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1. Hard GC, Seely JC, Kissling GE, Betz LJ: Spontaneous occurrence of a distinctive renal tubule tumor phenotype in rat carcinogenicity studies conducted by the national toxicology program. Toxicol Pathol; 2008 Apr;36(3):388-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spontaneous occurrence of a distinctive renal tubule tumor phenotype in rat carcinogenicity studies conducted by the national toxicology program.
  • The Toxicology Data Management System (TDMS) of the National Toxicology Program, National Institutes of Environmental Health Sciences, National Institutes of Health, was surveyed for occurrence and distribution of a distinctive renal tubule tumor type in rats.
  • It is referred to here as the amphophilic-vacuolar (AV) variant of renal tubule tumor.
  • Of 154 studies in which renal tubule tumors had been recorded in the standard single sections of kidney in the TDMS, there were collectively 1012 rats with renal adenomas, carcinomas, or adenocarcinomas, and of these, 100 displayed the distinctive AV morphology, representing 74 studies involving mostly the F344 rat, but also the Sprague-Dawley and Wistar strains.
  • The distribution of this renal tumor type was random across studies and dose groups, underscoring the likelihood that it was of spontaneous origin and not chemically induced.
  • Accordingly, it is suggested that this distinctive renal tumor phenotype be recorded as a separate category from conventional RTT when assessing the carcinogenic potential of a test compound.

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  • [Cites] Jpn J Cancer Res. 2000 Nov;91(11):1096-9 [11092972.001]
  • [Cites] Toxicol Pathol. 2007 Jun;35(4):589-93 [17654399.001]
  • [Cites] Jpn J Cancer Res. 2001 Nov;92(11):1147-9 [11714437.001]
  • [Cites] Toxicol Sci. 2002 Sep;69(1):30-41 [12215658.001]
  • [Cites] Cancer Sci. 2003 Feb;94(2):142-7 [12708488.001]
  • [Cites] Toxicol Pathol. 2004 Mar-Apr;32(2):171-80 [15200155.001]
  • [Cites] Crit Rev Toxicol. 2004 May-Jun;34(3):211-99 [15239388.001]
  • [Cites] Carcinogenesis. 1984 Aug;5(8):1047-50 [6744513.001]
  • [Cites] Toxicol Pathol. 1986;14(1):112-22 [3012758.001]
  • [Cites] J Urol. 1992 Dec;148(6):1932-6 [1433648.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11413-6 [7972075.001]
  • [Cites] Toxicol Pathol. 1994 Sep-Oct;22(5):489-96 [7899777.001]
  • [Cites] Nat Genet. 1995 Jan;9(1):70-4 [7704028.001]
  • [Cites] World J Urol. 1995;13(3):153-8 [7550386.001]
  • [Cites] Vet Pathol. 1995 Jul;32(4):419-22 [7483218.001]
  • [Cites] Prog Exp Tumor Res. 1999;35:95-108 [10377754.001]
  • [Cites] Toxicol Pathol. 2005;33(6):641-9 [16207638.001]
  • [Cites] Virchows Arch. 2006 Apr;448(4):463-71 [16447066.001]
  • [Cites] Food Chem Toxicol. 2007 Apr;45(4):600-8 [17156907.001]
  • [Cites] Toxicol Pathol. 2007 Feb;35(2):233-41 [17366317.001]
  • [Cites] Toxicol Pathol. 2001 May-Jun;29(3):379-86 [11442024.001]
  • (PMID = 18441261.001).
  • [ISSN] 1533-1601
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / N01ES95435; United States / Intramural NIH HHS / / ZIA ES045003-13; United States / NIEHS NIH HHS / ES / N01-ES-95435
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS143842; NLM/ PMC2905801
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2. Kokubo T, Kakinuma S, Kobayashi T, Watanabe F, Iritani R, Tateno K, Nishimura M, Nishikawa T, Hino O, Shimada Y: Age dependence of radiation-induced renal cell carcinomas in an Eker rat model. Cancer Sci; 2010 Mar;101(3):616-23
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  • [Title] Age dependence of radiation-induced renal cell carcinomas in an Eker rat model.
  • Toward this goal, we assessed the risk of developing renal cell carcinoma using Eker rats as a kidney tumor model.
  • In contrast, development of adenoma and adenocarcinoma were evident in animals irradiated at perinatal ages, being maximal at gestational day 19.
  • In conclusion, actively growing kidneys in perinatal-aged (F344 x Eker) F1 rats (Tsc2(+/-)) are at risk for radiation-induced malignant transformation of the renal epithelium associated with mTOR activation.
  • [MeSH-major] Carcinoma, Renal Cell / etiology. Kidney Neoplasms / etiology. Neoplasms, Radiation-Induced / etiology. Tumor Suppressor Proteins / genetics

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  • (PMID = 20132221.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Tumor Suppressor Proteins; 4JG2LF96VF / tuberous sclerosis complex 2 protein; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, rat; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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3. National Toxicology Program: NTP technical report on the toxicology and carcinogenesis studies of 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) (CAS No. 35065-27-1) in female Harlan Sprague-Dawley rats (Gavage studies). Natl Toxicol Program Tech Rep Ser; 2006 May;(529):4-168
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  • The dioxin TEF evaluation includes conducting multiple 2-year rat bioassays to evaluate the relative chronic toxicity and carcinogenicity of DLCs, structurally related PCBs, and mixtures of these compounds.
  • Absolute kidney weights of all exposed groups and the relative kidney weight of 3,000 microg/kg rats were significantly increased at week 53.
  • A single hepatocellular adenoma was observed in the 3,000 microg/kg core study group.
  • [MeSH-minor] Adenoma, Bile Duct / chemically induced. Adenoma, Bile Duct / pathology. Administration, Oral. Animals. Bile Duct Neoplasms / chemically induced. Bile Duct Neoplasms / pathology. Cell Enlargement / drug effects. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Female. Hepatocytes / drug effects. Hepatocytes / pathology. Liver / drug effects. Liver / pathology. Organ Size / drug effects. Rats. Rats, Sprague-Dawley. Thyroid Hormones / blood. Toxicity Tests

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  • (PMID = 16835634.001).
  • [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; 0 / Thyroid Hormones; DFC2HB4I0K / Polychlorinated Biphenyls; ZRU0C9E32O / 2,4,5,2',4',5'-hexachlorobiphenyl
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4. Tsuji A, Kikuchi Y, Sato Y, Koide S, Yuasa K, Nagahama M, Matsuda Y: A proteomic approach reveals transient association of reticulocalbin-3, a novel member of the CREC family, with the precursor of subtilisin-like proprotein convertase, PACE4. Biochem J; 2006 May 15;396(1):51-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adenoma / pathology. Amino Acid Sequence. Animals. COS Cells. Cell Line. Cell Line, Tumor / metabolism. Cercopithecus aethiops. Enzyme Activation. Furin / antagonists & inhibitors. Humans. Kidney / cytology. Molecular Sequence Data. Neoplasm Proteins / metabolism. Pituitary Neoplasms / pathology. Proprotein Convertase 5 / antagonists & inhibitors. Proprotein Convertases. Protein Binding. Proteomics. Rats. Recombinant Fusion Proteins / metabolism. Sequence Alignment. Sequence Homology, Amino Acid. Transfection. alpha 1-Antitrypsin / chemistry. alpha 1-Antitrypsin / genetics. alpha 1-Antitrypsin / metabolism

