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1. National Toxicology Program: Toxicology and carcinogenesis studies of dibromoacetic acid (Cas No. 631-64-1) in F344/N rats and B6C3F1 mice (drinking water studies). Natl Toxicol Program Tech Rep Ser; 2007 Apr;(537):1-320
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  • [Title] Toxicology and carcinogenesis studies of dibromoacetic acid (Cas No. 631-64-1) in F344/N rats and B6C3F1 mice (drinking water studies).
  • Dibromoacetic acid is a water disinfection by-product.
  • Drinking water was selected as the route of exposure to mimic human exposure to this chemical.
  • Male and female F344/N rats and B6C3F1 mice were exposed to dibromoacetic acid (greater than 99% pure) in drinking water for 2 weeks, 3 months, or 2 years.
  • 2-WEEK STUDY IN RATS: Groups of five male and five female rats were exposed to 0, 125, 250, 500, 1,000, or 2,000 mg/L dibromoacetic acid in drinking water for 2 weeks, equivalent to average daily doses of approximately 17, 32, 67, 134, 270 (males), or 257 (females) mg dibromoacetic acid/kg body weight.
  • Water consumption by exposed and control groups was similar.
  • Right testis weights of males exposed to 500 mg/L or greater were significantly decreased.
  • The incidences of hepatocytic cytoplasmic alteration were significantly increased in males exposed to 500 mg/L or greater and in 2,000 mg/L females.
  • Testicular lesions, characterized by a delay in spermiation and retained spermatids, were noted in males exposed to 500 mg/L or higher concentrations.
  • 2-WEEK STUDY IN MICE: Groups of five male and five female mice were exposed to 0, 125, 250, 500, 1,000, or 2,000 mg/L dibromoacetic acid (equivalent to average daily doses of approximately 24, 47, 95, 178, or 370 mg/kg to males and 22, 53, 88, 166, or 309 mg/kg to females) in drinking water for 2 weeks.
  • Water consumption by exposed and control groups was similar.
  • The incidences of morphological changes to the germinal epithelium of the testes were increased in males exposed to 1,000 or 2,000 mg/L. 3-MONTH STUDY IN RATS: Groups of 10 male and 10 female rats were exposed to 0, 125, 250, 500, 1,000, or 2,000 mg/L dibromoacetic acid (equivalent to average daily doses of approximately 10, 20, 40, 90, and 166 mg/kg to males and 12, 23, 48, 93, and 181 mg/kg to females) in drinking water for 3 months.
  • Water consumption by the 2,000 mg/L males at weeks 1 and 13 and by females at week 13 was less than that by controls.
  • The incidences of hepatocellular vacuolization were significantly increased in males exposed to 500 mg/L or greater and in females exposed to 2,000 mg/L.
  • Hematopoietic cell proliferation was noted in females in the 2,000 mg/L group.
  • 3-MONTH STUDY IN MICE: Groups of 10 male and 10 female mice were exposed to 0, 125, 250, 500, 1,000, or 2,000 mg/L dibromoacetic acid (equivalent to average daily doses of approximately 16, 30, 56, 115, and 230 mg/kg to males and 17, 34, 67, 132, and 260 mg/kg to females) in drinking water for 3 months.
  • Water consumption by males in the 2,000 mg/L group was decreased at weeks 1 and 13 relative to controls.
  • Small decreases in mean cell hemoglobin and platelet counts occurred in 2,000 mg/L male mice.
  • Liver weights of males and females exposed to 500 mg/L or greater were significantly increased.
  • 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were exposed to drinking water containing 0, 50, 500, and 1,000 mg/L dibromoacetic acid for 2 years (equivalent to average daily doses of approximately 2, 20, and 40 mg/kg to males and 2, 25, and 45 mg/kg to females).
  • Water consumption by males and females exposed to 1,000 mg/L was less than that by controls during year 2 of the study.
  • A positive trend in the incidence of mononuclear cell leukemia occurred in female rats, and the incidence in 1,000 mg/L females was significantly increased.
  • The incidences of mononuclear cell leukemia were increased in 50 and 500 mg/L males.
  • 2-YEAR STUDY IN MICE: Groups of 50 male and 50 female mice were exposed to drinking water containing 0, 50, 500, and 1,000 mg/L dibromoacetic acid for 2 years (equivalent to average daily doses of approximately 4, 45, and 87 mg/kg to males and 4, 35, and 65 mg/kg to females).
  • Water consumption by exposed mice was generally similar to that by controls throughout the study.
  • The incidences of multiple hepatocellular adenoma and hepatocellular adenoma or carcinoma (combined) were significantly increased in all exposed groups of males and in 500 and 1,000 mg/L females.
  • The incidences of hepatoblastoma were significantly increased in 500 and 1,000 mg/L males, and the incidences of hepatocellular carcinoma were significantly increased in 1,000 mg/L males and 500 mg/L females.
  • Increased frequencies of micronucleated normochromatic erythrocytes were observed in peripheral blood samples from male, but not female, mice administered dibromoacetic acid in drinking water for 3 months.
  • The increased incidences of mononuclear cell leukemia in male rats may have been related to dibromoacetic acid exposure.
  • There was some evidence of carcinogenic activity of dibromoacetic acid in female rats based on an increased incidence and positive trend of mononuclear cell leukemia.
  • There was clear evidence of carcinogenic activity of dibromoacetic acid in male and female mice based on increased incidences of hepatocellular neoplasms and hepatoblastoma (males only).
  • [MeSH-minor] Administration, Oral. Animals. Body Weight / drug effects. CHO Cells. Cricetinae. Cricetulus. Drug-Induced Liver Injury / etiology. Drug-Induced Liver Injury / pathology. Female. Kidney Diseases / chemically induced. Kidney Diseases / pathology. Liver / drug effects. Liver / pathology. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Lung Neoplasms / chemically induced. Lung Neoplasms / pathology. Male. Mesothelioma / chemically induced. Mesothelioma / secondary. Mice. Mice, Inbred Strains. Micronuclei, Chromosome-Defective / chemically induced. Organ Size / drug effects. Rats. Rats, Inbred F344. Salmonella typhimurium / drug effects. Salmonella typhimurium / genetics. Testis / drug effects. Testis / pathology. Water Supply

