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1. Stebbins KE, Johnson KA, Jeffries TK, Redmond JM, Haut KT, Shabrang SN, Stott WT: Chronic toxicity and oncogenicity studies of ingested 1, 3-dichloropropene in rats and mice. Regul Toxicol Pharmacol; 2000 Aug;32(1):1-13
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  • Histopathologic effects attributed to treatment in rats consisted of basal cell hyperplasia of the nonglandular mucosa of the stomach in males and females given 12.5 or 25 mg/kg/day for 12 and 24 months and an increased number of hepatocellular adenomas in males given 12.5 or 25 mg/kg/day and females given 25 mg/kg/day for 24 months.
  • The increase in hepatocellular adenomas was statistically identified by pairwise comparison only in males given 25 mg/kg/day.
  • An increased incidence of eosinophilic foci of altered cells in the liver was also noted in all treated groups of rats at 24 months.
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / pathology. Administration, Oral. Animals. Body Weight / drug effects. Carcinogenicity Tests. Chronic Disease. Diet. Drug Compounding. Female. Hepatocytes / drug effects. Hepatocytes / pathology. Hyperplasia. Kidney Diseases / chemically induced. Kidney Diseases / pathology. Lethal Dose 50. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Male. Mice. Mice, Inbred Strains. Neoplasms, Experimental / chemically induced. Neoplasms, Experimental / pathology. No-Observed-Adverse-Effect Level. Rats. Rats, Inbred F344. Stomach / drug effects. Stomach / pathology

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  • [Copyright] Copyright 2000 Academic Press.
  • (PMID = 11029263.001).
  • [ISSN] 0273-2300
  • [Journal-full-title] Regulatory toxicology and pharmacology : RTP
  • [ISO-abbreviation] Regul. Toxicol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Allyl Compounds; 0 / Insecticides; 9H780918D0 / 1,3-dichloro-1-propene
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2. Aiso S, Takeuchi T, Arito H, Nagano K, Yamamoto S, Matsushima T: Carcinogenicity and chronic toxicity in mice and rats exposed by inhalation to para-dichlorobenzene for two years. J Vet Med Sci; 2005 Oct;67(10):1019-29
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  • Incidences of hepatocellular carcinomas, hepatoblastomas and hepatic histiocytic sarcomas in the 300 ppm-exposed male mice, and hepatocellular adenomas and carcinomas and hepatoblastomas in the 300 ppm-exposed female mice were increased.
  • Treatment- and age-related increases in incidences of the eosinophilic globules of the respiratory and olfactory epithelia in female rats and incidences of the respiratory metaplasia of the nasal gland epithelium in mice and rats and the olfactory epithelium in mice were noted.

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  • (PMID = 16276058.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Chlorobenzenes; D149TYB5MK / 4-dichlorobenzene
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3. Harada T, Yamaguchi S, Ohtsuka R, Takeda M, Fujisawa H, Yoshida T, Enomoto A, Chiba Y, Fukumori J, Kojima S, Tomiyama N, Saka M, Ozaki M, Maita K: Mechanisms of promotion and progression of preneoplastic lesions in hepatocarcinogenesis by DDT in F344 rats. Toxicol Pathol; 2003 Jan-Feb;31(1):87-98
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  • Histologically, eosinophilic foci and hepatocellular adenomas increased in males at 50 ppm and both sexes at 500 ppm.
  • These results indicate that DDT may induce eosinophilic foci as a result of oxidative DNA damage and leads them to neoplasms in combination with its mitogenic activity and inhibitory effect on GJIC.
  • [MeSH-major] DDT / toxicity. Liver / drug effects. Liver Neoplasms, Experimental / chemically induced. Precancerous Conditions / chemically induced
  • [MeSH-minor] Animals. Carcinogenicity Tests. Cell Division / drug effects. Cytochrome P-450 Enzyme System / metabolism. Disease Progression. Dose-Response Relationship, Drug. Female. Gap Junctions / drug effects. Male. Oxidative Stress / drug effects. Rats. Rats, Inbred F344