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  • [Cites] Nat Rev Mol Cell Biol. 2002 Oct;3(10):753-66 [12360192.001]
  • [Cites] Biochem J. 1999 Dec 1;344 Pt 2:281-92 [10567207.001]
  • [Cites] J Biol Chem. 1975 May 25;250(10):4007-21 [236308.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Ann N Y Acad Sci. 1980;356:14-9 [6940493.001]
  • [Cites] Science. 1989 Oct 27;246(4929):482-6 [2683070.001]
  • [Cites] Electrophoresis. 1989 Nov;10(11):785-92 [2612479.001]
  • [Cites] J Biol Chem. 1990 Feb 25;265(6):2997-3000 [2154467.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Jan 15;88(2):340-4 [1988934.001]
  • [Cites] DNA Cell Biol. 1991 Dec;10(10):757-69 [1741956.001]
  • [Cites] J Biol Chem. 1992 Mar 25;267(9):5897-900 [1372895.001]
  • [Cites] J Biol Chem. 1993 Jan 5;268(1):699-705 [8416973.001]
  • [Cites] Exp Cell Res. 1993 Mar;205(1):101-10 [8453984.001]
  • [Cites] J Biochem. 1993 Feb;113(2):132-5 [8468318.001]
  • [Cites] Biochem J. 1994 Apr 1;299 ( Pt 1):1-18 [8166626.001]
  • [Cites] Cell. 1994 Jul 29;78(2):263-73 [7913882.001]
  • [Cites] Biochimie. 1994;76(3-4):217-25 [7819326.001]
  • [Cites] Cancer Res. 1996 Feb 1;56(3):448-51 [8564950.001]
  • [Cites] Biochem J. 1996 Mar 15;314 ( Pt 3):727-31 [8615762.001]
  • [Cites] J Biochem. 1996 Jul;120(1):29-34 [8864840.001]
  • [Cites] FEBS Lett. 1997 Feb 3;402(2-3):145-50 [9037184.001]
  • [Cites] EMBO J. 1997 Apr 1;16(7):1508-18 [9130696.001]
  • [Cites] J Biochem. 1997 May;121(5):941-8 [9192737.001]
  • [Cites] Biochem J. 1997 Nov 1;327 ( Pt 3):625-35 [9599222.001]
  • [Cites] FEBS Lett. 1998 Aug 28;434(1-2):155-9 [9738469.001]
  • [Cites] J Cell Biol. 1998 Nov 2;143(3):601-12 [9813083.001]
  • [Cites] J Biochem. 1999 Mar;125(3):627-33 [10050053.001]
  • [Cites] FEBS Lett. 2000 Jan 21;466(1):11-8 [10648803.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Jan 18;290(2):878-84 [11785985.001]
  • [Cites] Protein Eng. 2002 Feb;15(2):123-30 [11917148.001]
  • [Cites] J Biol Chem. 2002 Apr 12;277(15):12879-90 [11799113.001]
  • [Cites] Nature. 1970 Aug 15;227(5259):680-5 [5432063.001]
  • (PMID = 16433634.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Neoplasm Proteins; 0 / Protein Precursors; 0 / RCN3 protein, human; 0 / Recombinant Fusion Proteins; 0 / alpha 1-Antitrypsin; EC 3.4.- / Proprotein Convertases; EC 3.4.21.- / PCSK6 protein, human; EC 3.4.21.- / Pcsk6 protein, rat; EC 3.4.21.- / Proprotein Convertase 5; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.50 / lysyl endopeptidase; EC 3.4.21.75 / Furin
  • [Other-IDs] NLM/ PMC1449992
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5. Barmeyer C, Ye JH, Sidani S, Geibel J, Binder HJ, Rajendran VM: Characteristics of rat downregulated in adenoma (rDRA) expressed in HEK 293 cells. Pflugers Arch; 2007 Jun;454(3):441-50
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  • [Title] Characteristics of rat downregulated in adenoma (rDRA) expressed in HEK 293 cells.
  • Studies with apical membrane vesicles have shown that two distinct and separate anion exchange processes are present in rat distal colon, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS)-sensitive CL(-)-HCO(3)(-) exchange, and DIDS-resistant Cl(-)-OH(-) exchange.
  • These studies proposed that anion exchanger (AE)-1 isoform encodes the former as both apical membrane DIDS-sensitive CL(-)-HCO(3)(-) exchange, and AE1 specific mRNA are present only in surface cells and are downregulated in Na-depleted rats, whereas downregulated in adenoma (DRA) encodes the latter as both DIDS-resistant Cl(-)-OH(-) exchange, and DRA-specific proteins are present in apical membranes of both surface and crypt cells and are not altered in Na(+)-depleted rats.
  • Studies were, therefore, initiated to identify the function of rat DRA (rDRA) in vitro. rDRA cDNA isolated from rat distal colon encodes a 757-amino-acid protein which has 96 and 81% homology with mDRA and hDRA, respectively. rDRA-specific mRNA expression was detectable only in specific segments of the digestive tract (duodenum, ileum, cecum, proximal colon, and distal colon) but not in the stomach, jejunum, or in the kidney, brain, heart, and lung.
  • Our observations that rDRA mediates DIDS-insensitive, acid pH-dependent Cl(-) uptake are consistent with prior observations that rDRA does not mediate DIDS-sensitive Cl(-)-HCO(3)(-) exchange in rat distal colon.

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  • (PMID = 17492310.001).
  • [ISSN] 0031-6768
  • [Journal-full-title] Pflügers Archiv : European journal of physiology
  • [ISO-abbreviation] Pflugers Arch.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AF337809
  • [Grant] United States / NIDDK NIH HHS / DK / DK60069; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antiporters; 0 / Bicarbonates; 0 / Chlorides; 0 / DNA Primers; 0 / Fatty Acids, Volatile; 0 / Recombinant Proteins; 0 / Slc26a3 protein, rat; Q1O6DSW23R / 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
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6. National Toxicology Program: Toxicology and carcinogenesis studies of methyl isobutyl ketone (Cas No. 108-10-1) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2007 Feb;(538):1-236
Hazardous Substances Data Bank. 2-HEXANONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the standard evaluation of the kidney, there were slightly increased incidences of renal tubule adenoma and renal tubule adenoma or carcinoma (combined) in males exposed to 900 or 1,800 ppm, and renal tubule carcinoma in males exposed to 1,800 ppm.
  • The incidences of renal tubule hyperplasia were also significantly increased in the 450 and 1,800 ppm males, and the severities were greater than in the chamber controls.
  • The incidences of transitional epithelial hyperplasia of the renal pelvis in males exposed to 900 or 1,800 ppm and mineralization of the renal papilla in all groups of exposed males were significantly increased.
  • In addition, two female rats exposed to 1,800 ppm had renal mesenchymal tumors.
  • In the extended evaluation of the kidney, renal tubule adenomas and renal tubule hyperplasia occurred in all groups of exposed male rats.
  • In the combined single and step section analysis, the incidences of renal tubule adenoma and renal tubule adenoma or carcinoma (combined) were significantly increased in males exposed to 1,800 ppm.
  • The incidences of renal tubule hyperplasia were also significantly increased in all exposed groups of males.
  • The incidences of hepatocellular adenoma and hepatocellular adenoma or carcinoma (combined) were significantly increased in males and females exposed to 1,800 ppm.
  • GENETIC TOXICOLOGY: Methyl isobutyl ketone was not mutagenic in Salmonella typhimurium strains TA97, TA98, TA100, or TA1535 when tested with and without hamster or rat liver metabolic activation enzymes.
  • CONCLUSIONS: Under the conditions of these 2-year studies, there was some evidence of carcinogenic activity of methyl isobutyl ketone in male F344/N rats based on increased incidences of renal tubule neoplasms.
  • There was equivocal evidence of carcinogenic activity of methyl isobutyl ketone in female F344/N rats based on the occurrence of renal mesenchymal tumors in the 1,800 ppm group.
  • Exposure to methyl isobutyl ketone resulted in nonneoplastic lesions of the kidney characteristic of alpha2u-globulin accumulation in male rats and nephropathy in female rats.
  • [MeSH-minor] Administration, Oral. Adrenal Glands / drug effects. Animals. Body Weight / drug effects. Female. Kidney / drug effects. Kidney / pathology. Kidney Neoplasms / chemically induced. Kidney Neoplasms / pathology. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / pathology. Liver / drug effects. Liver / pathology. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Lung Neoplasms / chemically induced. Lung Neoplasms / pathology. Male. Mice. Mice, Inbred Strains. Occupational Exposure. Rats. Rats, Inbred F344. Water Supply

