of rats treated at an advanced stage of carcinomatosis.
  • Renal failure occurred in pigs receiving a total dose of 200 and 400 mg of cisplatin with IAP, but a dose of 100 mg was well tolerated.
  • CONCLUSIONS: Intraperitoneal chemotherapy with increased IAP, in comparison with conventional IP or IV chemotherapy, improved the tumor accumulation and the antitumor effect of cisplatin in rats bearing advanced peritoneal carcinomatosis.
  • [MeSH-major] Abdomen / physiology. Antineoplastic Agents / pharmacokinetics. Carcinoma / pathology. Cisplatin / pharmacokinetics. Peritoneal Neoplasms / pathology

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  • (PMID = 16794395.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC1570583
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5. Parada B, Sereno J, Reis F, Teixeira-Lemos E, Garrido P, Pinto AF, Cunha MF, Pinto R, Mota A, Figueiredo A, Teixeira F: Anti-inflammatory, anti-proliferative and antioxidant profiles of selective cyclooxygenase-2 inhibition as chemoprevention for rat bladder carcinogenesis. Cancer Biol Ther; 2009 Sep;8(17):1615-22
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  • [Title] Anti-inflammatory, anti-proliferative and antioxidant profiles of selective cyclooxygenase-2 inhibition as chemoprevention for rat bladder carcinogenesis.
  • PURPOSE: To evaluate the efficacy of a selective cyclooxygenase-2 (COX-2) inhibitor in rat bladder cancer chemoprevention, as well as to assess the relevance of inflammation, proliferation and oxidative stress in tumor growth and in its prevention.
  • RESULTS: The main findings were: (I) the incidence of carcinoma was: control: 0% (0/8); BBN: 65% (13/20); CEL: 0% (0/8) and BBN + CEL: 12.5% (1/8);.
  • (II) the mean tumor volume per rat with tumor and per tumor were significantly lower in the BBN + CEL group (21.2 and 5.3 +/- 0.4 mm(3)) vs. BBN (138.5 +/- 7.5 and 112.5 +/- 6.4 mm(3));.
  • (III) the incidence of pre-neoplasic (hyperplasia and dysplasia) and neoplasic (papillary tumors and carcinoma in situ-CIS) lesions were notoriously reduced in the CEL + BBN treatment;.
  • (V) CEL reduced MDA formation in serum (p < 0.001) and liver (p < 0.05) and also showed a trend to reduction in kidney.
  • METHODS: Drug treatments were performed during the first 8 w, followed by 12 w for tumor expression/prevention, in the following groups: control-vehicle; carcinogen-0.05% of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN); celecoxib (CEL)-10 mg/kg/day and preventive CEL + BBN.
  • [MeSH-minor] Animals. Celecoxib. Cell Growth Processes / drug effects. Inflammation / metabolism. Inflammation / pathology. Male. Oxidative Stress / drug effects. Rats. Rats, Wistar. Urinary Bladder / drug effects. Urinary Bladder / metabolism. Urinary Bladder / pathology. Urothelium / drug effects. Urothelium / metabolism. Urothelium / pathology

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  • (PMID = 19571668.001).
  • [ISSN] 1555-8576
  • [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 / Anticarcinogenic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; JCX84Q7J1L / Celecoxib
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6. Bhattacharya A, Tang L, Li Y, Geng F, Paonessa JD, Chen SC, Wong MK, Zhang Y: Inhibition of bladder cancer development by allyl isothiocyanate. Carcinogenesis; 2010 Feb;31(2):281-6
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  • Here, we report that allyl isothiocyanate (AITC), an ingredient of many common cruciferous vegetables, potently inhibited the proliferation of bladder carcinoma cell lines in vitro [half maximal inhibitory concentration (IC(50)) of 2.7-3.3 microM], which was associated with profound G(2)/M arrest and apoptosis.
  • AITC was then evaluated in two rat bladder cancer models in vivo (an orthotopic model and a subcutaneous model).
  • This differential effect was explained by our finding that urinary levels of AITC equivalent were two to three orders of magnitude higher than that in the plasma and that its levels in the orthotopic cancer tissues were also three orders of magnitude higher than that in the subcutaneous cancer tissues.
  • In conclusion, AITC is selectively delivered to bladder cancer tissue through urinary excretion and potently inhibits bladder cancer development and invasion.

