Models, mechanisms and clinical evidence for cancer dormancy

被引:1214
作者
Aguirre-Ghiso, Julio A. [1 ]
机构
[1] SUNY Albany, Sch Publ Hlth, Dept Biomed Sci, Ctr Excellence Canc Genom, Rensselaer, NY 12144 USA
关键词
D O I
10.1038/nrc2256
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Patients with cancer can develop recurrent metastatic disease with latency periods that range from years even to decades. This pause can be explained by cancer dormancy, a stage in cancer progression in which residual disease is present but remains asymptomatic. Cancer dormancy is poorly understood, resulting in major shortcomings in our understanding of the full complexity of the disease. Here, I review experimental and clinical evidence that supports the existence of various mechanisms of cancer dormancy including angiogenic dormancy, cellular dormancy(G0-G1 arrest) and immunosurveillance. The advances in this field provide an emerging picture of how cancer dormancy can ensue and how it could be therapeutically targeted.
引用
收藏
页码:834 / 846
页数:13
相关论文
共 141 条
[1]   Green fluorescent protein tagging of extracellular signal-regulated kinase and p38 pathways reveals novel dynamics of pathway activation during primary and metastatic growth [J].
Aguirre-Ghiso, JA ;
Ossowski, L ;
Rosenbaum, SK .
CANCER RESEARCH, 2004, 64 (20) :7336-7345
[2]   Urokinase receptor and fibronectin regulate the ERKMAPK to p38MAPK activity ratios that determine carcinoma cell proliferation or dormancy in vivo [J].
Aguirre-Ghiso, JA ;
Liu, D ;
Mignatti, A ;
Kovalski, K ;
Ossowski, L .
MOLECULAR BIOLOGY OF THE CELL, 2001, 12 (04) :863-879
[3]  
Aguirre-Ghiso JA, 2003, CANCER RES, V63, P1684
[4]   Intravascular origin of metastasis from the proliferation of endothelium-attached tumor cells: a new model for metastasis [J].
Al-Mehdi, AB ;
Tozawa, K ;
Fisher, AB ;
Shientag, L ;
Lee, A ;
Muschel, RJ .
NATURE MEDICINE, 2000, 6 (01) :100-102
[5]  
Allgayer H, 1997, CANCER RES, V57, P1394
[6]   Most early disseminated cancer cells detected in bone marrow of breast cancer patients have a putative breast cancer stem cell phenotype [J].
Balic, Marija ;
Lin, Henry ;
Young, Lillian ;
Hawes, Debra ;
Giuliano, Armando ;
McNamara, George ;
Datar, Ram H. ;
Cote, Richard J. .
CLINICAL CANCER RESEARCH, 2006, 12 (19) :5615-5621
[7]   Interaction of KAI1 on tumor cells with DARC on vascular endothelium leads to metastasis suppression [J].
Bandyopadhyay, Sucharita ;
Zhan, Rui ;
Chaudhuri, Asok ;
Watabe, Misako ;
Pai, Sudha K. ;
Hirota, Shigeru ;
Hosobe, Sadahiro ;
Tsukada, Taisei ;
Miura, Kunio ;
Takano, Yukio ;
Saito, Ken ;
Pauza, Mary E. ;
Hayashi, Sunao ;
Wang, Ying ;
Mohinta, Sonia ;
Mashimo, Tomoyuki ;
Iiizumi, Megumi ;
Furuta, Eiji ;
Watabe, Kounosuke .
NATURE MEDICINE, 2006, 12 (08) :933-938
[8]   Reversal of human cellular senescence:: roles of the p53 and p16 pathways [J].
Beauséjour, CM ;
Krtolica, A ;
Galimi, F ;
Narita, M ;
Lowe, SW ;
Yaswen, P ;
Campisi, J .
EMBO JOURNAL, 2003, 22 (16) :4212-4222
[9]   Tumorigenesis and the angiogenic switch [J].
Bergers, G ;
Benjamin, LE .
NATURE REVIEWS CANCER, 2003, 3 (06) :401-410
[10]   Detection of melanoma cells in sentinel lymph nodes, bone marrow and peripheral blood by a reverse transcription-polymerase chain reaction assay in patients with primary cutaneous melanoma: association with Breslow's tumour thickness [J].
Blaheta, HJ ;
Paul, T ;
Sotlar, K ;
Maczey, E ;
Schittek, B ;
Paul, A ;
Moehrle, M ;
Breuninger, H ;
Bueltmann, B ;
Rassner, G ;
Garbe, C .
BRITISH JOURNAL OF DERMATOLOGY, 2001, 145 (02) :195-202