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  • (PMID = 17554398.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acetates; 0 / Carcinogens; 0 / Environmental Pollutants; 0 / Mutagens; 631-64-1 / dibromoacetic acid
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2. Ko JM, Chan PL, Yau WL, Chan HK, Chan KC, Yu ZY, Kwong FM, Miller LD, Liu ET, Yang LC, Lo PH, Stanbridge EJ, Tang JC, Srivastava G, Tsao SW, Law S, Lung ML: Monochromosome transfer and microarray analysis identify a critical tumor-suppressive region mapping to chromosome 13q14 and THSD1 in esophageal carcinoma. Mol Cancer Res; 2008 Apr;6(4):592-603
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  • [Title] Monochromosome transfer and microarray analysis identify a critical tumor-suppressive region mapping to chromosome 13q14 and THSD1 in esophageal carcinoma.
  • Loss of chromosome 13q regions in esophageal squamous cell carcinoma (ESCC) is a frequent event.
  • Monochromosome transfer approaches provide direct functional evidence for tumor suppression by chromosome 13 in SLMT-1, an ESCC cell line, and identify critical regions at 13q12.3, 13q14.11, and 13q14.3.
  • Differential gene expression profiles of three tumor-suppressing microcell hybrids (MCH) and their tumorigenic parental SLMT-1 cell line were revealed by competitive hybridization using 19k cDNA oligonucleotide microarrays.
  • Nine candidate 13q14 tumor-suppressor genes (TSG), including RB1, showed down-regulation in SLMT-1, compared with NE1, an immortalized normal esophageal epithelial cell line; their average gene expression was restored in MCHs compared with SLMT-1.
  • Reverse transcription-PCR validated gene expression levels in MCHs and a panel of ESCC cell lines.
  • Results suggest that the tumor-suppressing effect is not attributed to RB1, but instead likely involves thrombospondin type I domain-containing 1 (THSD1), a novel candidate TSG mapping to 13q14.
  • Quantitative reverse transcription-PCR detected down-regulation of THSD1 expression in 100% of ESCC and other cancer cell lines.
  • Transfection of wild-type THSD1 into SLMT-1 resulted in significant reduction of colony-forming ability, hence providing functional evidence for its growth-suppressive activity.
  • [MeSH-minor] Alleles. Cell Line, Transformed. Cell Line, Tumor. Chromosome Segregation. DNA Methylation / drug effects. Deoxycytidine / pharmacology. Epithelial Cells / drug effects. Epithelial Cells / pathology. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Genome, Human / genetics. Humans. Hydroxamic Acids / pharmacology. In Situ Hybridization, Fluorescence. Microsatellite Repeats / genetics. Promoter Regions, Genetic / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Tumor Stem Cell Assay

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  • (PMID = 18403638.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hydroxamic Acids; 0 / THSD1 protein, human; 0 / Thrombospondins; 0W860991D6 / Deoxycytidine; 3X2S926L3Z / trichostatin A
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3. National Toxicology Program: Toxicology and carcinogenesis studies of formamide (Cas No. 75-12-7) in F344/N rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2008 Jul;(541):1-192
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  • Male and female F344/N rats and B6C3F1 mice were administered formamide (approximately 100% pure) in deionized water by gavage for 2 weeks, 3 months, or 2 years.
  • 3-MONTH STUDY IN RATS: Groups of 10 male and 10 female rats were administered 0, 10, 20, 40, 80, or 160 mg formamide/kg body weight in deionized water by gavage, 5 days per week for 14 weeks.
  • 3-MONTH STUDY IN MICE: Groups of 10 male and 10 female mice were administered 0, 10, 20, 40, 80, or 160 mg formamide/kg body weight in deionized water by gavage, 5 days per week for 14 weeks.
  • 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were administered 0, 20, 40, or 80 mg formamide/kg body weight, 5 days per week for 104 to 105 weeks in deionized water by gavage.
  • 2-YEAR STUDY IN MICE: Groups of 50 male and 50 female mice were administered 0, 20, 40, or 80 mg formamide/kg body weight, 5 days per week for 104 to 105 weeks in deionized water by gavage.
  • The incidence of hepatocellular adenoma or carcinoma (combined) in 80 mg/kg females was significantly increased.
  • The incidence of hematopoietic cell proliferation of the spleen was significantly increased in 80 mg/kg males.
  • There was clear evidence of carcinogenic activity of formamide in male B6C3F1 mice based on increased incidences of hemangiosarcoma of the liver.
  • There was equivocal evidence of carcinogenic activity of formamide in female B6C3F1 mice based on increased incidences of hepatocellular adenoma or carcinoma (combined).
  • Mineralization of the testicular arteries and tunic and hematopoietic cell proliferation of the spleen in male mice were also associated with administration of formamide.
  • [MeSH-minor] Administration, Oral. Animals. Body Weight / drug effects. Bone Marrow / drug effects. Bone Marrow / pathology. Calcinosis / chemically induced. Calcinosis / pathology. Female. Hyperplasia. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Male. Mice. Mice, Inbred Strains. Mutagenicity Tests. Rats. Rats, Inbred F344. Spleen / drug effects. Spleen / pathology. Testis / drug effects. Testis / pathology

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  • (PMID = 18716632.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Environmental Pollutants; 0 / Formamides; 4781T907ZS / formamide
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4. He W, Gong K, Zhu G, Smith DK, Ip NY: Membrane distal cytokine binding domain of LIFR interacts with soluble CNTFR in vitro. FEBS Lett; 2002 Mar 13;514(2-3):214-8
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  • Moreover, purified CBD1 partially blocks CNTF signaling, but not that of interleukin-6 or LIF, in human embryonal carcinoma cell line Ntera/D1 cells.
  • [MeSH-minor] Animals. Cell Line. Cytokines / pharmacology. Embryonal Carcinoma Stem Cells. Enzyme-Linked Immunosorbent Assay. Growth Inhibitors / pharmacology. Humans. Interleukin-6 / pharmacology. Leukemia Inhibitory Factor. Leukemia Inhibitory Factor Receptor alpha Subunit. Lymphokines / pharmacology. Macromolecular Substances. Neoplastic Stem Cells / cytology. Neoplastic Stem Cells / metabolism. PC12 Cells. Peptide Fragments / genetics. Peptide Fragments / metabolism. Peptide Fragments / pharmacology. Protein Binding / physiology. Protein Structure, Tertiary / physiology. Rats. Receptors, OSM-LIF. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Signal Transduction / drug effects. Signal Transduction / physiology

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  • (PMID = 11943154.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Growth Inhibitors; 0 / Interleukin-6; 0 / LIF protein, human; 0 / LIFR protein, human; 0 / Leukemia Inhibitory Factor; 0 / Leukemia Inhibitory Factor Receptor alpha Subunit; 0 / Lifr protein, rat; 0 / Lymphokines; 0 / Macromolecular Substances; 0 / Peptide Fragments; 0 / Receptor, Ciliary Neurotrophic Factor; 0 / Receptors, Cytokine; 0 / Receptors, OSM-LIF; 0 / Recombinant Fusion Proteins
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5. Zhou J, Cheng SC, Luo D, Xie Y: Study of multi-drug resistant mechanisms in a taxol-resistant hepatocellular carcinoma QGY-TR 50 cell line. Biochem Biophys Res Commun; 2001 Feb 9;280(5):1237-42
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  • [Title] Study of multi-drug resistant mechanisms in a taxol-resistant hepatocellular carcinoma QGY-TR 50 cell line.
  • A taxol-resistant cell line, QGY-TR50, derived from a human hepatocellular carcinoma (HCC) QGY-7703 cell line was used to investigate the mechanisms of taxol-resistance.
  • QGY-TR50 cells showed more than 250-fold resistance to taxol and exhibited cross-resistance to other drugs including actinomycin D, doxorubicin, vinblastine, and vincristine.
  • All results suggest that the P-glycoprotein could be one key factor involved in enhancing drug resistance in QGY-TR50 cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Hepatocellular / genetics. Drug Resistance, Multiple / genetics. Paclitaxel / pharmacology
  • [MeSH-minor] Cell Survival / drug effects. Dactinomycin / pharmacology. Doxorubicin / pharmacology. Drug Resistance, Neoplasm. Fluorouracil / pharmacology. Gene Expression Regulation, Neoplastic. Humans. Inhibitory Concentration 50. Mitomycin / pharmacology. P-Glycoprotein / genetics. P-Glycoproteins / genetics. Protein Isoforms / genetics. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tubulin / genetics. Tumor Cells, Cultured. Vinblastine / pharmacology. Vincristine / pharmacology

