British journal of cancer, 69(2), 217-221 (1994-02-01)
Sensitivity to platinum-containing drugs is believed to be a function of how much drug enters the cell, the extent of DNA adduct formation and the rate at which DNA is repaired. Activation of protein kinase C by 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was
The Journal of clinical investigation, 95(3), 1193-1198 (1995-03-01)
Cross-resistance between cisplatin (DDP) and metalloid salts in human cells was sought on the basis that mechanisms that mediate metalloid salt cross-resistance in prokaryotes are evolutionarily conserved. Two ovarian and two head and neck carcinoma cell lines selected for DDP
Cancer chemotherapy and pharmacology, 34(6), 484-490 (1994-01-01)
Cholecystokinin (CCK) is an important trophic hormone for the pancreas, and CCK receptors are present on pancreatic carcinoma cells. We sought to determine whether either CCK itself or an antagonist of CCK could modulate the sensitivity of the human pancreatic
Killing of human ovarian carcinoma 2008 cells by cisplatin (DDP) is in direct proportion to the amount of drug entering the cell. DDP and its analogue [3H]dichloro(ethylenediamine)platinum[II] ([3H]-DEP) enter cells relatively slowly. We found that the uptake of [3H]DEP into
The sequence specificity of DNA damage caused by cis-diamminedichloroplatinum(II) (cisplatin) and four analogues in human (HeLa) cells was studied using Taq DNA polymerase and a linear amplification system. The primer extension is inhibited by the drug-DNA adducts, and hence the
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