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  • (PMID = 17557116.001).
  • [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; 0 / Environmental Pollutants; 0 / Solvents; 6QDY60NH6N / Methyl n-Butyl Ketone; U5T7B88CNP / methyl isobutyl ketone
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7. National Toxicology Program: NTP toxicology and carcinogenesis studies of decalin (CAS No. 91-17-8) in F344/N rats and B6C3F(1) mice and a toxicology study of decalin in male NBR rats (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2005 Jan;(513):1-316
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  • Male NBR rats do not produce alpha2u-globulin; the NBR rats were included to study the relationship of alpha2u-globulin and renal lesion induction.
  • Renal toxicity studies were performed in male F344/N and NBR rats.
  • The numbers of labeled cells and the labeling indices in the left kidney of 200 and 400 ppm F344/N male rats were significantly greater than those in the chamber controls.
  • Kidney weights of male F344/N rats exposed to 50 ppm or greater were significantly increased.
  • Exposure-related hyaline droplet accumulation, degeneration and regeneration of renal cortical tubules, and granular casts occurred in the kidney of exposed F344/N male rats.
  • 3-MONTH STUDY IN RATS: Groups of 25 male and 20 female F344/N rats were exposed to 0, 25, 50, 100, 200, or 400 ppm decalin vapor 6 hours per day, 5 days per week for 2 (five male renal toxicity rats), 6 (10 male and 10 female clinical pathology rats), or 14 (10 core study rats) weeks.
  • Urinalysis results indicated that decalin exposure caused increases in urine glucose and protein concentrations and enzyme activities that were consistent with the renal lesions observed microscopically.
  • Renal toxicity studies were performed on rats sacrificed at 2 and 6 weeks and at the end of the study.
  • In kidney tissue examined for cell proliferation, the numbers of PCNA-labeled cells and labeling indices were generally significantly greater than those of the chamber controls in exposed groups of rats at all three time points.
  • Concentrations of alpha2u-globulin in the kidney as well as the alpha2u-globulin/soluble protein ratios were significantly increased at week 2 in all exposed groups and in the 200 and 400 ppm groups at week 6 and at the end of the study.
  • Absolute and/or relative kidney and liver weights of male rats exposed to 50 ppm or greater were increased.
  • Incidences of renal tubule regeneration and granular casts in the medulla of the kidney in exposed male rats were increased, and the severities of hyaline droplets generally increased with increasing exposure concentration.
  • Incidences of renal tubule adenoma and adenoma or carcinoma (combined) and of benign or malignant pheochromocytoma (combined) of the adrenal medulla in 100 and 400 ppm males were significantly increased.
  • Nonneoplastic lesions related to decalin exposure occurred in the kidney of male rats.
  • GENETIC TOXICOLOGY: Decalin was not mutagenic in S. typhimurium strains TA97, TA98, TA100, or TA1535, with or without induced hamster or rat liver S9 enzymes.
  • CONCLUSIONS: Under the conditions of these studies, there was clear evidence of carcinogenic activity of decalin in male F344/N rats based on increased incidences of renal tubule neoplasms.
  • Exposure of male rats to decalin resulted in nonneoplastic lesions of the kidney characteristic of alpha2u-globulin accumulation.
  • [MeSH-minor] Administration, Inhalation. Animal Feed / analysis. Animals. Atmosphere Exposure Chambers. Body Weight / drug effects. Female. Genitalia, Male / pathology. Kidney Diseases / chemically induced. Kidney Diseases / pathology. Male. Mice. Mice, Inbred Strains. Mutagens / toxicity. Organ Size / drug effects. Rats. Rats, Inbred F344. Reproduction / drug effects

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  • (PMID = 15891779.001).
  • [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; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mutagens; 0 / Naphthalenes; 88451Q4XYF / decalin
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8. Toxicology and carcinogenesis studies of benzophenone (CAS No. 119-61-9) in F344/N rats and B6C3F1 mice (feed studies). Natl Toxicol Program Tech Rep Ser; 2006 Feb;(533):1-264
Hazardous Substances Data Bank. BENZOPHENONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There was a positive trend in the incidences of renal tubule adenoma in males, and the incidences in 625 and 1,250 ppm males exceeded the historical control range for all routes; these neoplasms were accompanied by significantly increased incidences of renal tubule hyperplasia.
  • Due to these findings, additional kidney sections were evaluated; results indicated additional renal tubule adenomas in all groups of males and renal tubule hyperplasia in all groups of males and females.
  • In male mice, there were significantly increased incidences of hepatocellular adenoma in the 625 and 1,250 ppm groups, and these incidences exceeded the historical control range.
  • In female mice, the incidences of hepatocellular adenoma in the 625 and 1,250 ppm groups were higher than expected after adjusting for the lower body weights in these groups.
  • The incidences of kidney nephropathy and mineralization in exposed groups of females and the severity of nephropathy in exposed groups of males were significantly increased.
  • GENETIC TOXICOLOGY: Benzophenone was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537, with or without hamster or rat liver activation enzymes.
  • CONCLUSIONS: Under the conditions of these 2-year studies, there was some evidence of carcinogenic activity of benzophenone in male F344/N rats based on increased incidences of renal tubule adenoma; mononuclear cell leukemia in male F344/N rats may have been related to benzophenone exposure.
  • There was some evidence of carcinogenic activity of benzophenone in male B6C3F1 mice based on increased incidences of hepatocellular neoplasms, primarily adenoma.
  • There was some evidence of carcinogenic activity of benzophenone in female B6C3F1 mice based on increased incidences of histiocytic sarcoma; the incidences of hepatocellular adenoma in female B6C3F1 mice may have been related to benzophenone exposure.
  • Administration of benzophenone in feed resulted in increased incidences and/or severities of nonneoplastic lesions in the kidney and liver of male and female rats and in the liver, kidney, nose, and spleen of male and female mice.
  • [MeSH-minor] Animals. Body Weight / drug effects. Carcinogenicity Tests. Dose-Response Relationship, Drug. Female. Histiocytic Disorders, Malignant / chemically induced. Histiocytic Disorders, Malignant / pathology. Kidney Neoplasms / chemically induced. Kidney Neoplasms / pathology. Leukemia / chemically induced. Leukemia / pathology. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Longevity / drug effects. Male. Mice. Mice, Inbred C57BL. Mutagenicity Tests. Rats. Rats, Inbred F344. Sarcoma / chemically induced. Sarcoma / pathology. Toxicity Tests, Chronic

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  • (PMID = 16741556.001).
  • [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 / Benzophenones; 0 / Photosensitizing Agents; 701M4TTV9O / benzophenone
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9. Hard GC, Seely JC, Betz LJ, Hayashi SM: Re-evaluation of the kidney tumors and renal histopathology occurring in a 2-year rat carcinogenicity bioassay of quercetin. Food Chem Toxicol; 2007 Apr;45(4):600-8
Hazardous Substances Data Bank. QUERCETIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Re-evaluation of the kidney tumors and renal histopathology occurring in a 2-year rat carcinogenicity bioassay of quercetin.
  • Renal histopathology in the most recent 2-year carcinogenicity bioassay of quercetin, in Fischer 344 rats, was re-evaluated in an attempt to determine a mode of action underlying a small increase in renal tubule tumors reported in the males ().
  • The re-evaluation confirmed the reported increase in renal tumors in mid- and high-dose males, including a single carcinoma in a high-dose male, as well as an exacerbation of spontaneous, chronic progressive nephropathy (CPN) in male rats only.
  • The re-evaluation also showed that there were no cellular alterations in the kidney indicative of chemical toxicity at 6 months, 15 months, or 2 years.
  • This mode of action represents a secondary mechanism for renal tumor development, with no relevance for extrapolation to humans.
  • In addition, the single carcinoma present in the high-dose males, along with 4 other lesions ranging from ATH to adenoma in male and female groups, were considered to have a unique phenotype associated previously with neoplasms of spontaneous and familial origin.
  • [MeSH-major] Carcinogenicity Tests. Kidney / drug effects. Kidney Neoplasms / chemically induced. Quercetin / toxicity
  • [MeSH-minor] Animals. Female. Hyperplasia. Kidney Tubules / drug effects. Kidney Tubules / pathology. Male. Rats. Rats, Inbred F344

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  • (PMID = 17156907.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / 1-ES-95435
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 9IKM0I5T1E / Quercetin
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10. Inoue K, Yoshida M, Takahashi M, Shibutani M, Takagi H, Hirose M, Nishikawa A: Induction of kidney and liver cancers by the natural food additive madder color in a two-year rat carcinogenicity study. Food Chem Toxicol; 2009 Jan;47(1):184-91
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  • [Title] Induction of kidney and liver cancers by the natural food additive madder color in a two-year rat carcinogenicity study.
  • Our previous studies revealed MC to have obvious subchronic and chronic toxicity and potent carcinogenicity targeting rat liver and kidney.
  • Histopathologically, karyomegaly and atypical tubules/hyperplasias, as well as renal cell adenomas and carcinomas were significantly increased in treated groups of both sexes with dose-dependence.
  • These data provide clear evidence that MC exerts unequivocal carcinogenicity against renal tubule cells and hepatocytes in rats.
  • [MeSH-major] Food Additives / toxicity. Kidney Neoplasms / chemically induced. Liver Neoplasms / chemically induced. Plant Extracts / toxicity. Rubia / toxicity
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / pathology. Animals. Carcinoma / chemically induced. Carcinoma / pathology. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Kidney / pathology. Liver / pathology. Lymph Nodes / pathology. Male. Rats. Rats, Inbred F344. Sex Characteristics