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  • (PMID = 11162660.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / Protein Isoforms; 0 / RNA, Neoplasm; 0 / Tubulin; 1CC1JFE158 / Dactinomycin; 50SG953SK6 / Mitomycin; 5J49Q6B70F / Vincristine; 5V9KLZ54CY / Vinblastine; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel; U3P01618RT / Fluorouracil
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6. Pedrosa I, Alsop DC, Rofsky NM: Magnetic resonance imaging as a biomarker in renal cell carcinoma. Cancer; 2009 May 15;115(10 Suppl):2334-45
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  • [Title] Magnetic resonance imaging as a biomarker in renal cell carcinoma.
  • The ability to noninvasively discriminate the most common types of renal cell carcinoma (RCC) based on their magnetic resonance imaging (MRI) appearances or their magnetic resonance phenotypes is achievable.
  • Intracellular lipids, a histologic characteristic of the clear cell RCC, can be identified on chemical shift MRI.
  • In addition to morphologic imaging features, the different subtypes of RCC have distinct patterns of enhancement on dynamic contrast-enhanced MRI.
  • Clear cell tumors demonstrate much greater enhancement than papillary and chromophobe RCCs during the corticomedullary and nephrographic phases.
  • The MRI technique arterial spin labeling (ASL) uses magnetic fields to label the water protons in arterial blood and measures blood flow into tissue; quantitative images of blood flow can be generated without exogenous contrast media.
  • Multiple measurements of tumor perfusion may be repeated before and after a physiologic or drug challenge (ie, antiangiogenic therapy).
  • [MeSH-major] Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology. Magnetic Resonance Imaging / methods

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  • [Copyright] (c) 2009 American Cancer Society.
  • (PMID = 19402070.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 93
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7. Chan C, Harland ML, Webb SE, Chen J, Miller AL, Barritt GJ: Evaluation, using targeted aequorins, of the roles of the endoplasmic reticulum and its (Ca2++Mg2+)ATP-ases in the activation of store-operated Ca2+ channels in liver cells. Cell Calcium; 2004 Apr;35(4):317-31
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  • The process by which store-operated Ca2+ channels (SOCs) deliver Ca2+ to the endoplasmic reticulum (ER) and the role of (Ca2++Mg2+)ATP-ases of the ER in the activation of SOCs in H4-IIE liver cells were investigated using cell lines stably transfected with apo-aequorin targeted to the cytoplasmic space or the ER.
  • This was associated with a sharp transient increase in the cytoplasmic Ca2+ concentration ([Ca2+]cyt) of about 15 s duration (a Cao2+-induced [Ca2+]cyt spike) after which [Ca2+]cyt remained elevated slightly above the basal value for a period of about 2 min (low [Ca2+]cyt plateau).
  • [MeSH-major] Aequorin / metabolism. Ca(2+) Mg(2+)-ATPase / physiology. Calcium / metabolism. Calcium Channels / metabolism. Carcinoma, Hepatocellular / metabolism. Endoplasmic Reticulum / physiology. Liver / metabolism
  • [MeSH-minor] Animals. Calcium Channel Agonists / pharmacology. Calcium Channel Blockers / pharmacology. Cytoplasm / drug effects. Cytoplasm / metabolism. Drug Delivery Systems. Ethylenediamines / pharmacology. Fura-2 / metabolism. Hydroquinones / pharmacology. Mitochondria / drug effects. Mitochondria / metabolism. Rats. Thapsigargin / pharmacology

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  • (PMID = 15036949.001).
  • [ISSN] 0143-4160
  • [Journal-full-title] Cell calcium
  • [ISO-abbreviation] Cell Calcium
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Calcium Channel Agonists; 0 / Calcium Channel Blockers; 0 / Calcium Channels; 0 / Ethylenediamines; 0 / Hydroquinones; 16858-02-9 / N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine; 50934-79-7 / Aequorin; 67526-95-8 / Thapsigargin; 88-58-4 / 2,5-di-tert-butylhydroquinone; EC 3.6.1.- / Ca(2+) Mg(2+)-ATPase; SY7Q814VUP / Calcium; TSN3DL106G / Fura-2
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8. George MH, Olson GR, Doerfler D, Moore T, Kilburn S, DeAngelo AB: Carcinogenicity of bromodichloromethane administered in drinking water to Male F344/N Rats and B6C3F1 mice. Int J Toxicol; 2002 May-Jun;21(3):219-30
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  • [Title] Carcinogenicity of bromodichloromethane administered in drinking water to Male F344/N Rats and B6C3F1 mice.
  • A life-time exposure study was conducted to assess the carcinogenicity of bromodichloromethane (BDCM) administered in the drinking water to male F344/N rats and B6C3F(1) mice.
  • Time-weighted water consumption of 135, 97, and 89 ml/kg/day resulted in mean daily doses of 8.1, 27.2, and 43.4 mg BDCM/kg/day.
  • Time-weighted water consumption of 65, 63, and 59 ml/kg/day yielded 3.9, 20.6 and 36.3 mg BDCM/kg/day.
  • The prevalence of basophilic and clear cell, but not eosinophilic cells, altered foci of cells declined with increasing dose.
  • Under the conditions of the study, BDCM in the drinking water was not carcinogenic in the male B6C3F(1) mouse, but was carcinogenic in the male F344/N rat based on an increased hepatocellular neoplasia.
  • [MeSH-major] Carcinogens / toxicity. Carcinoma / chemically induced. Liver Neoplasms, Experimental / chemically induced. Trihalomethanes / toxicity
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Drinking / drug effects. Male. Mice. Mice, Inbred Strains. Organ Specificity. Rats. Rats, Inbred F344. Species Specificity. Water Supply / standards