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  • (PMID = 19955395.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA124627; United States / NCI NIH HHS / CA / R01CA124627; United States / NCI NIH HHS / CA / R25 CA114101
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Food Preservatives; 0 / Isothiocyanates; BN34FX42G3 / allyl isothiocyanate
  • [Other-IDs] NLM/ PMC2812574
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7. Karim M, Vaux E, Davies DR, Mason PD: Renal failure due to scleroderma with thrombotic microangiopathy developing in a woman treated with carboplatin for ovarian cancer. Clin Nephrol; 2002 Nov;58(5):384-8
Hazardous Substances Data Bank. CARBOPLATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Renal failure due to scleroderma with thrombotic microangiopathy developing in a woman treated with carboplatin for ovarian cancer.
  • Acute renal failure in association with microangiopathic hemolytic anemia and the pathological finding of thrombotic microangiopathy may occur in a number of conditions including hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and systemic sclerosis.
  • We present a patient who was treated with 5 doses of monthly carboplatin chemotherapy for stage IIb ovarian carcinoma and who subsequently developed acute renal failure and microangiopathic hemolysis together with some cutaneous features of systemic sclerosis.
  • Initial serological tests, including anti-nuclear antibody titers measured using rat hepatocytes, were normal, and renal biopsy showed features of microangiopathic hemolysis, fibrinoid change, patchy tubular atrophy, and concentric intimal proliferation.
  • Subsequent results from tests taken at the time of her presentation with acute renal failure revealed a normal von Willebrand factor qualitative distribution, and a positive anti-nuclear antibody titer (using a human cell line) in association with positive autoantibodies to RNA polymerase types I, II, and III.
  • We discuss the differential diagnoses, and the associations between these and malignancy and chemotherapy.
  • [MeSH-major] Acute Kidney Injury / etiology. Anemia, Hemolytic / chemically induced. Anemia, Hemolytic / complications. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Carboplatin / adverse effects. Carboplatin / therapeutic use. Carcinoma / drug therapy. Ovarian Neoplasms / drug therapy. Scleroderma, Systemic / chemically induced. Scleroderma, Systemic / complications. Thrombosis / chemically induced. Thrombosis / complications


8. Ruggeri B, Singh J, Gingrich D, Angeles T, Albom M, Yang S, Chang H, Robinson C, Hunter K, Dobrzanski P, Jones-Bolin S, Pritchard S, Aimone L, Klein-Szanto A, Herbert JM, Bono F, Schaeffer P, Casellas P, Bourie B, Pili R, Isaacs J, Ator M, Hudkins R, Vaught J, Mallamo J, Dionne C: CEP-7055: a novel, orally active pan inhibitor of vascular endothelial growth factor receptor tyrosine kinases with potent antiangiogenic activity and antitumor efficacy in preclinical models. Cancer Res; 2003 Sep 15;63(18):5978-91
The Lens. Cited by Patents in .

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  • Inhibition of the vascular endothelial growth factor VEGF-VEGF receptor (VEGF-R) kinase axes in the tumor angiogenic cascade is a promising therapeutic strategy in oncology.
  • Evaluation of the antiangiogenic activity of CEP-5214 revealed a dose-related inhibition of microvessel growth ex vivo in rat aortic ring explant cultures and in vitro on HUVEC capillary-tube formation on Matrigel at low nanomolar concentrations.
  • Single-dose p.o. or s.c. administration of CEP-7055 or CEP-5214 to CD-1 mice at 23.8 mg/kg/dose b.i.d. resulted in a reversible inhibition of VEGF-R2/FLK-1 phosphorylation in murine lung tissues.
  • Chronic p.o. administration of CEP-7055 at doses of 11.9 to 23.8 mg/kg/dose b.i.d. resulted in significant inhibition (50-90% maximum inhibition relative to controls) in the growth of a variety of established murine and human s.c. tumor xenografts in nude mice, including A375 melanomas, U251MG and U87MG glioblastomas, CALU-6 lung carcinoma, ASPC-1 pancreatic carcinoma, HT-29 and HCT-116 colon carcinomas, MCF-7 breast carcinomas, and SVR angiosarcomas.
  • Significant antitumor efficacy was observed similarly against orthotopically implanted LNCaP human prostate carcinomas in male nude mice and orthotopically implanted renal carcinoma (RENCA) tumors in BALB/c mice, in terms of a significant reduction in the metastatic score and the extent of pulmonary metastases.
  • The antitumor efficacy of chronic CEP-7055 administration was independent of initial tumor volume (in the ASPC-1 pancreatic carcinoma model) and reversible on withdrawal of treatment.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Antineoplastic Agents / pharmacology. Carbazoles / pharmacology. Neoplasms, Experimental / drug therapy. Vascular Endothelial Growth Factor Receptor-1 / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-3 / antagonists & inhibitors
  • [MeSH-minor] Administration, Oral. Animals. Endothelium, Vascular / cytology. Endothelium, Vascular / drug effects. Endothelium, Vascular / enzymology. Enzyme Inhibitors / pharmacokinetics. Enzyme Inhibitors / pharmacology. Female. In Vitro Techniques. Male. Mice. Mice, Nude. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / enzymology. Phosphorylation. Prodrugs / pharmacokinetics. Prodrugs / pharmacology. Rats. Rats, Sprague-Dawley. Solubility. Xenograft Model Antitumor Assays

