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Open AccessJournal ArticleDOI

Models, mechanisms and clinical evidence for cancer dormancy.

Julio A. Aguirre-Ghiso
- 01 Nov 2007 - 
- Vol. 7, Iss: 11, pp 834-846
TLDR
Experimental and clinical evidence is reviewed that supports the existence of various mechanisms of cancer dormancy including angiogenic dormancy, cellular dormancy (G0–G1 arrest) and immunosurveillance.
Abstract
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.

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Citations
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TL;DR: The paradoxical roles of the tumor microenvironment during specific stages of cancer progression and metastasis are discussed, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects.
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Cancer Immunoediting: Integrating Immunity’s Roles in Cancer Suppression and Promotion

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A Perspective on Cancer Cell Metastasis

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Microenvironmental regulation of metastasis

TL;DR: Experimental data demonstrating the role of the microenvironment in metastasis is described, areas for future research are identified and possible new therapeutic avenues are suggested.
References
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Journal ArticleDOI

The hallmarks of cancer.

TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
Journal ArticleDOI

Targeting HIF-1 for cancer therapy

TL;DR: Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes that are involved in crucial aspects of cancer biology, including angiogenesis, cell survival, glucose metabolism and invasion.
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Opposing Effects of ERK and JNK-p38 MAP Kinases on Apoptosis

TL;DR: The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells.
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Dissemination and growth of cancer cells in metastatic sites

TL;DR: Inhibition of the growth of metastases in secondary sites offers a promising approach for cancer therapy and could help to improve the treatment of metastatic disease.
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Tumour stem cells and drug resistance

TL;DR: Gaining a better insight into the mechanisms of stem-cell resistance to chemotherapy might lead to new therapeutic targets and better anticancer strategies.
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