Synergistic tumor suppressor activity of BRCA2 and p53 in a conditional mouse model for breast cancer

10.1038/ng747 ◽  
2001 ◽  
Vol 29 (4) ◽  
pp. 418-425 ◽  
Author(s):  
Jos Jonkers ◽  
Ralph Meuwissen ◽  
Hanneke van der Gulden ◽  
Hans Peterse ◽  
Martin van der Valk ◽  
...  
2015 ◽  
Vol 13 (10) ◽  
pp. 1398-1407 ◽  
Author(s):  
Hagai Ligumsky ◽  
Tami Rubinek ◽  
Keren Merenbakh-Lamin ◽  
Adva Yeheskel ◽  
Rotem Sertchook ◽  
...  

BMC Cancer ◽  
2011 ◽  
Vol 11 (1) ◽  
Author(s):  
Guihong Zhang ◽  
Abenaa Brewster ◽  
Baoxiang Guan ◽  
Zhen Fan ◽  
Powel H Brown ◽  
...  

2007 ◽  
Vol 67 (3) ◽  
pp. 1105-1112 ◽  
Author(s):  
Chengyin Min ◽  
Kathrin H. Kirsch ◽  
Yingshe Zhao ◽  
Sébastien Jeay ◽  
Amitha H. Palamakumbura ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nathan F. Schachter ◽  
Jessica R. Adams ◽  
Patryk Skowron ◽  
Katelyn. J. Kozma ◽  
Christian A. Lee ◽  
...  

AbstractThe most common events in breast cancer (BC) involve chromosome arm losses and gains. Here we describe identification of 1089 gene-centric common insertion sites (gCIS) from transposon-based screens in 8 mouse models of BC. Some gCIS are driver-specific, others driver non-specific, and still others associated with tumor histology. Processes affected by driver-specific and histology-specific mutations include well-known cancer pathways. Driver non-specific gCIS target the Mediator complex, Ca++ signaling, Cyclin D turnover, RNA-metabolism among other processes. Most gCIS show single allele disruption and many map to genomic regions showing high-frequency hemizygous loss in human BC. Two gCIS, Nf1 and Trps1, show synthetic haploinsufficient tumor suppressor activity. Many gCIS act on the same pathway responsible for tumor initiation, thereby selecting and sculpting just enough and just right signaling. These data highlight ~1000 genes with predicted conditional haploinsufficient tumor suppressor function and the potential to promote chromosome arm loss in BC.


2011 ◽  
Vol 42 (01) ◽  
Author(s):  
P. Monfared ◽  
T. Viel ◽  
G. Schneider ◽  
Y. Waerzeggers ◽  
S. Rapic ◽  
...  

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