Buscher H P
Medizinische Klinik, Universität Freiburg.
Klin Wochenschr. 1990 May 4;68(9):443-6. doi: 10.1007/BF01648895.
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.
在临床实践中，肿瘤获得性或新发的抗肿瘤化疗耐药性仍然是一个大问题。然而，在过去几年中，在理解两个主要机制方面取得了一些进展：代谢改变导致药物的细胞生长抑制或细胞毒性作用降低，以及药物在肿瘤细胞内的积累减少[15, 34, 35]。第二种现象通常归因于肿瘤细胞加速各种外源性物质外流的能力。这种现象被认为是多药耐药（MDR）产生的主要原因。然而，肿瘤细胞药物摄取的丧失或受损也可能导致对抗肿瘤药物的耐药性。本文重点介绍了支持这一观点的肝癌细胞的最新研究结果。