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  • (PMID = 12055023.001).
  • [ISSN] 1091-5818
  • [Journal-full-title] International journal of toxicology
  • [ISO-abbreviation] Int. J. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Trihalomethanes; 7LN464CH2O / bromodichloromethane
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9. Chan KT, Lung ML: Mutant p53 expression enhances drug resistance in a hepatocellular carcinoma cell line. Cancer Chemother Pharmacol; 2004 Jun;53(6):519-26
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  • [Title] Mutant p53 expression enhances drug resistance in a hepatocellular carcinoma cell line.
  • Chemoresistance is a major problem in the treatment of hepatocellular carcinoma.
  • Certain p53 mutants may enhance drug resistance in cancer cells.
  • To determine whether two frequently occurring p53 mutants, R248Q and R273C, would increase the drug resistance of liver cancer cells, stable cell lines expressing these specific p53 mutants were established by transfecting the p53-null Hep3B cells with mutant p53 expression vectors, and then treating them with the anticancer drugs doxorubicin and paclitaxel.
  • The cells expressing the p53 mutant, R248Q, but not R273C, displayed cross-resistance to both drugs, in contrast to the control cells expressing the vector alone.
  • Moreover, both the expression and the activity of the multiple drug resistance gene product, P-glycoprotein, were elevated in p53 mutant R248Q-expressing cells.
  • These results suggest that expression of the p53 mutant, R248Q, in liver cancer cells may enhance their drug resistance and that upregulation of P-glycoprotein activity may contribute to this protective effect.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Drug Resistance, Neoplasm / genetics. Liver Neoplasms / genetics. Mutation. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Survival / drug effects. DNA, Neoplasm / analysis. Doxorubicin / metabolism. Doxorubicin / pharmacology. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. In Situ Nick-End Labeling. P-Glycoprotein / metabolism. Paclitaxel / metabolism. Paclitaxel / pharmacology. Transfection. Up-Regulation

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  • (PMID = 15004724.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / P-Glycoprotein; 0 / Tumor Suppressor Protein p53; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel
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10. Ho CC, Siu WY, Chow JP, Lau A, Arooz T, Tong HY, Ng IO, Poon RY: The relative contribution of CHK1 and CHK2 to Adriamycin-induced checkpoint. Exp Cell Res; 2005 Mar 10;304(1):1-15
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  • Topoisomerase II poisons like Adriamycin (ADR, doxorubicin) are clinically important chemotherapeutic agents.
  • Adriamycin-induced DNA damage checkpoint activates ATM and ATR, which could in turn inhibit the cell cycle engine through either CHK1 or CHK2.
  • Several lines of evidence from dominant-negative mutants, short hairpin RNA (shRNA), and knockout cells indicated that CHK1, but not CHK2, is critical for Adriamycin-induced cell cycle arrest.
  • Disruption of CHK1 function bypassed the checkpoint, as manifested by the increase in CDC25A, activation of CDC2, increase in histone H3 phosphorylation, and reduction in cell survival after Adriamycin treatment.
  • Finally, we found that CHK1 was upregulated in primary hepatocellular carcinoma (HCC), albeit as an inactive form.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Doxorubicin / pharmacology. Protein Kinases / physiology. Protein-Serine-Threonine Kinases / physiology
  • [MeSH-minor] Base Sequence. Cell Line, Tumor. Checkpoint Kinase 2. DNA Damage. Genes, cdc. HeLa Cells. Humans. Molecular Sequence Data. Neoplasms / metabolism. RNA / metabolism

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  • (PMID = 15707569.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 63231-63-0 / RNA; 80168379AG / Doxorubicin; EC 2.7.- / Protein Kinases; EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Checkpoint kinase 1; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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11. Cheng SC, Zhou J, Xie Y: P-glycoprotein expression induced by glucose depletion enhanced the chemosensitivity in human hepatocellular carcinoma cell-lines. Cell Biol Int; 2005 Apr;29(4):269-75
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  • [Title] P-glycoprotein expression induced by glucose depletion enhanced the chemosensitivity in human hepatocellular carcinoma cell-lines.
  • In this study, P-gp was found gradually expressed in a human hepatocellular carcinoma (HCC) QGY-7703 cells after 48 h of culturing in glucose-free medium.
  • Mdr1-cDNA isolated from the cell line cultured in glucose-free conditions (namely QGY-7703G), was transiently transformed into the parent QGY-7703 cells, and multi-drug resistance was eventually induced.
  • Results from XTT cytotoxicity assays indicated that the mdr1 gene was functional and the P-gp could restore the QGY-7703 cell's ability to withstand high concentrations of a number of chemotherapeutic agents.
  • A P-gp inhibitor, verapamil, could completely reverse the cellular drug resistance when applied to the QGY-7703G cells.
  • Our results indicated that an alteration of a specific state in cells caused by an external stimulus in vitro may lead to an expression of stress proteins (e.g.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Glucose / metabolism. P-Glycoprotein / biosynthesis
  • [MeSH-minor] Carcinoma, Hepatocellular. Cell Line, Tumor. Culture Media. Dactinomycin / pharmacology. Doxorubicin / pharmacology. Drug Resistance, Multiple / physiology. Drug Resistance, Neoplasm. Fluorouracil / pharmacology. Humans. Inhibitory Concentration 50. Paclitaxel / pharmacology. Vinblastine / pharmacology. Vincristine / pharmacology

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  • (PMID = 15914037.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Culture Media; 0 / P-Glycoprotein; 1CC1JFE158 / Dactinomycin; 5J49Q6B70F / Vincristine; 5V9KLZ54CY / Vinblastine; 80168379AG / Doxorubicin; IY9XDZ35W2 / Glucose; P88XT4IS4D / Paclitaxel; U3P01618RT / Fluorouracil
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12. Chan AS, Ng LW, Poon LS, Chan WW, Wong YH: Dopaminergic and adrenergic toxicities on SK-N-MC human neuroblastoma cells are mediated through G protein signaling and oxidative stress. Apoptosis; 2007 Jan;12(1):167-79
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  • Dopamine, norepinephrine, as well as their corresponding synthetic agonists (SKF38393 and isoproterenol, respectively) triggered SK-N-MC cell death when applied at 50-100 muM persistently for 2 days.
  • This catecholamine-induced cell death appears to be neuronal specific, as demonstrated by their inabilities of triggering apoptosis of A549 lung carcinoma cells and Cos-7 kidney fibroblasts.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis / physiology. Dopamine / pharmacology. GTP-Binding Proteins / metabolism. Neuroblastoma / drug therapy. Neuroblastoma / metabolism. Norepinephrine / pharmacology
  • [MeSH-minor] 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / pharmacology. Adrenergic beta-Agonists / pharmacology. Caspase 3 / metabolism. Caspase 7 / metabolism. Cell Line, Tumor. DNA Fragmentation / drug effects. Dopamine Agonists / pharmacology. Humans. Isoproterenol / pharmacology. Models, Neurological. Nerve Degeneration / etiology. Nerve Degeneration / metabolism. Nerve Degeneration / pathology. Oxidative Stress / drug effects. Poly(ADP-ribose) Polymerases / metabolism. Signal Transduction / drug effects

