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Growth‐inhibitory effects of combination chemotherapy for human pancreatic cancer cell lines
Author(s) -
Matsuno Seiki,
Hisano Hirotake,
Kobari Masao,
Akaishi Satoshi
Publication year - 1990
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19901201)66:11<2369::aid-cncr2820661120>3.0.co;2-z
Subject(s) - medicine , aclarubicin , cisplatin , pancreatic cancer , chemotherapy , ic50 , doxorubicin hydrochloride , doxorubicin , pharmacology , growth inhibition , cancer , cell culture , cancer research , biology , genetics
Sensitivities to anti‐tumor drugs, mytomycin C (MMC), aclarubicin hydrochloride (ACR), doxorubicin hydrochloride (ADR), cisplatin, and 5‐fluorouracil (5FU), were examined using PK‐1, ‐8, ‐9, ‐12, ‐14, and ‐16 cell lines derived from human pancreatic cancer. These cell lines showed different sensitivities to each of the above anti‐tumor drugs. the concentrations required for 50% growth‐inhibition (IC 50 ) after 2 hours of exposure were 0.096 to 0.35 μg/ml for MMC, 0.0074 to 0.0076 μg/ml for ACR, 0.033 to 0.23 μg/ml for ADR, 0.35 to 1.9 μg/ml for cisplatin, and 21 to 42 μg/ml for 5FU. IC 50 of each anti‐tumor drug decreased significantly after 48 hours of exposure. the combination of any two out of MMC, ACR, and 5FU showed synergistic inhibition of the growth of PK‐1 and PK‐8 cell lines. These results show that MMC, ACR, ADR, cisplatin, and 5FU have sufficient anti‐tumor effect against six human pancreatic cancer cell lines even at clinically achievable concentrations and exposure times, and chemotherapy for pancreatic cancers requires naturally effective drug delivery into cancer tissues.