| First Author | Castellano E | Year | 2013 |
| Journal | Cancer Cell | Volume | 24 |
| Issue | 5 | Pages | 617-30 |
| PubMed ID | 24229709 | Mgi Jnum | J:206736 |
| Mgi Id | MGI:5551924 | Doi | 10.1016/j.ccr.2013.09.012 |
| Citation | Castellano E, et al. (2013) Requirement for interaction of PI3-kinase p110alpha with RAS in lung tumor maintenance. Cancer Cell 24(5):617-30 |
| abstractText | RAS proteins directly activate PI3-kinases. Mice bearing a germline mutation in the RAS binding domain of the p110alpha subunit of PI3-kinse are resistant to the development of RAS-driven tumors. However, it is unknown whether interaction of RAS with PI3-kinase is required in established tumors. The need for RAS interaction with p110alpha in the maintenance of mutant Kras-driven lung tumors was explored using an inducible mouse model. In established tumors, removal of the ability of p110alpha to interact with RAS causes long-term tumor stasis and partial regression. This is a tumor cell-autonomous effect, which is improved significantly by combination with MEK inhibition. Total removal of p110alpha expression or activity has comparable effects, albeit with greater toxicities. |
