Complementary effects of HDAC inhibitor 4-PB on gap junction communication and cellular export mechanisms support restoration of chemosensitivity of PDAC cells

@article{Ammerpohl2007ComplementaryEO,
  title={Complementary effects of HDAC inhibitor 4-PB on gap junction communication and cellular export mechanisms support restoration of chemosensitivity of PDAC cells},
  author={Ole Ammerpohl and Anna Trauzold and Bodo Schniewind and U Griep and Christian Pilarsky and R Grutzmann and Hans-Detlev Saeger and Ottmar Janssen and Bence Sipos and Gunter Kloppel and Holger Kalthoff},
  journal={British Journal of Cancer},
  year={2007},
  volume={96},
  pages={73 - 81}
}
Pancreatic ductal adenocarcinoma (PDAC) is a fatal disease and one of the cancer entities with the lowest life expectancy. Beside surgical therapy, no effective therapeutic options are available yet. Here, we show that 4-phenylbutyrate (4-PB), a known and well-tolerable inhibitor of histone deacetylases (HDAC), induces up to 70% apoptosis in all cell lines tested (Panc 1, T4M-4, COLO 357, BxPc3). In contrast, it leads to cell cycle arrest in only half of the cell lines tested. This drug… CONTINUE READING
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