EXPLOITING MULTIDRUG-RESISTANCE TO TREAT CANCER
EXPLOITING MULTIDRUG-RESISTANCE TO TREAT CANCER
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DOI：
10.1101/sqb.1994.059.01.078
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发表时间：
1994-01-01
期刊：
影响因子：
--
通讯作者：
PASTAN, I
中科院分区：
文献类型：
--
作者：
GOTTESMAN, MM;AMBUDKAR, SV;PASTAN, I
Of the 1,000,000 patients who present to their physicians each year in the United States with cancer, approximately 500,000 have tumors that have spread beyond their primary origin. Currently, the most effective therapy for metastatic and disseminated cancers is the use of chemotherapy, but chemotherapy eliminates only 5-10% of these cancers, including germ-cell cancers, leukemias, lymphomas, and childhood tumors. In most solid tumors, chemotherapy is either ineffective or, after a brief remission, becomes ineffective. The molecular basis of resistance to modern multiagent chemotherapy (multidrug resistance, MDR) has been the subject of considerable investigation. One major conclusion from these studies is that most resistance is cell-based, occurring because of the expression in cancer cells of drug resistance genes; or loss of pathways which sensitize cells to chemotherapy, such as those involved in metabolic activation of cytotoxins; or programmed cell death. Thus, drug-resistance phenomena can be modeled in cultured cancer cells selected for resistance to anticancer drugs. In Figure 1, we summarize a variety of different mechanisms thought to play a role in the intrinsic expression or acquisition of drug resistance in cancer.
