Cancer drug addiction is relayed by an ERK2-dependent phenotype switch
Xiangjun Kong,
Thomas Kuilman,
Aida Shahrabi,
Julia Boshuizen,
Kristel Kemper,
Ji-Ying Song,
Hans W. M. Niessen,
Elisa A. Rozeman,
Marnix H. Geukes Foppen,
Christian U. Blank and
Daniel S. Peeper ()
Additional contact information
Xiangjun Kong: The Netherlands Cancer Institute
Thomas Kuilman: The Netherlands Cancer Institute
Aida Shahrabi: The Netherlands Cancer Institute
Julia Boshuizen: The Netherlands Cancer Institute
Kristel Kemper: The Netherlands Cancer Institute
Ji-Ying Song: The Netherlands Cancer Institute
Hans W. M. Niessen: VU University Medical Center, ACS
Elisa A. Rozeman: The Netherlands Cancer Institute
Marnix H. Geukes Foppen: The Netherlands Cancer Institute
Christian U. Blank: The Netherlands Cancer Institute
Daniel S. Peeper: The Netherlands Cancer Institute
Nature, 2017, vol. 550, issue 7675, 270-274
Abstract:
The identification of an ERK2–JUNB–FRA1 signalling pathway that drives addiction to therapeutic drugs in cancer cells, and an ERK2-dependent phenotype switch that precedes cell death after drug withdrawal, may help to guide therapies that exploit the addiction phenotype.
Date: 2017
References: Add references at CitEc
Citations: View citations in EconPapers (2)
Downloads: (external link)
https://www.nature.com/articles/nature24037 Abstract (text/html)
Access to the full text of the articles in this series is restricted.
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:550:y:2017:i:7675:d:10.1038_nature24037
Ordering information: This journal article can be ordered from
https://www.nature.com/
DOI: 10.1038/nature24037
Access Statistics for this article
Nature is currently edited by Magdalena Skipper
More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().