Modulation of G2 arrest enhances cell death induced by the antitumor 1-nitroacridine derivative, Nitracrine

Apoptosis

Volumn 7, Issue 4, 2002, Pages 347-359

  Skladanowski, A ^a  

^a GDANSK UNIVERSITY OF TECHNOLOGY   (Poland)

Author keywords

Antitumor drug; Apoptosis; Cell death; DNA cross linking; G2 arrest; Nitracrine

Indexed keywords

CAFFEINE; CAMPTOTHECIN; CISPLATIN; DNA FRAGMENT; DNA TOPOISOMERASE INHIBITOR; NITRACRINE; VINBLASTINE; NUCLEIC ACID SYNTHESIS INHIBITOR;

ANIMAL CELL; ANTINEOPLASTIC ACTIVITY; APOPTOSIS; CELL CYCLE; CELL CYCLE G2 PHASE; CELL CYCLE S PHASE; CELL DEATH; CONTROLLED STUDY; COVALENT BOND; CYTOTOXICITY; DNA CROSS LINKING; DNA DAMAGE; DNA SYNTHESIS; DNA TEMPLATE; FLOW CYTOMETRY; HUMAN; HUMAN CELL; MITOSIS INDEX; MOUSE; NICK END LABELING; NONHUMAN; PRIORITY JOURNAL; REVIEW; ARTICLE; DOSE RESPONSE; DRUG EFFECT; HELA CELL;

APOPTOSIS; CAMPTOTHECIN; CISPLATIN; DNA FRAGMENTATION; DOSE-RESPONSE RELATIONSHIP, DRUG; FLOW CYTOMETRY; G2 PHASE; HELA CELLS; HUMAN; IN SITU NICK-END LABELING; NITRACRINE; NUCLEIC ACID SYNTHESIS INHIBITORS; S PHASE; SUPPORT, NON-U.S. GOV'T; HUMANS;

ANIMALIA; MURINAE;

EID: 0036022409     PISSN: 13608185     EISSN: None     Source Type: Journal    
DOI: 10.1023/A:1016127513947     Document Type: Review

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