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  • (PMID = 17136323.001).
  • [ISSN] 1360-8185
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic beta-Agonists; 0 / Dopamine Agonists; 67287-49-4 / 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP7 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7; EC 3.6.1.- / GTP-Binding Proteins; L628TT009W / Isoproterenol; VTD58H1Z2X / Dopamine; X4W3ENH1CV / Norepinephrine
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13. Gao QT, Cheung JK, Choi RC, Cheung AW, Li J, Jiang ZY, Duan R, Zhao KJ, Ding AW, Dong TT, Tsim KW: A Chinese herbal decoction prepared from Radix Astragali and Radix Angelicae Sinensis induces the expression of erythropoietin in cultured Hep3B cells. Planta Med; 2008 Mar;74(4):392-5
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  • Danggui Buxue Tang (DBT), a Chinese medicinal decoction used commonly for treating women's ailments, contains Radix Astragali (RA) and Radix Angelicae Sinensis (RAS).
  • According to Chinese medicinal theory, this decoction is to nourish the blood function; this, however, has not been demonstrated on the molecular level.
  • In order to reveal the hematopoietic effect of this decoction, DBT was applied to cultured Hep3B human hepatocellular carcinoma cells.
  • [MeSH-minor] Cell Line, Tumor. Drugs, Chinese Herbal. Gene Expression Regulation / drug effects. Humans. Medicine, Chinese Traditional. Plant Preparations

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  • (PMID = 18484529.001).
  • [ISSN] 0032-0943
  • [Journal-full-title] Planta medica
  • [ISO-abbreviation] Planta Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Plant Extracts; 0 / Plant Preparations; 0 / danggui buxue decoction; 11096-26-7 / Erythropoietin
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14. Kwitniewski M, Jankowski D, Jaskiewicz K, Dziadziuszko H, Juzeniene A, Moan J, Ma LW, Peksa R, Kunikowska D, Graczyk A, Kwasny M, Kaliszewski M, Glosnicka R: Photodynamic therapy with 5-aminolevulinic acid and diamino acid derivatives of protoporphyrin IX reduces papillomas in mice without eliminating transformation into squamous cell carcinoma of the skin. Int J Cancer; 2009 Oct 1;125(7):1721-7
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  • [Title] Photodynamic therapy with 5-aminolevulinic acid and diamino acid derivatives of protoporphyrin IX reduces papillomas in mice without eliminating transformation into squamous cell carcinoma of the skin.
  • In this study, we used 5-aminolevulinic (ALA) acid and 3 water soluble photosensitizers-PP(Arg)(2), PP(Ser)(2)Arg(2), PP(Ala)(2)Arg(2), all diamino acid derivatives of protoporphyrin IX-to treat benign papillomas in FVB/N mice induced by 7,12-dimethylbenz(a)anthracene (DMBA)-12-O-tetradecanoyl-phorbol-13-acetate (TPA).
  • Of these drugs, ALA and PP(Arg)(2) were found the most efficient.
  • PDT reduced the number of papillomas, but with increasing effectiveness of the drugs, the risk of malignant transformation of the papillomas into squamous cell carcinomas increased.
  • The underlying mechanisms are not clear and further investigations are needed.
  • [MeSH-major] Aminolevulinic Acid / therapeutic use. Carcinoma, Squamous Cell / etiology. Cell Transformation, Neoplastic / pathology. Papilloma / drug therapy. Photochemotherapy / methods. Photosensitizing Agents / therapeutic use. Protoporphyrins / therapeutic use. Skin Neoplasms / drug therapy. Skin Neoplasms / etiology
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene. Animals. Carcinogens. Kaplan-Meier Estimate. Mice. Mice, Inbred Strains. Tetradecanoylphorbol Acetate

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  • (PMID = 19521986.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Photosensitizing Agents; 0 / Protoporphyrins; 553-12-8 / protoporphyrin IX; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 88755TAZ87 / Aminolevulinic Acid; NI40JAQ945 / Tetradecanoylphorbol Acetate
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15. Cheng SC, Luo D, Xie Y: Taxol induced Bcl-2 protein phosphorylation in human hepatocellular carcinoma QGY-7703 cell line. Cell Biol Int; 2001;25(3):261-5
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  • [Title] Taxol induced Bcl-2 protein phosphorylation in human hepatocellular carcinoma QGY-7703 cell line.
  • Bcl-2 family proteins play a critical role in the regulation of apoptosis.
  • Treatment of a human hepatocellular carcinoma cell line, QGY-7703, with Taxol induced apoptosis and Bcl-2 protein phosphorylation.
  • Other Bcl-2 family proteins, including Bax (a heterodimerization partner of Bcl-2), Bcl-XL, Bak and Bad, were expressed, but at constant levels.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma, Hepatocellular / metabolism. Liver Neoplasms / metabolism. Paclitaxel / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. Blotting, Western. DNA Fragmentation / drug effects. Humans. Phosphorylation / drug effects. Tumor Cells, Cultured

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  • [Copyright] Copyright 2001 Academic Press.
  • (PMID = 11352500.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Proto-Oncogene Proteins c-bcl-2; P88XT4IS4D / Paclitaxel
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16. Seguchi K, Kawauchi S, Morimoto Y, Arai T, Asanuma H, Hayakawa M, Kikuchi M: Critical parameters in the cytotoxicity of photodynamic therapy using a pulsed laser. Lasers Med Sci; 2002;17(4):265-71
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  • Photodynamic therapy (PDT) using a pulsed laser is becoming popular, but its cytotoxic effect is still not clear.
  • Mice renal cell carcinoma cells were incubated with PAD-S31, a water-soluble photosensitiser of which the excitation peak is 670 nm, and were then irradiated with either a tungsten lamp, a CW diode laser, or a nanosecond pulsed Nd:YAG laser-based optical parametric oscillator system.
  • [MeSH-major] Carcinoma, Renal Cell / pathology. Laser Therapy. Photochemotherapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Division / radiation effects. Mice. Porphyrins / administration & dosage. Radiation Dosage. Radiation-Sensitizing Agents / administration & dosage. Tumor Cells, Cultured

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  • (PMID = 12417981.001).
  • [ISSN] 0268-8921
  • [Journal-full-title] Lasers in medical science
  • [ISO-abbreviation] Lasers Med Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 13,17-bis(1-carboxypropionyl)carbamoylethyl-3-ethenyl-8-ethoxyiminoethylidene-7-hydroxy-2,7,12,18-tetramethyl porphyrin; 0 / Porphyrins; 0 / Radiation-Sensitizing Agents
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17. Chan KT, Cheng SC, Xie H, Xie Y: A humanized monoclonal antibody constructed from intronless expression vectors targets human hepatocellular carcinoma cells. Biochem Biophys Res Commun; 2001 Jun 1;284(1):157-67
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  • [Title] A humanized monoclonal antibody constructed from intronless expression vectors targets human hepatocellular carcinoma cells.
  • An anti-human hepatocellular carcinoma (HCC) monoclonal antibody, hHP-1, was genetically humanized from a murine monoclonal antibody.
  • In vitro binding activity assay showed that the hHP-1 had retained its binding function to a human HCC SMMC-7721 cell-line, without cross binding to other human normal tissues.
  • [MeSH-major] Antibodies, Monoclonal / physiology. Antibody Specificity / immunology. Carcinoma, Hepatocellular / immunology. Genetic Vectors / metabolism. Liver Neoplasms / immunology
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Binding, Competitive / drug effects. Binding, Competitive / immunology. CHO Cells. Chromatography, Affinity. Cricetinae. Cytomegalovirus / genetics. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Fluorescent Antibody Technique. Humans. Immunoglobulin G / isolation & purification. Immunoglobulin G / pharmacology. Immunoglobulin G / physiology. Immunoglobulin Heavy Chains / genetics. Immunoglobulin kappa-Chains / genetics. Introns / genetics. Mice. Molecular Sequence Data. Serologic Tests. Tumor Cells, Cultured