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  • [ErratumIn] Food Chem Toxicol. 2009 Jun;47(6):1400
  • (PMID = 19032970.001).
  • [ISSN] 1873-6351
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Food Additives; 0 / Plant Extracts; 0 / madder color
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11. Inoue K, Shibutani M, Masutomi N, Toyoda K, Takagi H, Takahashi M, Fujimoto H, Hirose M, Nishikawa A: One-year chronic toxicity of madder color in F344 rats--induction of preneoplastic/neoplastic lesions in the kidney and liver. Food Chem Toxicol; 2008 Oct;46(10):3303-10
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  • [Title] One-year chronic toxicity of madder color in F344 rats--induction of preneoplastic/neoplastic lesions in the kidney and liver.
  • Relative weights of the liver were significantly increased from 1.0% in both sexes, and those of the kidney were significantly increased from 1.0% in males and from 0.2% in females.
  • Histopathologically, atypical renal tubule hyperplasias were increased at 1.0% or higher in both sexes in association with increase of cell proliferative activity in the tubules.
  • A renal cell adenoma was observed in a male rat receiving 5.0% MC.
  • These results indicate that MC has chronic toxicity targeting kidney, liver and blood cells.
  • Moreover, the results strongly suggest that MC may have the carcinogenic potential in the kidney and the liver.
  • [MeSH-major] Kidney Neoplasms / chemically induced. Liver Neoplasms / chemically induced. Plant Extracts / administration & dosage. Plant Extracts / toxicity. Precancerous Conditions / chemically induced. Rubia / toxicity
  • [MeSH-minor] Animals. Cell Proliferation. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Kidney / cytology. Male. Rats. Rats, Inbred F344. Toxicity Tests, Chronic

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  • (PMID = 18723070.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / madder color
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12. Kouchi M, Okimoto K, Matsumoto I, Tanaka K, Yasuba M, Hino O: Natural history of the Nihon (Bhd gene mutant) rat, a novel model for human Birt-Hogg-Dubé syndrome. Virchows Arch; 2006 Apr;448(4):463-71
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  • [Title] Natural history of the Nihon (Bhd gene mutant) rat, a novel model for human Birt-Hogg-Dubé syndrome.
  • In the Nihon rat, an established model of hereditary renal cell carcinoma (RCC), the propensity for tumor development, is inherited as an autosomal dominant trait due to a single germline nucleotide insertion mutation in the rat Bhd ortholog.
  • The Birt-Hogg-Dubé (BHD) syndrome is a rare autosomal dominant disease characterized by fibrofolliculoma, pulmonary cysts, spontaneous pneumothorax, and renal neoplasm.
  • The renal lesions of the Nihon rat are characterized, and extrarenal lesions are also described in this work.
  • The earliest lesion of the RCC was identified as an altered tubule at as early as 3 weeks of age and rapidly progressed through adenoma to carcinoma with the primary cell type being clear/acidophilic where some similarities were evident to RCCs in BHD syndrome.
  • The Nihon rats demonstrate a heterotopic ossification within RCCs and three extrarenal lesions, clear cell hyperplasia/adenoma of the endometrium, clear cell change of the epithelium of striated portions of salivary glands, and cardiac rhabdomyomatosis.
  • This rat model of hereditary RCC provides a useful tool for analyzing the series of events leading to renal tumorigenesis and for studying BHD gene functions.
  • [MeSH-major] Carcinoma, Renal Cell / pathology. Disease Models, Animal. Genetic Diseases, Inborn / genetics. Germ-Line Mutation / genetics. Kidney Neoplasms / pathology. Proteins / genetics
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Animals. Blood Chemical Analysis. Body Weight / physiology. Endometrial Hyperplasia / genetics. Endometrial Hyperplasia / pathology. Endometrial Neoplasms / genetics. Endometrial Neoplasms / pathology. Female. Heart Neoplasms / genetics. Heart Neoplasms / pathology. Hematologic Tests. Humans. Male. Phenotype. Rats. Rats, Mutant Strains. Rhabdomyoma / genetics. Rhabdomyoma / pathology. Salivary Glands / pathology

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  • (PMID = 16447066.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Flcn protein, rat; 0 / Proteins
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13. Hard GC, Seely JC: Recommendations for the interpretation of renal tubule proliferative lesions occurring in rat kidneys with advanced chronic progressive nephropathy (CPN). Toxicol Pathol; 2005;33(6):641-9
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  • [Title] Recommendations for the interpretation of renal tubule proliferative lesions occurring in rat kidneys with advanced chronic progressive nephropathy (CPN).
  • Several proliferative lesions were identified as common in advanced CPN with no apparent evidence supporting a role in renal tubule carcinogenesis.
  • Criteria were developed to distinguish these CPN-associated lesions from atypical tubule hyperplasia, a precursor of adenoma, both of which were also represented in this survey of advanced CPN.
  • [MeSH-major] Adenoma / diagnosis. Aging / pathology. Carcinogens / toxicity. Kidney Diseases / diagnosis. Kidney Neoplasms / diagnosis. Kidney Tubules / pathology. Precancerous Conditions / diagnosis

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  • (PMID = 16207638.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens
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14. Mattioli F, Martelli A, Gosmar M, Garbero C, Manfredi V, Varaldo E, Torre GC, Brambilla G: DNA fragmentation and DNA repair synthesis induced in rat and human thyroid cells by chemicals carcinogenic to the rat thyroid. Mutat Res; 2006 Oct 30;609(2):146-53
Hazardous Substances Data Bank. NITROBENZENE .

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  • [Title] DNA fragmentation and DNA repair synthesis induced in rat and human thyroid cells by chemicals carcinogenic to the rat thyroid.
  • [MeSH-minor] Adenocarcinoma, Follicular / chemically induced. Adenoma / chemically induced. Animals. Bromates / toxicity. Cells, Cultured. DNA Damage. Ethylenethiourea / toxicity. Humans. In Vitro Techniques. Kidney / drug effects. Kidney / metabolism. Liver / drug effects. Liver / metabolism. Male. Methimazole / toxicity. Nitrobenzenes / toxicity. Rats. Rats, Sprague-Dawley. Thiourea / analogs & derivatives. Thiourea / toxicity. Thyroid Neoplasms / chemically induced

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  • (PMID = 16942904.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Bromates; 0 / Carcinogens; 0 / Nitrobenzenes; 04MB35W6ZA / potassium bromate; 24FOJ4N18S / Ethylenethiourea; 26914-14-7 / diethylthiourea; 554Z48XN5E / Methimazole; E57JCN6SSY / nitrobenzene; GYV9AM2QAG / Thiourea
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15. Brown AL, Odell EW, Mantle PG: DNA ploidy distribution in renal tumours induced in male rats by dietary ochratoxin A. Exp Toxicol Pathol; 2007 Oct;59(2):85-95
Hazardous Substances Data Bank. OCHRATOXIN A .

