Mechanisms of disseminated cancer cell dormancy: an awakening field

被引:841
作者
Sosa, Maria Soledad [1 ,2 ]
Bragado, Paloma [1 ,2 ]
Aguirre-Ghiso, Julio A. [1 ,2 ]
机构
[1] Ichan Sch Med Mt Sinai, Tisch Canc Inst, Dept Otolaryngol, Div Hematol & Oncol,Dept Med, New York, NY 10029 USA
[2] Ichan Sch Med Mt Sinai, Black Family Stem Cell Inst, New York, NY 10029 USA
基金
美国国家卫生研究院;
关键词
UNFOLDED PROTEIN RESPONSE; BREAST-CANCER; BONE-MARROW; TUMOR DORMANCY; HEMATOPOIETIC STEM; PROSTATE-CANCER; METASTATIC OUTGROWTH; UROKINASE RECEPTOR; PROGENITOR CELLS; BALANCED PROLIFERATION;
D O I
10.1038/nrc3793
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Metastases arise from residual disseminated tumour cells (DTCs). This can happen years after primary tumour treatment because residual tumour cells can enter dormancy and evade therapies. As the biology of minimal residual disease seems to diverge from that of proliferative lesions, understanding the underpinnings of this new cancer biology is key to prevent metastasis. Analysis of approximately 7 years of literature reveals a growing focus on tumour and normal stem cell quiescence, extracellular and stromal microenvironments, autophagy and epigenetics as mechanisms that dictate tumour cell dormancy. In this Review, we attempt to integrate this information and highlight both the weaknesses and the strengths in the field to provide a framework to understand and target this crucial step in cancer progression.
引用
收藏
页码:611 / 622
页数:12
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