Carcinogenesis Advance Access originally published online on May 2, 2008
Carcinogenesis 2008 29(6):1092-1095; doi:10.1093/carcin/bgn104
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Mechanisms of malignant progression
Department of Biology, Ludwig Center for Molecular Oncology, Whitehead Institute for Biomedical Research, MIT, Cambridge, MA 02142, USA
* To whom correspondence should be addressed. Email: weinberg@wi.mit.edu
Abbreviations: EMT, epithelial–mesenchymal transition; TF, transcription factor
| The first 150 words of the full text of this article appear below. |
While a coherent picture has begun to emerge about the biological and molecular mechanisms that create primary tumors, the processes that lead subsequently to invasion and metastasis have, until recently, been relatively obscure. However, over the past 5 years, research of diverse sorts has begun to generate the conceptual outlines that explain how high-grade malignancies arise. These discussions invariably are motivated by a widely accepted depiction of how metastatic dissemination occurs—the sequence termed the invasion–metastasis cascade (1). Thus, primary tumor cells invade locally, enter into the circulation (intravasation), are transported through the circulation, are lodged in microvessels in distant tissues, invade the parenchyma of such tissue (extravasation) and form micrometastatic deposits, some of which eventually grow into macroscopic metastases, the last process being termed colonization.
| Early determination |
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A major issue concerns the timing of acquisition of the ability to invade and metastasize. Is this ability a function of the great
| Determinants of invasiveness |
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| Induction of expression of EMT-inducing TFs |
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| The EMT and the invasion–metastasis cascade |
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| Permanent EMT |
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| An emerging pattern |
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| Funding |
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