Apoptosis primarily accounts for the growth-inhibitory properties of sulindac metabolites and involves a mechanism that is independent of cyclooxygenase inhibition, cell cycle arrest, and p53 induction

Cancer Research

Volumn 57, Issue 12, 1997, Pages 2452-2459

  Piazza, Gary A ^a   Rahm, Alanna K ^a   Finn, Tyler S ^a   Fryer, Benjamin H ^a   Li, Han ^a   Stoumen, Alan L ^a   Pamukcu, Rifat ^a   Ahnen, Dennis J ^b  

^a Cell Pathways Inc   (United States)

^b UNIVERSITY OF COLORADO   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

FLUOROURACIL; PROTEIN P53; SULINDAC;

ANIMAL CELL; APOPTOSIS; ARTICLE; CELL CYCLE; CELL GROWTH; CELL PROLIFERATION; COLON ADENOCARCINOMA; COLON MUCOSA; DRUG EFFECT; ENZYME INHIBITION; GROWTH INHIBITION; MITOSIS INHIBITION; NONHUMAN; PRIORITY JOURNAL; TUMOR GROWTH;

16,16-DIMETHYLPROSTAGLANDIN E2; ADENOCARCINOMA; ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL; APOPTOSIS; CELL CYCLE; CELL DIVISION; CELL SURVIVAL; COLONIC NEOPLASMS; CYCLOOXYGENASE INHIBITORS; DOSE-RESPONSE RELATIONSHIP, DRUG; FLUOROURACIL; GROWTH INHIBITORS; HUMANS; PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES; SULINDAC; TIME FACTORS; TUMOR CELLS, CULTURED; TUMOR SUPPRESSOR PROTEIN P53;

EID: 0030968757     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

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