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  • [Title] DNA ploidy distribution in renal tumours induced in male rats by dietary ochratoxin A.
  • DNA ploidy distribution, measured in experimental renal tumours that occurred in twelve ageing male Fischer rats derived from carcinogenicity experiments on ochratoxin A (OTA) in response to chronic dietary exposure, was diploid in all renal adenomas and aneuploid in all carcinomas, correlating with their typical organised and disorganised histopathology, respectively.
  • Aneuploidy was also detected in renal tissue in which karyomegaly, induced by OTA, was analogous to that caused by the fungus Penicillium polonicum.
  • Thus, the experimental rat renal carcinoma could arise within an adenoma directly from certain persistent karyomegalic tubular epithelial cells long after their particular genetic damage has been caused during a protracted period of OTA insult.
  • [MeSH-major] Adenoma / genetics. Aneuploidy. Carcinogens / toxicity. Carcinoma / genetics. DNA, Neoplasm / genetics. Kidney Neoplasms / genetics. Ochratoxins / toxicity

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  • (PMID = 17629687.001).
  • [ISSN] 0940-2993
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carcinogens; 0 / DNA, Neoplasm; 0 / Ochratoxins; 1779SX6LUY / ochratoxin A
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16. Habib SL: Tuberous sclerosis complex and DNA repair. Adv Exp Med Biol; 2010;685:84-94
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  • Tuberous sclerosis complex (TSC) is an autosomal dominant disorder in humans characterized by the development of hamartomas in several organs, including renal angiomyolipomas, cardiac rhabdomyomas and subependymal giant cell astrocytomas.
  • TSC is associated with hamartomas and renal cell carcinoma (RCC) as well as sporadic tumors in TSC patient.
  • Renal angiomyolipomas associated with TSC tend to be larger, bilateral, multifocal and present at a younger age compared with sporadic forms.
  • Deficiency ofTSC2 in Eker rat is associated with the development of tumors in several organs including kidney.
  • The majority of renal cell tumors observed in the Eker rat originates from renal proximal tubules and are histologically similar to renal cell carcinoma in humans.
  • Moreover, knockout mice in OGG1 developed spontaneously adenoma and carcinoma.
  • We recently show that the constitutive expression of OGG1 in heterozygous (TSC2+/-) Eker rat and in angiomyolipomas kidney tissue from human is 2-3fold less than in kidney from wild-type rats and control human subjects.
  • In addition, we show that loss of TSC2 in kidney tumor of Eker rat is associated with loss of OGG1 and accumulation significant levels of oxidative DNA damage 8-oxo-deoxyguanine suggesting that TSC2 and OGG1 play a major role in renal tumorigenesis.
  • [MeSH-major] Chromosome Disorders. DNA Repair-Deficiency Disorders. Kidney Neoplasms. Tuberous Sclerosis. Tumor Suppressor Proteins
  • [MeSH-minor] Animals. DNA Glycosylases / genetics. DNA Glycosylases / metabolism. DNA Repair / genetics. DNA, Neoplasm / genetics. DNA, Neoplasm / metabolism. Humans. Kidney Tubules, Proximal / metabolism. Kidney Tubules, Proximal / pathology. Mice. Multiprotein Complexes / genetics. Multiprotein Complexes / metabolism. Oxidation-Reduction. Rats

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  • (PMID = 20687497.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Multiprotein Complexes; 0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein; 4JG2LF96VF / tuberous sclerosis complex 2 protein; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / OGG1 protein, rat; EC 3.2.2.- / Ogg1 protein, mouse; EC 3.2.2.- / oxoguanine glycosylase 1, human
  • [Number-of-references] 70
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17. Hall WC, Elder B, Walker CL, Cai SL, Peters DG, Goodman DG, Ulland BM, Borzelleca JF: Spontaneous renal tubular hyperplastic and neoplastic lesions in three Sprague-Dawley rats from a 90-day toxicity study. Toxicol Pathol; 2007 Feb;35(2):233-41
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  • [Title] Spontaneous renal tubular hyperplastic and neoplastic lesions in three Sprague-Dawley rats from a 90-day toxicity study.
  • Multiple renal tubular cell adenomas and atypical tubular hyperplasia were diagnosed in 2 high-dose and 1 mid-dose female Sprague-Dawley (Crl:CD (SD)IGS BR) rats from a 90-day toxicity study of an amino acid found in green tea.
  • The tumors were bilateral multicentric adenomas accompanied by atypical foci of renal tubular hyperplasia in both kidneys of the 3 animals.
  • Toxic tubular changes that typically accompany renal carcinogenesis were not seen in any of the other animals of the study, suggesting rather, an underlying germline mutation of a tumor suppressor gene in these three rats.
  • The histological appearance of these tumors and short latency was reminiscent of the spontaneous lesions reported to arise in Sprague-Dawley rats in the Nihon rat model.
  • Nihon rats develop kidney tumors as a result of a spontaneous mutation in the rat homologue of the Birt-Hogg-Dubé gene (Bhd).
  • Interestingly, rats obtained from two other sources (n = 17) only carried the nt106G-allele, consistent with the published rat sequence for this gene.
  • Taken together, these data suggest that the tumors observed in these animals arose spontaneously as a result of a shared genetic susceptibility leading to the development of renal tubular neoplasms.
  • [MeSH-major] Adenoma / chemically induced. Glutamates / toxicity. Kidney Neoplasms / chemically induced. Kidney Tubules / pathology

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  • (PMID = 17366317.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 63613; United States / NIEHS NIH HHS / ES / ES 07784
  • [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 / Flcn protein, rat; 0 / Glutamates; 0 / Proteins; 8021PR16QO / theanine
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18. Michal M, Hes O, Nemcova J, Sima R, Kuroda N, Bulimbasic S, Franco M, Sakaida N, Danis D, Kazakov DV, Ohe C, Hora M: Renal angiomyoadenomatous tumor: morphologic, immunohistochemical, and molecular genetic study of a distinct entity. Virchows Arch; 2009 Jan;454(1):89-99
The Lens. Cited by Patents in .

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  • [Title] Renal angiomyoadenomatous tumor: morphologic, immunohistochemical, and molecular genetic study of a distinct entity.
  • We present a series of a distinct tumorous entity named renal angiomyoadenomatous tumor (RAT).
  • RAT is a distinct morphologic entity, being different morphologically, immunohistochemically, and genetically from all renal tumors including conventional clear cell carcinoma and mixed epithelial and stromal tumor of kidney.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Kidney Neoplasms / metabolism. Kidney Neoplasms / pathology

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  • [CommentIn] Virchows Arch. 2009 Apr;454(4):479-80 [19205727.001]
  • (PMID = 19020896.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / CAM 5.2 antigen; 0 / Keratin-20; 0 / Keratin-7; 0 / Mucin-1; 0 / Vimentin; 68238-35-7 / Keratins; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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19. National Toxicology Program: Toxicology and carcinogenesis studies of divinylbenzene-HP (Cas No. 1321-74-0) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2006 Nov;(534):1-290
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  • Relative kidney weights of 50 ppm or greater males and relative liver weights of 200 and 400 ppm males were significantly greater than those of the chamber controls.
  • Kidney and liver weights of exposed groups of females were significantly greater than those of the chamber controls.
  • Renal tubule necrosis and regeneration occurred at 200 ppm.
  • Kidney and liver weights of exposed groups of males and of 400 ppm females were generally greater than those of the chamber controls.
  • Exposure to divinylbenzene was associated with necrosis of the liver and kidney in 200 ppm males and females dying early.
  • Renal tubule carcinomas occurred in two of 50 males exposed to 400 ppm in the original kidney sections, an incidence that exceeded the historical control range.
  • In 400 ppm males, the incidence of renal tubule hyperplasia was increased, and the incidence of nephropathy was significantly increased.
  • Following combined analysis of single and step-section data, the incidences of renal tubule adenoma and adenoma or carcinoma (combined) were marginally higher in 200 and 400 ppm males, and the incidence of renal tubule hyperplasia was significantly increased in 400 ppm males.
  • The incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) in 100 ppm males were greater than chamber control incidences, but the incidences of adenoma or carcinoma (combined) were within the historical control range.
  • The incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) in all exposed groups of females were generally greater than those of the chamber controls; the incidences were at the upper end or exceeded the historical control ranges.
  • GENETIC TOXICOLOGY: Divinylbenzene-HP was not mutagenic in any of three independent gene mutation assays using Salmonella typhimurium strains TA97, TA98, TA100, TA1535, or TA1537 or Escherichia coli tester strain WP2 uvrA with or without induced hamster or rat liver enzymes.
  • CONCLUSIONS: Under the conditions of this 2-year inhalation study, there was equivocal evidence of carcinogenic activity of divinylbenzene-HP in male F344/N rats based upon the occurrence of carcinomas in the kidney and glial tumors in the brain.
  • There was equivocal evidence of carcinogenic activity of divinylbenzene-HP in female B6C3F1 mice based on the incidences of alveolar/bronchiolar adenoma or carcinoma (combined) in the lung.
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Female. Inhalation Exposure. Kidney / drug effects. Kidney / pathology. Liver / drug effects. Liver / pathology. Male. Mice. Mice, Inbred Strains. Organ Size / drug effects. Rats. Rats, Inbred F344