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  • [Copyright] Copyright 2001 Academic Press.
  • (PMID = 11374885.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin G; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin kappa-Chains
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18. Salnikov AV, Iversen VV, Koisti M, Sundberg C, Johansson L, Stuhr LB, Sjöquist M, Ahlström H, Reed RK, Rubin K: Lowering of tumor interstitial fluid pressure specifically augments efficacy of chemotherapy. FASEB J; 2003 Sep;17(12):1756-8
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  • Here, it is argued that a condition of raised interstitial fluid pressure (IFP) that can be observed in many tumors is a major factor in preventing optimal access of systemically administered chemotherapeutic agents.
  • These experiments uniquely demonstrate a clear and, according to the starting hypothesis, logical, synergistic effect of PGE1 and 5-FU that offers hope for better treatment of many tumors in which raised IFP is likely to be inhibiting optimal results with water-soluble cancer chemotherapeutic agents.
  • [MeSH-major] Alprostadil / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Carcinoma / drug therapy. Fluorouracil / therapeutic use
  • [MeSH-minor] Animals. Blood Pressure. Cell Division. Drug Synergism. Extracellular Space / drug effects. Models, Biological. Pressure. Rats

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  • (PMID = 12958200.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; F5TD010360 / Alprostadil; U3P01618RT / Fluorouracil
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19. Yip EC, Chan AS, Pang H, Tam YK, Wong YH: Protocatechuic acid induces cell death in HepG2 hepatocellular carcinoma cells through a c-Jun N-terminal kinase-dependent mechanism. Cell Biol Toxicol; 2006 Jul;22(4):293-302
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  • [Title] Protocatechuic acid induces cell death in HepG2 hepatocellular carcinoma cells through a c-Jun N-terminal kinase-dependent mechanism.
  • Protocatechuic acid (PCA), chlorogenic acid (CA) and luteolin (LT) are plant phenols found in Chinese medicinal herbs such as Lonicera japonica.
  • Cytotoxicity assays showed that PCA, CA and LT (at 100 micromol/L) effectively killed the HepG2 hepatocellular carcinoma cells.
  • Coincidently, PCA-induced cell death was rescued by specific inhibitors for JNK and p38, while the cytotoxicities of CA and LT were partially eliminated by the antioxidant effect of N-acetyl-L-cysteine (NAC).
  • Further investigation demonstrated that the aqueous extract of Lonicera japonica also triggered HepG2 cell death in a JNK-dependent manner, but the amount of PCA alone in this herbal extract was insufficient to contribute the subsequent cytotoxic effect.
  • Collectively, our results suggest that PCA is a naturally occurring compound capable of inducing JNK-dependent hepatocellular carcinoma cell death.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Hepatocellular / drug therapy. Hydroxybenzoates / pharmacology. JNK Mitogen-Activated Protein Kinases / metabolism. Liver Neoplasms / drug therapy
  • [MeSH-minor] Cell Death. Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. Lonicera / metabolism. MAP Kinase Signaling System. Models, Chemical. Phosphorylation. Plant Extracts / pharmacology. p38 Mitogen-Activated Protein Kinases / metabolism

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  • [ErratumIn] Cell Biol Toxicol. 2007 Mar;23(2):139
  • (PMID = 16835731.001).
  • [ISSN] 0742-2091
  • [Journal-full-title] Cell biology and toxicology
  • [ISO-abbreviation] Cell Biol. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxybenzoates; 0 / Plant Extracts; 36R5QJ8L4B / protocatechuic acid; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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20. National Toxicology Program: Toxicology and carcinogenesis studies of sodium dichromate dihydrate (Cas No. 7789-12-0) in F344/N rats and B6C3F1 mice (drinking water studies). Natl Toxicol Program Tech Rep Ser; 2008 Jul;(546):1-192
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  • [Title] Toxicology and carcinogenesis studies of sodium dichromate dihydrate (Cas No. 7789-12-0) in F344/N rats and B6C3F1 mice (drinking water studies).
  • Sodium dichromate dihydrate is one of a number of inorganic compounds containing hexavalent chromium (Cr VI) found in drinking water source supplies as a contaminant resulting from various industrial processes including electroplating operations, leather tanning, and textile manufacturing.
  • Because of the lack of adequate experimental data on the toxicity and carcinogenicity of hexavalent chromium ingested orally and because hexavalent chromium has been found in drinking water source supplies, the California Congressional Delegation, the California Environmental Protection Agency, and the California Department of Health Services nominated hexavalent chromium to the National Toxicology Program for study.
  • In the current study, male and female F344/N rats and B6C3F1 mice were exposed to sodium dichromate dihydrate (greater than 99.7% pure) in drinking water for 2 years.
  • 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were exposed to drinking water containing 0, 14.3, 57.3, 172, or 516 mg/L sodium dichromate dihydrate (equivalent to 0, 5, 20, 60, or 180 mg/L chromium) for 2 years (equivalent to average daily doses of approximately 0.6, 2.2, 6, or 17 mg sodium dichromate dihydrate/kg body weight for males and 0.7, 2.7, 7, or 20 mg/kg for females).
  • The lower body weights were partly attributed to poor palatability of the dosed water and consequent reductions in water consumption.
  • Water consumption by 172 and 516 mg/L rats was less than that by the controls throughout the study.
  • The incidences of squamous cell carcinoma in the oral mucosa of 516 mg/L male and female rats were significantly greater than those in the controls.
  • The incidence in 172 mg/L females exceeded the historical control ranges for drinking water studies and for all routes of administration.
  • The incidences of squamous cell papilloma or squamous cell carcinoma (combined) of the oral mucosa or tongue of 516 mg/L male and female rats were significantly greater than those in the controls.
  • Exposure concentration-related nonneoplastic liver lesions were observed in males and females exposed to 57.3 mg/L or greater.
  • These included histiocytic cellular infiltration, chronic inflammation, fatty change (females), basophilic focus (males), and clear cell focus (females).
  • Increased incidences of histiocytic cellular infiltration also occurred in the small intestine (duodenum), mesenteric lymph node, and pancreatic lymph node of males and/or females exposed to 57.3 mg/L or greater.
  • 2-YEAR STUDY IN MICE: Groups of 50 male mice were exposed to drinking water containing 0, 14.3, 28.6, 85.7, or 257.4 mg/L sodium dichromate dihydrate (equivalent to 0, 5, 10, 30, or 90 mg/L chromium) for 2 years (equivalent to average daily doses of approximately 1.1, 2.6, 7, or 17 mg sodium dichromate dihydrate/kg body weight).
  • Groups of 50 female mice were exposed to drinking water containing 0, 14.3, 57.3, 172, or 516 mg/L sodium dichromate dihydrate (equivalent to 0, 5, 20, 60, or 180 mg/L chromium) for 2 years (equivalent to average daily doses of approximately 1.1, 3.9, 9, or 25 mg/kg).
  • The lower body weights were partly attributed to poor palatability of the dosed water and consequent reductions in water consumption.
  • Water consumption by 85.7 and 257.4 mg/L males and 172 and 516 mg/L females was less than that by the controls throughout the study.
  • The incidence of carcinoma of the duodenum was significantly increased in 516 mg/L females.
  • When the incidences of adenoma and carcinoma were combined for all sites of the small intestine, the incidences were significantly increased in 85.7 and 257.4 mg/L males and 172 and 516 mg/L females compared to those in the controls.
  • The incidences in 57.3 mg/L females exceeded the historical control ranges for drinking water studies and for all routes of administration.
  • CONCLUSIONS: Under the conditions of these 2-year drinking water studies, there was clear evidence of carcinogenic activity of sodium dichromate dihydrate in male and female F344/N rats based on increased incidences of squamous cell neoplasms of the oral cavity.
  • There was clear evidence of carcinogenic activity of sodium dichromate dihydrate in male and female B6C3F1 mice based on increased incidences of neoplasms of the small intestine (duodenum, jejunum, or ileum).
  • [MeSH-major] Chromates / toxicity. Neoplasms, Experimental / etiology. Toxicity Tests. Water Pollutants, Chemical / toxicity
  • [MeSH-minor] Administration, Oral. Animals. Female. Intestinal Neoplasms / chemically induced. Intestinal Neoplasms / pathology. Intestine, Small / drug effects. Intestine, Small / pathology. Liver / drug effects. Liver / pathology. Lymph Nodes / drug effects. Lymph Nodes / pathology. Male. Mice. Mice, Inbred Strains. Mouth Neoplasms / chemically induced. Mouth Neoplasms / pathology. Rats. Rats, Inbred F344. Water Supply