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  • [ErratumIn] Cancer Res. 2003 Nov 1;63(21):7543
  • (PMID = 14522925.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-(5,6,7,13-tetrahydro-9-((1-methylethoxy)methyl)-5-oxo-12H-indeno(2,1-a)pyrrolo(3,4-c)carbazol-12-yl)propanol; 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Enzyme Inhibitors; 0 / N,N-dimethylglycine 3-(5,6,7,13-tetrahydro-9-((1-methylethoxy)methyl)-5-oxo-12H-indeno(2,1-a)pyrrolo(3,4-c)carbazol-12-yl)propyl ester; 0 / Prodrugs; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
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9. Boschi A, Uccelli L, Duatti A, Colamussi P, Cittanti C, Filice A, Rose AH, Martindale AA, Claringbold PG, Kearney D, Galeotti R, Turner JH, Giganti M: A kit formulation for the preparation of 188Re-lipiodol: preclinical studies and preliminary therapeutic evaluation in patients with unresectable hepatocellular carcinoma. Nucl Med Commun; 2004 Jul;25(7):691-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A kit formulation for the preparation of 188Re-lipiodol: preclinical studies and preliminary therapeutic evaluation in patients with unresectable hepatocellular carcinoma.
  • Renal activity peaked at 1.7%, diminishing to 0.6% over 48 h.
  • Rat whole body gamma imaging showed gut activity in addition to hepatic uptake at 6 and 24 h, but only liver was evident from 48 to 72 h.
  • Kidneys were not demonstrable at any imaging time point.
  • Computed tomography/single-photon emission computed tomography (CT/SPECT) imaging at 1 and 24 h confirmed the retention of 188Re-lipiodol in the hepatoma, with minimal gut uptake and no lung activity over 24 h.
  • Repeated treatments were performed on two to three occasions in three patients without evident toxicity.
  • It is concluded that 188Re-lipiodol, prepared using our novel kit formulation, is stable in vivo and provides safe and effective therapy of unresectable hepatocellular carcinoma when given via the hepatic artery, either alone or in combination with transarterial chemoembolization.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / radiotherapy. Isotope Labeling / methods. Liver Neoplasms / metabolism. Liver Neoplasms / radiotherapy. Organometallic Compounds / administration & dosage. Organometallic Compounds / pharmacokinetics
  • [MeSH-minor] Animals. Drug Evaluation, Preclinical. Drug Stability. Humans. Injections, Intravenous. Male. Metabolic Clearance Rate. Organ Specificity. Pilot Projects. Radiopharmaceuticals / administration & dosage. Radiopharmaceuticals / adverse effects. Radiopharmaceuticals / chemical synthesis. Radiopharmaceuticals / pharmacokinetics. Rats. Rats, Wistar. Tissue Distribution. Treatment Outcome

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  • [ErratumIn] Nucl Med Commun. 2004 Sep;25(9):983. Claringbold, Paul G [corrected to Claringbold, Phillip G]; Turner, Harvey J [corrected to Turner, J Harvey]
  • (PMID = 15208496.001).
  • [ISSN] 0143-3636
  • [Journal-full-title] Nuclear medicine communications
  • [ISO-abbreviation] Nucl Med Commun
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / (188)Re-lipiodol; 0 / Organometallic Compounds; 0 / Radiopharmaceuticals
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10. 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
Hazardous Substances Data Bank. N-NITROSODIMETHYLAMINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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).
  • The organ-ablative efficacy was evaluated in models of unilateral hypertension and chemically induced renal tumors (i.e., dimethyl-nitrosamine).
  • Prior to the vaso-occlusion, the volume of the arterial system of the kidney is determined by perfusion of the kidney with contrast-dye via a blocked balloon-catheter.
  • 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 model of chemically induced renal tumors, complete necrosis of T2 stages could be achieved in 83% using Ethibloc compared to only 63% with Gelfoam particles, and 17% after ligation.
  • 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.
  • After an interval of up to 28 days, complete necrosis of the renal tumor could be achieved in tumors up to 9 cm in diameter.
  • DISCUSSION: Capillary chemoembolization represents an effective concept for ablation of malignant renal tumors.
  • 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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11. Johnston MR, Mullen JB, Pagura ME, Howard RB: Validation of an orthotopic model of human lung cancer with regional and systemic metastases. Ann Thorac Surg; 2001 Apr;71(4):1120-5
Hazardous Substances Data Bank. (L)-Phenylalanine .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: We developed an orthotopic model of human lung cancer that exhibits highly predictable regional and systemic metastases.
  • This study examines the response of the model when treated with conventional and experimental chemotherapy.
  • METHODS: NCI-H460 tumor fragments were implanted into the right caudal lung lobe of a nude rat.
  • Treatment commenced 2 weeks later.
  • We also calculated the incidence of metastasis to kidney, bone, brain, and contralateral lung in treated versus untreated animals.
  • High-dose cisplatin caused renal toxicity that shortened survival.
  • CONCLUSIONS: Responses were similar to NCI-H460 in vitro data and consistent with clinical experience for these drugs.
  • Drug-related toxicities similar to those seen in clinical practice were detected.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Large Cell / drug therapy. Carcinoma, Large Cell / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Phenylalanine / analogs & derivatives. Xenograft Model Antitumor Assays / standards
  • [MeSH-minor] Analysis of Variance. Animals. Cisplatin / pharmacology. Disease Models, Animal. Doxorubicin / pharmacology. Humans. Male. Mitomycin / pharmacology. Neoplasm Invasiveness. Neoplasm Transplantation. Rats. Rats, Nude. Survival Rate. Thiophenes / pharmacology. Treatment Outcome

