Apoptosis and melanoma chemoresistance

被引:670
作者
Soengas, MS [1 ]
Lowe, SW
机构
[1] Univ Michigan, Ctr Comprehens Canc, Dept Dermatol, Melanoma Program, Ann Arbor, MI USA
[2] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
关键词
skin cancer; drug resistance; apoptosis; cancer therapy; chemotherapeutic targets;
D O I
10.1038/sj.onc.1206454
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Melanoma is the most aggressive form of skin cancer and is notoriously resistant to all current modalities of cancer therapy. A large set of genetic, functional and biochemical studies suggest that melanoma cells become 'bullet proof' against a variety of chemotherapeutic drugs by exploiting their intrinsic resistance to apoptosis and by reprogramming their proliferation and survival pathways during melanoma progression. In recent years, the identification of molecules involved in the regulation and execution of apoptosis, and their alteration in melanoma, have provided new insights into the molecular basis for melanoma chemoresistance. With this knowledge in hand, the challenge is now to devise strategies potent enough to compensate or bypass these cell death defects and improve the actual poor prognosis of patients at late stages of the disease.
引用
收藏
页码:3138 / 3151
页数:14
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