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  • (PMID = 18716633.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromates; 0 / Water Pollutants, Chemical; C9G6VY6ZZ4 / sodium bichromate
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21. Toxicology and carcinogenesis studies of acrylonitrile (CAS No. 107-13-1) in B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2001 Oct;(506):1-201
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  • Male and female B6C3F1 mice received acrylonitrile (greater than 99% pure) in deionized water by gavage for 14 weeks or 2 years.
  • 14-WEEK STUDY: Groups of 10 male and 10 female mice were administered 0, 5, 10, 20, 40, or 60 mg acrylonitrile/kg body weight in deionized water by gavage, 5 days per week, for 14 weeks.
  • 2-YEAR STUDY: Groups of 50 male and 50 female mice were administered acrylonitrile in deionized water by gavage at doses of 0, 2.5, 10, or 20 mg/kg, 5 days per week, for 104 to 105 weeks.
  • Pathology Findings The incidences of squamous cell papilloma, squamous cell carcinoma, and squamous cell papilloma or carcinoma (combined) of the forestomach occurred with positive trends in males and females, and were present in 50% or greater of mice administered 10 or 20 mg/kg.
  • The incidences of harderian gland adenoma and adenoma or carcinoma (combined) were significantly increased in all dosed groups of males and in 10 and 20 mg/kg females, and the incidence of harderian gland hyperplasia was significantly increased in 10 mg/kg males.
  • The incidence of benign or malignant granulosa cell tumor (combined) in the ovary of 10 mg/kg females was greater than that in the vehicle controls.
  • The incidence of alveolar/bronchiolar adenoma or carcinoma (combined) in 10 mg/kg females was significantly increased.
  • CONCLUSIONS: Under the conditions of this 2-year gavage study, there was clear evidence of carcinogenic activity of acrylonitrile in male and female B6C3F1 mice based on increased incidences of forestomach and harderian gland neoplasms.
  • [MeSH-minor] Animals. Body Weight / drug effects. Carcinogenicity Tests. Female. Male. Mice. Mice, Inbred Strains. Mutagenicity Tests. Neoplasms / chemically induced. Neoplasms / pathology. Sex Characteristics. Survival Analysis. Time Factors

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  • (PMID = 11803701.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; MP1U0D42PE / Acrylonitrile
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22. Zhou P, Li Z, Chau Y: Synthesis, characterization, and in vivo evaluation of poly(ethylene oxide-co-glycidol)-platinate conjugate. Eur J Pharm Sci; 2010 Nov 20;41(3-4):464-72
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  • We showed that this new bioconjugation material is biocompatible by its lack of toxicity on fibroblast cell growth, inactivity in hemolysis, and the absence of side effects after injection in mice.
  • The usefulness of poly(EO-co-Gly) as a polymeric drug carrier was demonstrated via the preparation and characterization of a new anticancer polymer-drug conjugate, poly(EO-co-Gly)-platinate.
  • The drug loading was 9.1-12.6% (cisplatin/conjugate w/w), at least four times higher than a PEG conjugate of similar molecular weight.
  • The release of active drugs was confirmed by the antitumor activity of poly(EO-co-Gly)-platinate in vitro against HONE-1 (human nasopharyngeal carcinoma) and MCF-7 (human breast cancer), albeit at a potency lower than free cisplatin.
  • These findings support that poly(EO-co-Gly) is a suitable drug carrier.
  • [MeSH-minor] Animals. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Cell Line. Cisplatin / chemistry. Cisplatin / pharmacology. Mice. Mice, Nude. Molecular Structure. Neoplasms, Experimental / drug therapy

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  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20709170.001).
  • [ISSN] 1879-0720
  • [Journal-full-title] European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
  • [ISO-abbreviation] Eur J Pharm Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biocompatible Materials; 0 / Malonates; 0 / Platinum Compounds; 30IQX730WE / Polyethylene Glycols; Q20Q21Q62J / Cisplatin
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24. Zhang Z, Du X, Wang F: Biological activities of procyanidins from the bark of Pinus caribaea Morelet. Nat Prod Res; 2009;23(8):696-703
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  • [Title] Biological activities of procyanidins from the bark of Pinus caribaea Morelet.
  • The extraction and biological activities of procyanidins from the bark of Pinus caribaea Morelet (P. caribaea) have been studied for the first time in our research.
  • The focus of this study is to investigate the biological activities of the procyanidins from the bark of P. caribaea.
  • Free-radical scavenging activity of the procyanidins was measured by means of 2,2-diphenyl-1-picrylhydrazyl (DPPH) method, and it was clear that the procyanidins product had a strong radical scavenging ability.
  • The results indicated that the procyanidins extracted with water had a stronger inhibition on promycelocytic cells HL-60, an effective inhibition on human stomach adenocarcinoma cells BGC-823 and human hepatocellular carcinoma cells BEL-7402, but no effect on human lung carcinoma cells A549, whereas the procyanidins extracted with ethanol had an effective inhibition on HL-60 and BGC-823, but no effect on A549 or BEL-7402.
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. HL-60 Cells. Humans