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  • (PMID = 17342197.001).
  • [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 / Vinyl Compounds; IZ715T4SBU / divinyl benzene
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20. National Toxicology Program: Toxicology and carcinogenesis studies of alpha-methylstyrene (Cas No. 98-83-9) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2007 Nov;(543):1-210
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  • Kidney weights were significantly increased in 1,000 ppm males and 600 and 1,000 ppm females.
  • The incidences of renal hyaline droplet accumulation were similar between exposed groups and chamber control groups, but the severity of hyaline droplet accumulation in 600 and 1,000 ppm males was greater than in chamber controls.
  • Two 1,000 ppm males and one 300 ppm male had renal tubule carcinomas, and one 300 ppm male had a renal tubule adenoma.
  • Because of the neoplasms observed in 300 and 1,000 ppm males at the end of the 2-year study and the finding of alpha2μ-globulin accumulation in the kidneys at 3 months, which is often associated with kidney neoplasms, additional step sections of kidney were prepared; additional males with focal hyperplasia or adenoma were identified.
  • The incidences of renal tubule adenoma and carcinoma (combined) in the 1,000 ppm males were significantly greater than those in the chamber controls when the single and step sections were combined.
  • The incidence of mineralization of the renal papilla was significantly increased in 1,000 ppm males.
  • The incidences of hepatocellular adenoma or carcinoma (combined) were significantly increased in the 100 and 600 ppm males and in all exposed groups of females.
  • The incidences of hepatocellular adenoma were significantly increased in all exposed groups of females, and the incidences in all exposed groups of males and females exceeded the historical range for chamber controls.
  • GENETIC TOXICOLOGY: alpha-Methylstyrene was not mutagenic in four strains of Salmonella typhimurium, with or without rat or hamster liver metabolic activation enzymes (S9).
  • CONCLUSIONS: Under the conditions of this 2-year inhalation study, there was some evidence of carcinogenic activity of alpha-methylstyrene in male F344/N rats based on increased incidences of renal tubule adenomas and carcinomas (combined).
  • There was equivocal evidence of carcinogenic activity of alpha-methylstyrene in male B6C3F1 mice based on marginally increased incidences of hepatocellular adenoma or carcinoma (combined).
  • Exposure of rats to alpha-methylstyrene resulted in kidney toxicity, which in males exhibited some features of alpha2μ-globulin nephropathy.
  • Exposure to alpha-methylstyrene resulted in nonneoplastic lesions of the nose in male and female rats and mice and of the liver and kidney in female mice.
  • [MeSH-minor] Animals. Body Weight / drug effects. CHO Cells. Cricetinae. Cricetulus. DNA Damage. Female. Inhalation Exposure. Kidney / drug effects. Kidney / pathology. Kidney Neoplasms / chemically induced. Kidney Neoplasms / pathology. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / pathology. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Male. Mice. Mice, Inbred Strains. Micronuclei, Chromosome-Defective / chemically induced. Nose Diseases / chemically induced. Rats. Rats, Inbred F344

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  • (PMID = 18685715.001).
  • [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 / Air Pollutants, Occupational; 0 / Carcinogens; 0 / Mutagens; 0 / Styrenes; 98-83-9 / alpha-methylstyrol
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21. NTP technical report on the toxicology and carcinogenesis studies of 1,2-dibromo-2,4-dicyanobutane (CAS No. 35691-65-7) in F344/N rats and B6C3F1 mice (dermal studies). Natl Toxicol Program Tech Rep Ser; 2010 Jun;(555):1-171
Hazardous Substances Data Bank. 1,2-DIBROMO-2,4-DICYANOBUTANE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The liver and kidney weights of 300 and 600 mg/kg females were significantly increased.
  • The heart weights of 600 and 1,200 mg/kg males and the kidney weights of 150 and 600 mg/kg males were significantly increased.
  • One 2 mg/kg female rat died on day 91.
  • The combined incidence of mammary gland fibroadenoma, adenoma, or adenocarcinoma occurred with a negative trend, and the incidence was significantly decreased in 6 mg/kg female rats.
  • GENETIC TOXICOLOGY: 1,2-Dibromo-2,4-dicyanobutane was not mutagenic in any of several strains of Salmonella typhimurium or Escherichia coli when tested with and without hamster and/or rat liver metabolic activation enzymes (S9).

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  • (PMID = 20725155.001).
  • [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 / Nitriles; YX089CPS05 / 1,2-dibromo-2,4-dicyanobutane
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22. Habib SL: Molecular mechanism of regulation of OGG1: tuberin deficiency results in cytoplasmic redistribution of transcriptional factor NF-YA. J Mol Signal; 2009;4:8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • TSC-2 gene encodes tuberin, a protein involved in the pathogenesis of kidney tumors, both angiomyolipomas and renal cell carcinomas.
  • On the other hand, mice-deficient in the DNA repair enzyme OGG1 spontaneously develop adenoma and carcinoma.
  • In addition, tuberin haploinsufficiency is associated with the loss of OGG1 and accumulation of 8-oxodG in rat kidney tumor.
  • Deficiency in tuberin results in decreased OGG1 and NF-YA protein expression and increased 8-oxodG in kidney tumor from TSC patients.
  • The deficiency of tuberin was associated with a significant decrease in NF-YA and loss of OGG1 in kidney tumors of Eker rat.
  • Downregulation of tuberin by siRNA resulted in a marked decrease in NF-YA and OGG1 protein expression in human renal epithelial cells.
  • This mechanism may be important in the pathogenesis of kidney tumors in patients with TSC disease.

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  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Toxicol Pathol. 2002 Nov-Dec;30(6):675-80 [12512868.001]
  • [Cites] Oncogene. 1998 Jun 11;16(23):3083-6 [9662341.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Nov 9;96(23):13300-5 [10557315.001]
  • [Cites] Biochimie. 2000 Jan;82(1):59-64 [10717388.001]
  • [Cites] Arch Biochem Biophys. 2000 May 1;377(1):1-8 [10775435.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4740-4 [10987279.001]
  • [Cites] Mutat Res. 2000 Oct 16;461(2):109-18 [11018584.001]
  • [Cites] Mol Cancer. 2009;8:1 [19128456.001]
  • [Cites] Carcinogenesis. 2003 Mar;24(3):573-82 [12663520.001]
  • [Cites] J Biol Chem. 2003 Sep 26;278(39):37288-96 [12867426.001]
  • [Cites] Mutat Res. 2003 Oct 29;531(1-2):127-39 [14637250.001]
  • [Cites] J Biol Chem. 2004 Mar 12;279(11):9857-66 [14688259.001]
  • [Cites] J Med Genet. 2004 Jan;41(1):1-5 [14729816.001]
  • [Cites] Am J Physiol Renal Physiol. 2008 Jan;294(1):F281-90 [17989114.001]
  • [Cites] Mol Cancer. 2008;7:10 [18218111.001]
  • [Cites] J Biol Chem. 1995 Jul 7;270(27):16409-14 [7608212.001]
  • (PMID = 20040097.001).
  • [ISSN] 1750-2187
  • [Journal-full-title] Journal of molecular signaling
  • [ISO-abbreviation] J Mol Signal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2807420
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23. National Toxicology Program: Multigenerational reproductive study of genistein (Cas No. 446-72-0) in Sprague-Dawley rats (feed study). Natl Toxicol Program Tech Rep Ser; 2008 Mar;(539):1-266
Hazardous Substances Data Bank. GENISTEIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Because of these concerns, genistein was selected as one of the compounds to be examined in a protocol utilizing Sprague-Dawley rats to evaluate the effects of multigenerational and long-term exposures to doses of estrogenic agents that produce subtle reproductive tract lesions in developmentally exposed Sprague-Dawley rat pups.
  • For this study, 140 animals of each sex were obtained from the NCTR CD (Sprague-Dawley) rat colony at weaning and placed on a soy- and alfalfa-free diet that was used throughout the study in an attempt to maintain consistently low background exposure to phytoestrogens.
  • Exposure-related microscopic lesions were confined to males, with the mammary gland and kidney affected.
  • Statistically significant effects of genistein on the incidences of generally minimal to mild kidney lesions in males were confined to the continuously exposed F(1) and F(2) generations.
  • Incidences of renal tubule mineralization were significantly increased in 100 and 500 ppm males in the F(1) and F(2) generations, and incidences of inflammation and renal tubule regeneration were significantly increased in 500 ppm males in the F(1) generation.
  • [MeSH-minor] Adenocarcinoma / chemically induced. Adenocarcinoma / pathology. Adenoma / chemically induced. Adenoma / pathology. Animals. Female. Male. Mammary Neoplasms, Animal / chemically induced. Mammary Neoplasms, Animal / pathology. Pituitary Neoplasms / chemically induced. Pituitary Neoplasms / pathology. Pregnancy. Rats. Rats, Sprague-Dawley. Recovery of Function. Withholding Treatment

