Imperial College London
Alternate

DrLauraYates

Faculty of Medicine, National Heart & Lung Institute

Research Manager
 
 
 
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Contact

 

+44 (0)20 7594 3792l.yates Website

 
 
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Location

 

363Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Elsum:2013:10.1038/onc.2013.498,
author = {Elsum, IA and Yates, LL and Pearson, HB and Phesse, TJ and Long, F and O'Donoghue, R and Ernst, M and Cullinane, C and Humbert, PO},
doi = {10.1038/onc.2013.498},
journal = {Oncogene},
pages = {5523--5533},
title = {Scrib heterozygosity predisposes to lung cancer and cooperates with KRas hyperactivation to accelerate lung cancer progression in vivo.},
url = {http://dx.doi.org/10.1038/onc.2013.498},
volume = {33},
year = {2013}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Lung cancer is the leading cause of cancer deaths worldwide with non small-cell lung cancer (NSCLC) accounting for 80% of all lung cancers. Although activating mutations in genes of the RAS-MAPK pathway occur in up to 30% of all NSCLC, the cooperating genetic lesions that are required for lung cancer initiation and progression remain poorly understood. Here we identify a role for the cell polarity regulator Scribble (Scrib) in NSCLC. A survey of genomic databases reveals deregulation of SCRIB in human lung cancer and we show that Scrib+/- mutant mice develop lung cancer by 540 days with a penetrance of 43%. To model NSCLC development in vivo, we used the extensively characterized LSL-KRasG12D murine model of NSCLC. We show that loss of Scrib and activated oncogenic KRas cooperate in vivo, resulting in more aggressive lung tumors, likely due to a synergistic elevation in RAS-MAPK signaling. Finally, we provide data consistent with immune infiltration having an important role in the acceleration of tumorigenesis in KRasG12D lung tumors following Scrib loss
AU  - Elsum,IA
AU  - Yates,LL
AU  - Pearson,HB
AU  - Phesse,TJ
AU  - Long,F
AU  - O'Donoghue,R
AU  - Ernst,M
AU  - Cullinane,C
AU  - Humbert,PO
DO  - 10.1038/onc.2013.498
EP  - 5533
PY  - 2013///
SN  - 0950-9232
SP  - 5523
TI  - Scrib heterozygosity predisposes to lung cancer and cooperates with KRas hyperactivation to accelerate lung cancer progression in vivo.
T2  - Oncogene
UR  - http://dx.doi.org/10.1038/onc.2013.498
UR  - https://www.nature.com/articles/onc2013498
VL  - 33
ER  -
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