TY - JOUR
T1 - Sensitivity of cultured human pancreatic carcinoma cells to dihydroxyanthracenedione
AU - Fountzilas, George
AU - Gratzner, Howard
AU - Lim, Lori O.
AU - Yunis, Adel A.
PY - 1984/3/15
Y1 - 1984/3/15
N2 - We tested the effectiveness of dihydroxyanthracenedione (DHAD) on cell growth of two human pancreatic carcinoma cell lines MlA PaCa‐2 and PANC‐1. At the level of ID50, the drug was almost equally effective against both cell lines. When the time exposure of MIA PaCa‐2 cells to the drug was increased from 1 h to continuous exposure for 5 days, the ID50 was decreased about three‐fold only (1.4 × 10−8 M and 4 × 10−9 M respectively). At the level of ID50 also the difference between 6 h exposure and continuous exposure for 5 days was minimal. In equimolar concentrations and with 1 h exposure, DHAD was more effective against MIA PaCa‐2 cells than other chemotherapeutic agents including adriamycin, mitomycin‐C, 5‐FU, vincristine, vindesine, vinblastine, VP‐16–213, bleomycin, cis‐platinum, asparaginase and acivicin. In concentrations of 5 × 10−7 M, DHAD caused about 40% inhibition of 14C‐thymidine incorporation of MIA PaCa‐2 cells. Treatment of MIA PaCa‐2 cells with the ID50 of DHAD for 1 h caused retardation of cellular traverse, with the major effect appearing to be in G2+M phase of the cycle. From these data DHAD appears to be a potent drug against human pancreatic carcinoma in vitro.
AB - We tested the effectiveness of dihydroxyanthracenedione (DHAD) on cell growth of two human pancreatic carcinoma cell lines MlA PaCa‐2 and PANC‐1. At the level of ID50, the drug was almost equally effective against both cell lines. When the time exposure of MIA PaCa‐2 cells to the drug was increased from 1 h to continuous exposure for 5 days, the ID50 was decreased about three‐fold only (1.4 × 10−8 M and 4 × 10−9 M respectively). At the level of ID50 also the difference between 6 h exposure and continuous exposure for 5 days was minimal. In equimolar concentrations and with 1 h exposure, DHAD was more effective against MIA PaCa‐2 cells than other chemotherapeutic agents including adriamycin, mitomycin‐C, 5‐FU, vincristine, vindesine, vinblastine, VP‐16–213, bleomycin, cis‐platinum, asparaginase and acivicin. In concentrations of 5 × 10−7 M, DHAD caused about 40% inhibition of 14C‐thymidine incorporation of MIA PaCa‐2 cells. Treatment of MIA PaCa‐2 cells with the ID50 of DHAD for 1 h caused retardation of cellular traverse, with the major effect appearing to be in G2+M phase of the cycle. From these data DHAD appears to be a potent drug against human pancreatic carcinoma in vitro.
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U2 - 10.1002/ijc.2910330311
DO - 10.1002/ijc.2910330311
M3 - Article
C2 - 6698638
AN - SCOPUS:0021358753
VL - 33
SP - 347
EP - 353
JO - International Journal of Cancer
JF - International Journal of Cancer
SN - 0020-7136
IS - 3
ER -