Abstract
The polycomb group (PcG) gene BMI1, which is required for proliferation of both differentiated cells and adult stem cells, is overexpressed in various cancers and acts as an oncogene. Its oncogenic function has been attributed primarily to repression of the CDKN2A locus, which encodes the tumour suppressors INK4a and ARF. However, some defects in Bmi1-knockout mice seem to be independent of INK4a and ARF, so Maarten van Lohuizen and colleagues set out to determine whether the same was true for BMI1-dependent tumorigenesis.
Full Text 
Sign-in/Register to access full text options
Sign-in/Register to access full text options 
Published version (
Free)
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