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  • (PMID = 12597452.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9035-51-2 / Cytochrome P-450 Enzyme System; CIW5S16655 / DDT
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4. Toyosawa K, Okimoto K, Kobayashi I, Kijima K, Kikawa E, Kohchi M, Koujitani T, Tanaka K, Matsuoka N: Di(2-ethylhexyl)phthalate induces hepatocellular adenoma in transgenic mice carrying a human prototype c-Ha-ras gene in a 26-week carcinogenicity study. Toxicol Pathol; 2001 Jul-Aug;29(4):458-66
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  • [Title] Di(2-ethylhexyl)phthalate induces hepatocellular adenoma in transgenic mice carrying a human prototype c-Ha-ras gene in a 26-week carcinogenicity study.
  • To evaluate the transgenic mouse carrying a human prototype c-Ha-ras gene (rasH2 mouse) as a model for 26-week carcinogenicity tests, Di(2-ethylhexyl)phthalate (DEHP), a peroxisome proliferator, was administered to 15 rasH2 mice/sex/group at concentrations of 1,500, 3,000 or 6,000 ppm, and to 15 wild-type (non-Tg) mice/sex/group at a concentration of 6,000 ppm in their diets for 26 weeks.
  • Common findings related to treatment with DEHP in rasH2 and non-Tg mice included hypertrophy with coarse granules and deposit of pigment in the liver, hydronephrosis and tubular regeneration in the kidney, focal atrophy in the testis, and increased eosinophilic body in the nasal cavity.
  • Hepatocellular adenoma was induced by treatment with DEHP, and was confined to male rasH2; mice the incidence being 7%(1/15), 13%(2/15), and 27%(4/15) in the 1,500-, 3,000-, and 6,000-ppm group, respectively.
  • Point mutation was not detected in codon 12 and 61 of human c-Ha-ras transgene upon DNA analyses on frozen samples taken from these hepatocellular adenomas.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Diethylhexyl Phthalate / toxicity. Genes, ras. Liver Neoplasms, Experimental / genetics. Peroxisome Proliferators / toxicity
  • [MeSH-minor] Administration, Oral. Animals. Carcinogenicity Tests / methods. Dose-Response Relationship, Drug. Female. Kidney / drug effects. Kidney / pathology. Kidney Tubules / drug effects. Kidney Tubules / pathology. Liver / drug effects. Liver / pathology. Male. Mice. Mice, Transgenic. Nasal Cavity / drug effects. Nasal Cavity / pathology. Polymorphism, Single-Stranded Conformational. Sex Factors. Survival Rate. Testis / drug effects. Testis / pathology. Time Factors

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  • (PMID = 11560251.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peroxisome Proliferators; C42K0PH13C / Diethylhexyl Phthalate
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5. 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
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  • 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.
  • In females, the incidences of mammary gland fibroadenoma were significantly decreased in the 20 and 50 mg/kg groups, the incidences of mammary gland hyperplasia were significantly decreased in all dosed groups, and the incidences of mammary gland cyst were significantly decreased in the 10 and 50 mg/kg groups.
  • In the liver of males, the incidences of basophilic focus in all dosed groups, the incidence of clear cell focus in the 20 mg/kg group, and the incidence of eosinophilic focus in the 50 mg/kg group were significantly increased.
  • 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.
  • Incidences of multiple hepatocellular adenomas and carcinomas were significantly increased in 10 and 50 mg/kg males, and there was an increased incidence of multiple hepatocellular adenomas in 50 mg/kg females.
  • The incidence of eosinophilic focus was significantly increased in 50 mg/kg males, and the incidences of mixed cell focus and cytoplasmic vacuolization were significantly increased in 50 mg/kg females.
  • 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 incidences of clitoral gland hyperplasia and clitoral gland duct dilatation were significantly increased in 10 and 50 mg/kg females.
  • 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.
  • [MeSH-minor] Animal Feed. Animals. Biomarkers. Body Weight / drug effects. Carcinogenicity Tests. Chemistry, Pharmaceutical. Dose-Response Relationship, Drug. Drug-Induced Liver Injury / metabolism. Drug-Induced Liver Injury / pathology. Estrous Cycle. Female. Genitalia / drug effects. Intubation, Gastrointestinal. Male. Mice. Mice, Inbred Strains. Micronucleus Tests. Mutagens / toxicity. Organ Size / drug effects. Rats. Rats, Inbred F344

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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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6. Mete O, Asa SL: Aldosterone-producing adrenal cortical adenoma with oncocytic change and cytoplasmic eosinophilic globular inclusions. Endocr Pathol; 2009;20(3):182-5
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  • [Title] Aldosterone-producing adrenal cortical adenoma with oncocytic change and cytoplasmic eosinophilic globular inclusions.
  • The laparoscopic left adrenalectomy specimen revealed an adrenal cortical adenoma composed of varying proportions of oncocytic and clear cells, predominantly showing central oncocytic change.
  • Oncocytes also exhibited numerous eosinophilic intracytoplasmic globular inclusions, which are not commonly observed in aldosterone-producing adrenal cortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Aldosterone / secretion. Inclusion Bodies / pathology
  • [MeSH-minor] Aged. Antihypertensive Agents / therapeutic use. Female. Humans. Hyperaldosteronism / etiology. Hypertension / drug therapy. Hypertension / etiology. Microscopy, Electron, Transmission