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  • (PMID = 18685713.001).
  • [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 / Carcinogens; 0 / Phytoestrogens; DH2M523P0H / Genistein
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24. Grijelmo C, Rodrigue C, Svrcek M, Bruyneel E, Hendrix A, de Wever O, Gespach C: Proinvasive activity of BMP-7 through SMAD4/src-independent and ERK/Rac/JNK-dependent signaling pathways in colon cancer cells. Cell Signal; 2007 Aug;19(8):1722-32
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The cytokine was identified by immunohistochemistry in surface epithelial cells and crypts in the normal colon mucosa, ACF in sigmoiditis, sporadic high grade dysplastic adenoma, and in 9 of 16 colon carcinomas (56.2%).
  • In addition, the conditioned medium collected from the adenoma PC/AA/C1 and carcinoma HCT8/S11 and SW48 cell lines in culture contained significant levels of BMP-7 ranging from 0.17 to 0.38 ng/ml.
  • We found that BMP-7 induced scattering and proinvasive responses (EC50=1 ng/ml) in kidney and colon cancer cell lines through SMAD4 and src -independent pathways and signaling cascades using FAK phosphorylation at Y925 and activation of ERK1/2, Rac1 and JNK.

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  • (PMID = 17478078.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMP7 protein, human; 0 / Bmp7 protein, rat; 0 / Bone Morphogenetic Protein 7; 0 / Bone Morphogenetic Proteins; 0 / SMAD4 protein, human; 0 / Smad4 Protein; 0 / Transforming Growth Factor beta; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.6.5.2 / rac GTP-Binding Proteins
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25. National Toxicology Program: Toxicology and carcinogenesis studies of genistein (Cas No. 446-72-0) in Sprague-Dawley rats (feed study). Natl Toxicol Program Tech Rep Ser; 2008 Jan;(545):1-240
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Because of these concerns, genistein was selected as one of the compounds to be examined using a protocol designed to evaluate the effects of multigenerational and long-term exposures to doses of estrogenic agents that produce subtle reproductive tract lesions in developmentally exposed Sprague-Dawley rat pups.
  • In F(1)C females, there was a significant positive trend in the incidences of mammary gland adenoma or adenocarcinoma (combined) regardless of whether an unmodified or natural log-transformed dose scale was used in the analysis, and the incidence in the 500 ppm group was significantly greater than that in the control group.
  • In 5 and 100 ppm F(1)T140 females, the combined incidences of adenoma and adenocarcinoma were less than those in the control or 500 ppm groups, although these were not statistically significant differences.
  • When the natural log-transformed dose scale was used, a marginally significant positive trend occurred in the incidences of adenoma or adenocarcinoma (combined) in F(3)T21 females.
  • There were positive trends in the incidences of adenoma or carcinoma (combined) in the pars distalis of the pituitary gland of females in the F(1)C and F(1)T140 arms, and the incidence in the 500 ppm group was significantly greater than that in the controls in the F(1)C study arm.
  • In F(1)C males, a significant positive trend (unmodified dose scale only) occurred in the incidences of combined adenoma or carcinoma of the pancreatic islets.
  • There was some evidence of carcinogenic activity of genistein in female Sprague-Dawley rats based on increased incidences of mammary gland adenoma or adenocarcinoma (combined) and pituitary gland neoplasms.
  • There was equivocal evidence of carcinogenic activity of genistein in female Sprague-Dawley rats based on increased incidences of mammary gland adenoma or adenocarcinoma (combined).
  • [MeSH-minor] Animals. Body Weight / drug effects. Estrous Cycle / drug effects. Female. Kidney / drug effects. Kidney / pathology. Litter Size / drug effects. Longevity / drug effects. Male. Mammary Glands, Animal / drug effects. Mammary Glands, Animal / pathology. Mammary Neoplasms, Animal / chemically induced. Mammary Neoplasms, Animal / pathology. Pituitary Neoplasms / chemically induced. Pituitary Neoplasms / pathology. Pregnancy. Prenatal Exposure Delayed Effects / chemically induced. Prenatal Exposure Delayed Effects / pathology. Rats. Rats, Sprague-Dawley

  • Hazardous Substances Data Bank. GENISTEIN .
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  • (PMID = 18685716.001).
  • [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 / Phytoestrogens; 0 / Xenobiotics; DH2M523P0H / Genistein
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26. Toxicology and carcinogenesis studies of androstenedione (CAS No. 63-05-8) in F344/N rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Sep;(560):1, 7-31,33-171 passim
Hazardous Substances Data Bank. ANDROSTENEDIONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Genetic toxicology studies were conducted in Salmonella typhimurium, Escherichia coli, rat bone marrow cells, and mouse peripheral blood erythrocytes.
  • Incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) were significantly increased in 20 mg/kg males.
  • The incidence of testicular interstitial cell adenoma (including bilateral) was significantly decreased in 50 mg/kg males.
  • The incidences of hepatocellular adenoma in males and females were significantly increased in the 50 mg/kg groups.
  • Incidences of hepatocellular adenoma or carcinoma (combined) in males and females were significantly increased in the 50 mg/kg groups.
  • There was a marginally increased incidence of pancreatic islet adenoma in 50 mg/kg males and in 10 and 50 mg/kg females, with an earlier day of first incidence in males.
  • The incidence of glomerular metaplasia of the kidney was significantly increased in 50 mg/kg females, and the incidences of cytoplasmic alteration of the submandibular salivary gland were significantly increased in all dosed female groups.
  • The increased incidences of cytoplasmic alteration of the submandibular salivary gland and glomerular metaplasia of the kidney in female mice indicated a masculinizing effect from androstenedione treatment.
  • CONCLUSIONS: under the conditions of these 2-year gavage studies, there was equivocal evidence of carcinogenic activity of androstenedione in male F344/N rats based on increased incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined).
  • There was clear evidence of carcinogenic activity of androstenedione in male B6C3F1 mice based on increased incidences of multiple hepatocellular adenoma and hepatocellular carcinoma and increased incidence of hepatoblastoma.
  • There was clear evidence of carcinogenic activity of androstenedione in female B6C3F1 mice based on increased incidences of hepatocellular adenoma and hepatocellular carcinoma.
  • Increased incidences of pancreatic islet adenoma in male and female mice were also considered chemical related.
  • Androstenedione administration caused increased incidences in nonneoplastic lesions of the liver in male and female rats and mice; pancreatic islets and exocrine pancreas of female rats; and clitoral gland, kidney, and submandibular salivary gland of female mice.
  • Decreases in the incidences of testicular interstitial cell adenoma in male rats, mammary gland fibroadenoma, cysts, and hyperplasia in female rats, and malignant lymphoma in female mice were considered related to androstenedione administration.

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  • (PMID = 21037592.001).
  • [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; Review; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Mutagens; 409J2J96VR / Androstenedione
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27. Mantle P, Kulinskaya E: Lifetime, low-dose ochratoxin A dietary study on renal carcinogenesis in male Fischer rats. Food Addit Contam Part A Chem Anal Control Expo Risk Assess; 2010 Nov;27(11):1566-73
Hazardous Substances Data Bank. OCHRATOXIN A .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lifetime, low-dose ochratoxin A dietary study on renal carcinogenesis in male Fischer rats.
  • Carcinoma arising from male rat renal parenchyma is an aspect of the nephrotoxicity of ochratoxin A (OTA) and is a factor in considering application of animal data to human health risk assessment.
  • From 34 rats, only four unilateral renal carcinomas (12%) developed during a 2-year exposure to dietary OTA, contaminated to give the same weekly overall dosage as in the 50 µg kg(-1) gavage-dosing regimen of an NTP study (30%).
  • However, absence of microscopic neoplastic renal lesions in premature decedents argues for minimal effect of the 47% leukaemia on carcinoma expression in the present experiment.
  • [MeSH-major] Carcinogens / administration & dosage. Carcinogens / toxicity. Carcinoma / chemically induced. Food Contamination. Kidney Neoplasms / chemically induced. Ochratoxins / administration & dosage. Ochratoxins / toxicity
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / pathology. Adenoma / urine. Aneuploidy. Animals. Aspergillus ochraceus / metabolism. Body Weight / drug effects. Dose-Response Relationship, Drug. Leukemia, Experimental / chemically induced. Leukemia, Experimental / pathology. Leukemia, Experimental / urine. Male. Rats. Rats, Inbred F344. Risk Assessment. Survival Analysis. Toxicity Tests, Chronic

