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senescence “barrier”, which in turn generate more aggressive sub-populations capable of driving metastasis.
Identifying, or molecularly defining, which cells possess the capability to escape senescence may allow us
to predict the aggressiveness of a patient’s metastatic burden and open potential avenues for targeting cells
with the potential to escape senescence. Ultimately, targeting the signaling responsible for plasticity, both in
pre-malignant and fully transformed cells, will enhance the efficacy of chemotherapies and suppress a key
driving force responsible for patient death.
DECLARATIONS
Authors’ contributions
Figure concept/design and writing of the manuscript: Smigiel JM
Writing of the manuscript: Taylor SE, Bryson BL, Tamagno I, Polak K, Jackson MW
Availability of data and materials
Not applicable.
Financial support and sponsorship
This work is supported by F30 (NIH NCIF30 CA224979) to Taylor SE.
Conflicts of interest
All authors declared that there are no conflicts of interest.
Ethical approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Copyright
© The Author(s) 2019.
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