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  • (PMID = 19462261.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 4964P6T9RB / Aldosterone
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7. 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
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  • Methyl isobutyl ketone is used as a denaturant for rubbing alcohol; as a solvent for paints, varnishes, nitrocellulose, lacquers, and protective coatings; in industrial extraction processes; in dry-cleaning preparations; and in the synthesis of methyl isobutyl carbinol.
  • 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.
  • 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 hepatocellular adenoma and hepatocellular adenoma or carcinoma (combined) were significantly increased in males and females exposed to 1,800 ppm.
  • The incidences of eosinophilic foci were significantly increased in 450 and 1,800 ppm females.
  • [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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8. National Toxicology Program: Toxicology and carcinogenesis studies of indium phosphide (CAS No. 22398-90-7) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2001 Jul;(499):7-340
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  • In general, body weight gains were significantly less in males and females exposed to 3 mg/m3 or greater compared to those of the chamber controls.
  • Animals in the 0.1 and 0.3 mg/m3 group were maintained on filtered air from exposure termination at week 22 until the end of the studies.
  • Pathology Findings: At 2 years, exposure to indium phosphide caused increased incidences of alveolar/bronchiolar adenomas and carcinomas in rats.
  • Exposure to indium phosphide also caused increased incidences of benign and malignant pheochromocytomas of the adrenal gland in males and females.
  • Marginal increases in the incidences of mononuclear cell leukemia in males and females, fibroma of the skin in males, and carcinoma of the mammary gland in females may have been related to exposure to indium phosphide.
  • Animals in the 0.1 and 0.3 mg/m3 groups were maintained on filtered air from exposure termination at week 21 until the end of the studies.
  • Survival and Body Weights: In general, exposure to indium phosphide for 2 years reduced survival and body weight gain in exposed males and females.
  • Pathology Findings:At 2 years, exposure to indium phosphide caused increased incidences of alveolar/bronchiolar carcinomas in males and alveolar/bronchiolar adenomas and carcinomas in females.
  • Exposed groups of males and females had increased incidences of eosinophilic foci of the liver at 2 years.
  • [MeSH-minor] Administration, Inhalation. Animals. Carcinogenicity Tests. Dose-Response Relationship, Drug. Female. Male. Mice. Mice, Inbred Strains. Rats. Rats, Inbred F344

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  • (PMID = 12087422.001).
  • [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 / Phosphines; 045A6V3VFX / Indium; 22398-80-7 / indium phosphide
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9. Koehler A, Alpermann T, Lauritzen B, Van Noorden CJ: Clonal xenobiotic resistance during pollution-induced toxic injury and hepatocellular carcinogenesis in liver of female flounder (Platichthys flesus (L.)). Acta Histochem; 2004;106(2):155-70
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  • Tumour frequencies up to 70% were found macroscopically in livers of adult female flounder which had progressed to adenomas and carcinomas in the most polluted site.
  • Because male adult flounder show only up to 50% of livers containing early preneoplastic foci but never malignancies, we focussed our study on female individuals. (Pre)neoplastic changes ranged from early eosinophilic foci to basophilic foci, adenomas and hepatocellular carcinomas.
  • Adenomas were generally eosinophilic whereas carcinomas were mainly basophilic.
  • With a quantitative immunohistochemical approach, we studied expression of P-glycoprotein (P-gp)-mediated multixenobiotic resistance (MXR), cytochrome P4501A1, glutathione-S-transferase-A which are key proteins in xenobiotic metabolism and elimination.
  • We observed upregulation of G6PDH activity already in early preneoplastic eosinophilic foci and subsequent further upregulation in basophilic foci and carcinomas.
  • [MeSH-major] Adaptation, Physiological. Adenoma / veterinary. Carcinogens, Environmental / toxicity. Fish Diseases / chemically induced. Liver Neoplasms / veterinary. Water Pollutants, Chemical / toxicity. Xenobiotics / toxicity
  • [MeSH-minor] Animals. Basophils / metabolism. Basophils / pathology. Biomarkers, Tumor / metabolism. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / metabolism. Enzymes / metabolism. Eosinophils / enzymology. Eosinophils / pathology. Female. Flounder. Gene Expression Regulation, Neoplastic. Liver / enzymology. Liver / pathology. Male. Sex Factors. Up-Regulation

