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Frontiers in Bioscience-Elite
Article . 2012 . Peer-reviewed
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Frontiers in Bioscience-Elite
Article . 2012 . Peer-reviewed
Data sources: Crossref
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Endogenous anticancer mechanisms metastasis

Authors: Scott, Valastyan;

Endogenous anticancer mechanisms metastasis

Abstract

Metastases, rather than the primary tumors from which these malignant growths are spawned, are culpable for greater than 90 % of human cancer-associated mortality. Metastases arise through the completion of a series of cell-biological events - collectively termed "the invasion-metastasis cascade" - which involve the dissemination of tumor cells to distant organ sites and their subsequent adaptation to these foreign microenvironments. Importantly, a number of endogenous mechanisms exist that serve to prevent metastatic progression. These safeguards must be overcome by incipient metastatic tumor cells in order for them to generate detectable metastases. Here, I highlight four endogenous mechanisms that protect against the development of metastatic disease in breast carcinomas. I discuss how the expression of these genes are dampened during malignant progression, the downstream responses they orchestrate, and clinical opportunities to therapeutically target these mechanisms. Indeed, one potentially effective strategy for the remediation of metastatic disease involves the reactivation of endogenous anti-metastasis mechanisms. Therefore, knowledge regarding endogenous anti-metastasis mechanisms may both further our comprehension of the basic etiology of metastasis and also guide the treatment of human tumors.

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Keywords

MicroRNAs, Animals, Humans, Neoplasm Invasiveness, NM23 Nucleoside Diphosphate Kinases, Neoplasm Metastasis, Cadherins

  • BIP!
    Impact byBIP!
    selected citations
    These citations are derived from selected sources.
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    2
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Average
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Average
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Average
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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
2
Average
Average
Average
gold
Related to Research communities
Cancer Research