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  • (PMID = 19418352.001).
  • [ISSN] 1478-6427
  • [Journal-full-title] Natural product research
  • [ISO-abbreviation] Nat. Prod. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proanthocyanidins
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26. Cheung WM, Chu AH, Chu PW, Ip NY: Cloning and expression of a novel nuclear matrix-associated protein that is regulated during the retinoic acid-induced neuronal differentiation. J Biol Chem; 2001 May 18;276(20):17083-91
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  • RA treatment induces growth arrest and terminal differentiation of a human embryonal carcinoma cell line (NT2) into postmitotic central nervous system neurons.
  • The transcript expression of ramp is closely correlated with the cell proliferation rate of NT2 cells.
  • Taken together, our data suggest that Ramp plays a role in the proliferation of the human embryonal carcinoma cells.
  • [MeSH-major] Gene Expression Regulation / physiology. Neurons / physiology. Nuclear Matrix / metabolism. Nuclear Proteins / genetics. Transcription, Genetic. Tretinoin / pharmacology
  • [MeSH-minor] Adult. Alkaline Phosphatase / genetics. Amino Acid Sequence. Carcinoma, Embryonal. Cell Differentiation / drug effects. Cell Differentiation / physiology. Cloning, Molecular. Embryo, Mammalian. Female. Gene Library. Humans. Male. Molecular Sequence Data. Organ Specificity. Placenta / metabolism. Pregnancy. Promoter Regions, Genetic. Protein Conformation. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. Ubiquitin-Protein Ligases

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  • (PMID = 11278750.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AF345896
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 5688UTC01R / Tretinoin; EC 3.1.3.1 / Alkaline Phosphatase; EC 6.3.2.19 / DTL protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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27. Cai SQ, Chen LR, Zheng M: [Acitretin induces apoptosis and changes of relative signaling pathway in epidermoid carcinoma cell line A431]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2006 Mar;35(2):182-8
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  • [Title] [Acitretin induces apoptosis and changes of relative signaling pathway in epidermoid carcinoma cell line A431].
  • OBJECTIVE: To study the effects of Acitretin on growth inhibition and apoptosis of epidermoid carcinoma cell line A431 and its molecular mechanisms.
  • The inhibition of cell growth was determined by MTT method, morphological changes were observed by electron microscopy, apoptosis was assessed by flow cytometry and Annexin-V staining.
  • Morphological changes revealed characteristics of cell apoptosis.
  • CONCLUSION: (1)Acitretin plays an inhibitory role in the tumor cell growth and induces the cell apoptosis in A431 cells. (2)The regulation of the Jak/STAT3 signaling pathway may play an important role in inducing growth inhibition and apoptosis by Acitretin in A431 cells.
  • [MeSH-major] Acitretin / pharmacology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Carcinoma, Squamous Cell / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Cell Line, Tumor. Humans. Signal Transduction / drug effects

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  • (PMID = 16610086.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; LCH760E9T7 / Acitretin
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28. Pruijn FB, Sturman JR, Liyanage HD, Hicks KO, Hay MP, Wilson WR: Extravascular transport of drugs in tumor tissue: effect of lipophilicity on diffusion of tirapazamine analogues in multicellular layer cultures. J Med Chem; 2005 Feb 24;48(4):1079-87
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  • [Title] Extravascular transport of drugs in tumor tissue: effect of lipophilicity on diffusion of tirapazamine analogues in multicellular layer cultures.
  • The extravascular diffusion of antitumor agents is a key determinant of their therapeutic activity, but the relationships between physicochemical properties of drugs and their extravascular transport are poorly understood.
  • It is well-known that drug lipophilicity plays an important role in transport across biological membranes, but the net effect of lipophilicity on transport through multiple layers of tumor cells is less clear.
  • This study examines the influence of lipophilicity (measured as the octanol-water partition coefficient P) on the extravascular transport properties of the hypoxic cytotoxin tirapazamine (TPZ, 1) and a series of 13 neutral analogues, using multicellular layers (MCLs) of HT29 human colon carcinoma cells as an in vitro model for the extravascular compartment of tumors.
  • Flux of drugs across MCLs was determined using diffusion chambers, with the concentration-time profile on both sides of the MCL measured by HPLC.
  • Correcting for M(r) differences, lipophilic compounds (log P > 1.5) had ca.
  • Using a pharmacokinetic/pharmacodynamic (PK/PD) model in which diffusion in the extravascular compartment of tumors is considered explicitly, we demonstrated that hypoxic cell kill is very sensitive to changes in extravascular diffusion coefficient of TPZ analogues within this range.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Triazines / pharmacokinetics
  • [MeSH-minor] Biological Transport. Diffusion. HT29 Cells. Humans. Models, Biological. Solubility

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  • (PMID = 15715475.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA82566
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Triazines; 1UD32YR59G / tirapazamine
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29. Ma WW, Jimeno A: Temsirolimus. Drugs Today (Barc); 2007 Oct;43(10):659-69
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  • Temsirolimus (CCI-779), a small molecule inhibitor of mTOR protein, is a water-soluble synthetic rapamycin ester that has been developed in both oral and intravenous (i.v.) formulations.
  • Inhibition of mTOR protein abrogates pathway-mediated cellular transcription and translation, leading to cell cycle arrest, antiangiogenesis and apoptosis.
  • The drug has significant in vitro antitumor effect against a number of cancer cell lines and has demonstrated in vivo cytostatic activity in xenograft models.
  • Biological activity was observed at all these doses.
  • However, the frequency and intensity of the toxicities increased at higher doses and more high-dose patients had to reduce the dose or discontinue the drug.
  • Temsirolimus is farther along in clinical development than any other mTOR inhibitor in its class and has demonstrated significant activity in patients with poor-risk clear-cell renal cell carcinoma.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Neoplasms / drug therapy. Sirolimus / analogs & derivatives
  • [MeSH-minor] Carcinoma, Renal Cell / drug therapy. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Clinical Trials, Phase III as Topic. Drug Delivery Systems. Humans. Protein Kinases / drug effects. Protein Kinases / metabolism. TOR Serine-Threonine Kinases

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  • [Copyright] 2007 Prous Science
  • (PMID = 17987219.001).
  • [ISSN] 1699-3993
  • [Journal-full-title] Drugs of today (Barcelona, Spain : 1998)
  • [ISO-abbreviation] Drugs Today
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  • [Number-of-references] 83
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