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  • (PMID = 11308147.001).
  • [ISSN] 0003-4975
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Thiophenes; 47E5O17Y3R / Phenylalanine; 50SG953SK6 / Mitomycin; 80168379AG / Doxorubicin; BK349F52C9 / batimastat; Q20Q21Q62J / Cisplatin
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12. Chu TF, Rupnick MA, Kerkela R, Dallabrida SM, Zurakowski D, Nguyen L, Woulfe K, Pravda E, Cassiola F, Desai J, George S, Morgan JA, Harris DM, Ismail NS, Chen JH, Schoen FJ, Van den Abbeele AD, Demetri GD, Force T, Chen MH: Cardiotoxicity associated with tyrosine kinase inhibitor sunitinib. Lancet; 2007 Dec 15;370(9604):2011-9
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  • BACKGROUND: Sunitinib, a multitargeted tyrosine-kinase inhibitor, which is approved by both US and European Commission regulatory agencies for clinical use, extends survival of patients with metastatic renal-cell carcinoma and gastrointestinal stromal tumours, but concerns have arisen about its cardiac safety.
  • We investigated potential mechanisms of sunitinib-associated cardiac effects by studies in isolated rat cardiomyocytes and in mice.
  • Sunitinib induced increases in mean systolic and diastolic blood pressure, and 35 of 75 (47%) individuals developed hypertension (>150/100 mm Hg).
  • Sunitinib caused mitochondrial injury and cardiomyocyte apoptosis in mice and in cultured rat cardiomyocytes.

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  • (PMID = 18083403.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL61688; United States / NHLBI NIH HHS / HL / R01 HL067371; United States / NHLBI NIH HHS / HL / R01 HL061688-11; United States / NHLBI NIH HHS / HL / HL061688-10; United States / NHLBI NIH HHS / HL / R01 HL061688; United States / NHLBI NIH HHS / HL / HL061688-11; United States / NHLBI NIH HHS / HL / R01 HL061688-10; United States / NHLBI NIH HHS / HL / HL67371; United States / NHLBI NIH HHS / HL / R01 HL061688-09; United States / NHLBI NIH HHS / HL / HL061688-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ NIHMS37146; NLM/ PMC2643085
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13. Lo ST, Stern S, Clogston JD, Zheng J, Adiseshaiah PP, Dobrovolskaia M, Lim J, Patri AK, Sun X, Simanek EE: Biological assessment of triazine dendrimer: toxicological profiles, solution behavior, biodistribution, drug release and efficacy in a PEGylated, paclitaxel construct. Mol Pharm; 2010 Aug 2;7(4):993-1006
Hazardous Substances Data Bank. TAXOL .

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  • [Title] Biological assessment of triazine dendrimer: toxicological profiles, solution behavior, biodistribution, drug release and efficacy in a PEGylated, paclitaxel construct.
  • Paclitaxel release occurs in vitro in human, rat, and mouse plasma and is nonlinear, ranging from 7 to 20% cumulative release over a 48 h incubation period.
  • The construct is 2-3 orders of magnitude less toxic than Taxol by weight in human hepatocarcinoma (Hep G2), porcine renal proximal tubule (LLC-PK1), and human colon carcinoma (LS174T) cells, but shows similar cytotoxicity to Abraxane in LS174T cells.

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  • (PMID = 20481608.001).
  • [ISSN] 1543-8392
  • [Journal-full-title] Molecular pharmaceutics
  • [ISO-abbreviation] Mol. Pharm.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM064560-08S1; United States / PHS HHS / / R01 65460; United States / NIGMS NIH HHS / GM / R01 GM064560-08S1; United States / NCI NIH HHS / CA / U24 CA126608; United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / N01-CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Dendrimers; 0 / Triazines; 30IQX730WE / Polyethylene Glycols; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS218356; NLM/ PMC2914493
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