| First Author | Finch A | Year | 2006 |
| Journal | Cancer Cell | Volume | 10 |
| Issue | 2 | Pages | 113-20 |
| PubMed ID | 16904610 | Mgi Jnum | J:112704 |
| Mgi Id | MGI:3663210 | Doi | 10.1016/j.ccr.2006.06.017 |
| Citation | Finch A, et al. (2006) Bcl-xL gain of function and p19 ARF loss of function cooperate oncogenically with Myc in vivo by distinct mechanisms. Cancer Cell 10(2):113-20 |
| abstractText | Overexpression of Bcl-xL, loss of p19 ARF, and loss of p53 all accelerate Myc oncogenesis. All three lesions are implicated in suppressing Myc-induced apoptosis, suggesting that this is a common mechanism by which they synergize with Myc. However, using an acutely switchable model of Myc-induced tumorigenesis, we demonstrate that each lesion cooperates with Myc in vivo by a distinct mechanism. While Bcl-xL blocks Myc-induced apoptosis, inactivation of p19 ARF enhances it. However, this increase in apoptosis is matched by increased Myc-induced proliferation. p53 inactivation shares features of both lesions, partially suppressing apoptosis while augmenting proliferation. Bcl-xL and p19 ARF loss together synergize to further accelerate Myc oncogenesis. Thus, differing lesions cooperate oncogenically with Myc by discrete mechanisms that can themselves synergize with each other. |
