Transgenic disruption of gap junctional intercellular communication enhances early but not late stage hepatocarcinogenesis in the rat

Toxicologic Pathology

Volumn 33, Issue 6, 2005, Pages 695-701

  Hokaiwado, Naomi ^a   Asamoto, Makoto ^a   Ogawa, Kumiko ^a   Shirai, Tomoyuki ^a  

^a NAGOYA CITY UNIVERSITY GRADUATE SCHOOL OF MEDICAL SCIENCES   (Japan)

Author keywords

Carcinogenesis; Connexin 32; Gap junction; Liver

Indexed keywords

CONNEXIN 32; DIETHYLNITROSAMINE; GLUTATHIONE TRANSFERASE; PHENOBARBITAL;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CANCER INCIDENCE; CANCER STAGING; CANCER SUSCEPTIBILITY; CELL COMMUNICATION; CHEMICAL CARCINOGENESIS; CONTROLLED STUDY; FEMALE; GAP JUNCTION; LIVER ADENOMA; LIVER CARCINOGENESIS; LIVER CELL CARCINOMA; LIVER INJURY; MALE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; RAT;

ALKYLATING AGENTS; ANIMALS; ANIMALS, GENETICALLY MODIFIED; CELL COMMUNICATION; COCARCINOGENESIS; CONNEXINS; DIETHYLNITROSAMINE; DISEASE SUSCEPTIBILITY; ENZYME INDUCTION; GAP JUNCTIONS; GLUTATHIONE TRANSFERASE; HEPATECTOMY; LIVER NEOPLASMS, EXPERIMENTAL; LIVER REGENERATION; MALE; MUTATION; PHENOBARBITAL; PRECANCEROUS CONDITIONS; RATS; TIME FACTORS;

ANIMALIA;

EID: 31544476877     PISSN: 01926233     EISSN: 15331601     Source Type: Journal    
DOI: 10.1080/01926230500330313     Document Type: Article

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