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  • (PMID = 20694869.001).
  • [ISSN] 1944-0057
  • [Journal-full-title] Food additives & contaminants. Part A, Chemistry, analysis, control, exposure & risk assessment
  • [ISO-abbreviation] Food Addit Contam Part A Chem Anal Control Expo Risk Assess
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Ochratoxins; 1779SX6LUY / ochratoxin A
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28. National Toxicology Program: NTP Toxicology and carcinogenesis studies of bromodichloromethane (CAS No. 75-27-4) in male F344/N rats and female B6C3F1 mice (Drinking Water Studies). Natl Toxicol Program Tech Rep Ser; 2006 Feb;(532):1-248
Hazardous Substances Data Bank. BROMODICHLOROMETHANE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bromodichloromethane has been shown to be carcinogenic at multiple sites in rats (large intestine and kidney) and in mice (liver and kidney) after administration by gavage in corn oil.
  • Relative kidney weights of rats in the 175, 350, and 700 mg/L groups were significantly greater than that of the controls.
  • Relative liver, kidney, and thymus weights of mice in the 350 and 700 mg/L groups were significantly greater than those of the controls.
  • The incidences of hepatocellular adenoma or carcinoma (combined) occurred with a negative trend, and the incidence in the 700 mg/L group was significantly decreased relative to the control group.
  • In contrast to the negative results in Salmonella, tests for mutation induction in mouse lymphoma L5178Y/tk(+/-)cells were positive in the presence of induced rat liver S9; no mutagenic activity occurred in tests conducted without S9.
  • In cytogenetic tests with cultured Chinese hamster ovary cells, bromodichloromethane induced a small increase in sister chromatid exchanges (SCEs) in one of four trials conducted in the presence of induced rat liver S9 enzymes; no significant increase in SCEs occurred without S9, and no induction of chromosomal aberrations occurred in bromodichloromethane-treated Chinese hamster ovary cells with or without S9.

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  • (PMID = 16741555.001).
  • [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 / Carcinogens; 0 / Mutagens; 0 / Trihalomethanes; 7LN464CH2O / bromodichloromethane
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29. National Toxicology Program: Toxicology and carcinogenesis studies of a mixture of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (Cas No. 1746-01-6), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) (Cas No. 57117-31-4), and 3,3',4,4',5-pentachlorobiphenyl (PCB 126) (Cas No. 57465-28-8) in female Harlan Sprague-Dawley rats (gavage studies). Natl Toxicol Program Tech Rep Ser; 2006 Sep;(526):1-180
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The dioxin TEF evaluation includes conducting multiple 2-year rat bioassays to evaluate the relative chronic toxicity and carcinogenicity of DLC's, structurally related PCBs, and mixtures of these compounds.
  • At 2 years, there were significant increases in the incidences of hepatocellular adenoma and cholangiocarcinoma of the liver.
  • At 2 years, incidences of acinar adenoma or acinar carcinoma that exceeded the historical control ranges were seen in all dosed groups except the 100 ng TEQ/kg group.
  • Treatment-related increases in the incidences of nonneoplastic lesions were seen in other organs including hyperplasia, cystic degeneration, atrophy, and cytoplasmic vacuolization of the adrenal cortex; gingival squamous hyperplasia of the oral mucosa; squamous metaplasia of the uterus; atrophy of the thymus (incidence and severity); chronic active inflammation of the ovary; nephropathy of the kidney (incidence and severity); cardiomyopathy; bone marrow hyperplasia; transitional epithelium of the urinary bladder; chronic active inflammation of the mesenteric artery; and follicular cell hypertrophy of the thyroid gland. (ABSTRACT TRUNCATED).

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  • (PMID = 17342195.001).
  • [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 / Benzofurans; 0 / Carcinogens; DFC2HB4I0K / Polychlorinated Biphenyls; TSH69IA9XF / 3,4,5,3',4'-pentachlorobiphenyl; U4C2RV3124 / 2,3,4,7,8-pentachlorodibenzofuran
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30. 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
Hazardous Substances Data Bank. DIBROMOACETIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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 alveolar/bronchiolar adenoma occurred with positive trends in males and females, and the incidence in 500 mg/L male mice was significantly greater than that in controls.
  • GENETIC TOXICOLOGY: Dibromoacetic acid was mutagenic in Salmonella typhimurium strain TA100 with and without rat or hamster liver metabolic activation enzymes (S9); no activity was detected in strain TA98, with or without S9.
  • [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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31. National Toxicology Program: NTP toxicology and carcinogenesis studies of 5-(Hydroxymethyl)-2-furfural (CAS No. 67-47-0) in F344/N rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Jun;(554):7-13, 15-9, 21-31 passim
Hazardous Substances Data Bank. FURFURAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Except for one 1,500 mg/kg core study male rat, all rats survived to the end of the study.
  • The incidences of minimal to mild cytoplasmic alteration of the kidney were significantly increased in males administered 188 mg/kg or greater.
  • The incidences of hepatocellular adenoma were significantly increased in 188 and 375 mg/kg females.
  • There was some evidence of carcinogenic activity of 5-(hydroxymethyl)-2-furfural in female B6C3F1 mice based on increased incidences of hepatocellular adenoma in the 188 and 375 mg/kg groups.

  • Hazardous Substances Data Bank. 5-Hydroxymethyl-2-furfuraldehyde .
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  • (PMID = 20725154.001).
  • [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] 70ETD81LF0 / 5-hydroxymethylfurfural; DJ1HGI319P / Furaldehyde
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32. National Toxicology Program: Toxicology and carcinogenesis studies of 2,3',4,4',5-pentachlorobiphenyl (PCB 118) (CAS No. 31508-00-6) in female harlan Sprague-Dawley rats (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Nov;(559):1-174

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This PCB 118 study was conducted as part of the dioxin TEF evaluation that included multiple 2-year rat bioassays to evaluate the relative chronic toxicity and carcinogenicity of DLCs, structurally related PCBs, and mixtures of these compounds.
  • At the 53-week interim evaluation, three 4,600 g/kg rats had liver cholangiocarcinoma and one had hepatocellular adenoma.
  • At 2 years, there were significant treatment-related increases in the incidences of cholangiocarcinoma and hepatocellular adenoma.
  • At 2 years, there were marginally increased incidences of exocrine pancreatic adenoma or carcinoma in the 460, 1,000, and 4,600 g/kg core study groups.
  • Numerous nonneoplastic effects were seen in other organs including: adrenal cortical atrophy and cytoplasmic vacuolization, pancreatic acinar cell cytoplasmic vacuolization and arterial chronic active inflammation, follicular cell hypertrophy of the thyroid gland, inflammation and respiratory epithelial hyperplasia of the nose, and kidney pigmentation.
  • CONCLUSIONS: Under the conditions of this 2-year gavage study, there was clear evidence of carcinogenic activity of PCB 118 in female Harlan Sprague-Dawley rats based on increased incidences of neoplasms of the liver (cholangiocarcinoma, hepatocholangioma, and hepatocellular adenoma) and cystic keratinizing epithelioma of the lung.
  • Administration of PCB 118 caused increased incidences of nonneoplastic lesions in the liver, lung, adrenal cortex, pancreas, thyroid gland, nose, and kidney.

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  • (PMID = 21383778.001).
  • [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] 31508-00-6 / 2,3',4,4',5-pentachlorobiphenyl; DFC2HB4I0K / Polychlorinated Biphenyls; DO80M48B6O / Tetrachlorodibenzodioxin
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33. Chakravarti B, Dwivedi SK, Mithal A, Chattopadhyay N: Calcium-sensing receptor in cancer: good cop or bad cop? Endocrine; 2009 Jun;35(3):271-84
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CaR plays a key role in the defense against hypercalcemia by "sensing" extracellular calcium levels in the parathyroid and kidney, the key organs maintaining systemic calcium homeostasis.
  • One situation is loss of CaR expression, resulting in loss of growth suppressing effects of elevated extracellular Ca(2+) by CaR, reported in parathyroid adenoma and in colon carcinoma.
  • Studies on H-500 rat Leydig cells, a xenotransplantable model of humoral hypercalcemia of malignancy has shed much light on the mechanisms of CaR-induced cancer cell growth and survival.

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  • (PMID = 19011996.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Calcium-Sensing
  • [Number-of-references] 203
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