Defective drug uptake contributing to multidrug resistance in hepatoma cells can be evaluated in vitro.
In clinical practice the acquired or de novo resistance of tumors to antitumor chemotherapy remains a big problem. However, in the past few years some progress has been made in understanding the two principal mechanisms: metabolic alterations leading to a reduced cytostatic or cytotoxic effect of drugs, and reduced accumulation of drugs within the tumor cells [15, 34, 35]. The second phenomenon is usually attributed to the ability of tumor cells to accelerate the efflux of various xenobiotics. This phenomenon is considered primarily responsible for the development of multidrug resistance (MDR). However, loss or impairment of drug uptake by the tumor cells may also contribute to resistance to antitumor drugs. This paper focuses on recent findings with hepatoma cells, which support this view.
Buscher
H P
HP
Medizinische Klinik, Universität Freiburg.
D000970:Antineoplastic Agents / Q000493:pharmacokinetics* / Q000494:pharmacology; D006528:Carcinoma, Hepatocellular; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology*; D015179:Colorectal Neoplasms; D004351:Drug Resistance; D006801:Humans; D008658:Inactivation, Metabolic / Q000502:physiology; D008113:Liver Neoplasms; D014407:Tumor Cells, Cultured / Q000187:drug effects / Q000378:metabolism*
D000970:Antineoplastic Agents