Is peroxisome proliferation an obligatory precursor step in the carcinogenicity of Di(2-ethylhexyl)phthalate (DEHP)?

Environmental Health Perspectives

Volumn 109, Issue 5, 2001, Pages 437-442

  Melnick, Ronald L ^a  

^a NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES   (United States)

Author keywords

Apoptosis; Cell proliferation; Di(2 ethylhexyl)phthalate; Hypolipidemic drugs; Peroxisome proliferation; Peroxisome proliferator activated receptor

Indexed keywords

ANTILIPEMIC AGENT; CARCINOGEN; FIBRIC ACID DERIVATIVE; PEROXISOME PROLIFERATOR; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR; PHTHALIC ACID BIS(2 ETHYLHEXYL) ESTER; TRANSCRIPTION FACTOR;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CANCER EPIDEMIOLOGY; CANCER RESEARCH; CANCER RISK; CARCINOGEN TESTING; CARCINOGENICITY; CELL TRANSFORMATION; CHEMICAL CARCINOGENESIS; CLINICAL PATHWAY; CONTROLLED STUDY; ENVIRONMENTAL EXPOSURE; EPIDEMIOLOGICAL DATA; FEMALE; HUMAN; HUMAN CELL; HUMAN EXPERIMENT; HUMAN TISSUE; HYPOTHESIS; LIVER TUMOR; MALE; MOUSE; NATIONAL HEALTH SERVICE; NONHUMAN; PEROXISOME; PLEIOTROPY; PRECURSOR; PRIORITY JOURNAL; PROTEIN EXPRESSION; RAT; REGULATORY MECHANISM; RISK ASSESSMENT; SIGNAL TRANSDUCTION; TOXICITY TESTING; TRANSCRIPTION INITIATION; TUMOR GROWTH; UNITED STATES;

ANIMALIA; RODENTIA;

EID: 0035325333     PISSN: 00916765     EISSN: None     Source Type: Journal    
DOI: 10.1289/ehp.01109437     Document Type: Article

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