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  • (PMID = 15147637.001).
  • [ISSN] 0065-1281
  • [Journal-full-title] Acta histochemica
  • [ISO-abbreviation] Acta Histochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carcinogens, Environmental; 0 / Enzymes; 0 / Water Pollutants, Chemical; 0 / Xenobiotics
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10. 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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  • There was a significantly enhanced prevalence and multiplicity of hepatocellular adenomas at 3.9 mg BDCM/kg/day (15.5% and 0.16/animal vs. 2.2% and 0.02/animal for the control).
  • The prevalence of basophilic and clear cell, but not eosinophilic cells, altered foci of cells declined with increasing dose.
  • [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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11. 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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  • alpha-Methylstyrene is used in the production of acrylonitrile-butadiene-styrene resins and copolymers, which improve the impact and heat-resistant properties of polymers, specialty grades of plastics, rubber, and protective coatings. alpha-Methylstyrene also moderates polymerization rates and improves product clarity in coatings and resins.
  • Morphologic changes were not detected in the liver.
  • The incidences of hyaline degeneration, characterized by the accumulation of eosinophilic globules in the cytoplasm of the respiratory epithelium, were significantly increased in females exposed to 150 ppm or greater.
  • 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 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.
  • The incidences of hepatocellular carcinoma and eosinophilic foci of the liver were significantly increased in 600 ppm females.
  • 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).
  • There was clear evidence of carcinogenic activity of alpha-methylstyrene in female B6C3F1 mice based on increased incidences of hepatocellular adenomas and carcinomas.
  • [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

  • Hazardous Substances Data Bank. ALPHA-METHYL STYRENE .
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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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12. Spencer PJ, Crissman JW, Stott WT, Corley RA, Cieszlak FS, Schumann AM, Hardisty JF: Propylene glycol monomethyl ether (PGME): inhalation toxicity and carcinogenicity in Fischer 344 rats and B6C3F1 mice. Toxicol Pathol; 2002 Sep-Oct;30(5):570-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary treatment-related effects included: initial sedation of animals exposed to 3,000 ppm and its subsequent resolution correlating with induction of hepatic mixed function oxidase activity and S-phase DNA synthesis; elevated mortality in high-exposure male rats and mice (chronic study); elevated deposition of alpha2u-globulin (alpha2U-G) and associated nephropathy and S-phase DNA synthesis in male rat kidneys; accelerated atrophy of the adrenal gland X-zone in female mice (subchronic study only); and increased occurrence and/or severity of eosinophilic foci of altered hepatocytes in male rats.
  • A numerical increase in the incidence of kidney adenomas occurred in intermediate-exposure male rats; however, the association with alpha2U-G nephropathy, a male rat specific effect, indicated a lack of relevance for human risk assessment.
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / metabolism. Adenoma / pathology. Administration, Inhalation. Alpha-Globulins / metabolism. Animals. Carcinogenicity Tests. DNA / biosynthesis. DNA Replication / drug effects. Dose-Response Relationship, Drug. Enzyme Induction / drug effects. Female. Kidney Neoplasms / chemically induced. Kidney Neoplasms / metabolism. Kidney Neoplasms / pathology. Liver / drug effects. Liver / enzymology. Longevity / drug effects. Male. Mice. Mice, Inbred Strains. Mixed Function Oxygenases / biosynthesis. Rats. Rats, Inbred F344. S Phase / drug effects. S Phase / physiology

  • Hazardous Substances Data Bank. 1-METHOXY-2-HYDROXYPROPANE .
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
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  • (PMID = 12371666.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alpha-Globulins; 0 / Carcinogens; 0 / Propylene Glycols; 0 / alpha 2u globulin; 74Z7JO8V3U / propylene glycol methyl ether; 9007-49-2 / DNA; EC 1.- / Mixed Function Oxygenases
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13. Goertz RS, Janka R, Nägel A, Strobel D: Eosinophilic infiltration of the liver and pancreas mimicking metastatic disease. Z Gastroenterol; 2010 Sep;48(9):1138-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Eosinophilic infiltration of the liver and pancreas mimicking metastatic disease.
  • Other lesions presenting hypoenhancement in the late phase are abscesses, hepatocellular and cholangiocellular carcinomas, adenomas, avascular necrosis, haematomas and rarely inflammatory masses.
  • The histopathological work-up surprisingly identified the hepatic lesions to be eosinophilic infiltration.
  • [MeSH-major] Drug-Induced Liver Injury / etiology. Drug-Induced Liver Injury / ultrasonography. Eosinophilia / chemically induced. Eosinophilia / ultrasonography. Fluoroquinolones / adverse effects. Pancreatic Diseases / chemically induced. Pancreatic Diseases / ultrasonography






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