Medical Oncology Branch, National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892, United States.
Mol Pharm. 2011 Dec 5;8(6):2021-31. doi: 10.1021/mp200329f. Epub 2011 Oct 7.
The histone deacetylase inhibitors (HDIs) have shown promise in the treatment of a number of hematologic malignancies, leading to the approval of vorinostat and romidepsin for the treatment of cutaneous T-cell lymphoma and romidepsin for the treatment of peripheral T-cell lymphoma by the U.S. Food and Drug Administration. Despite these promising results, clinical trials with the HDIs in solid tumors have not met with success. Examining mechanisms of resistance to HDIs may lead to strategies that increase their therapeutic potential in solid tumors. However, relatively few examples of drug-selected cell lines exist, and mechanisms of resistance have not been studied in depth. Very few clinical translational studies have evaluated resistance mechanisms. In the current review, we summarize many of the purported mechanisms of action of the HDIs in clinical trials and examine some of the emerging resistance mechanisms.
组蛋白去乙酰化酶抑制剂(HDIs)在治疗多种血液恶性肿瘤方面显示出良好的效果,已促使美国食品和药物管理局批准伏立诺他和罗米地辛用于治疗皮肤 T 细胞淋巴瘤,以及罗米地辛用于治疗外周 T 细胞淋巴瘤。尽管取得了这些有希望的结果,但在实体瘤中进行的 HDIs 临床试验并未取得成功。研究对 HDIs 的耐药机制可能会导致增加其在实体瘤中治疗潜力的策略。然而,存在的药物选择细胞系的例子相对较少,并且耐药机制尚未深入研究。很少有临床转化研究评估耐药机制。在当前的综述中,我们总结了临床试验中 HDIs 的许多推测作用机制,并研究了一些新出现的耐药机制。