| First Author | Cui M | Year | 2014 |
| Journal | Mol Cancer Res | Volume | 12 |
| Issue | 5 | Pages | 654-9 |
| PubMed ID | 24482365 | Mgi Jnum | J:209151 |
| Mgi Id | MGI:5566560 | Doi | 10.1158/1541-7786.MCR-13-0554 |
| Citation | Cui M, et al. (2014) PTEN Is a Potent Suppressor of Small Cell Lung Cancer. Mol Cancer Res 12(5):654-9 |
| abstractText | Small cell lung carcinoma (SCLC) is a highly metastatic tumor type with neuroendocrine features and a dismal prognosis. PTEN mutations and PIK3CA activating mutations have been reported in SCLC but the functional relevance of this pathway is unknown. The PTEN/PIK3CA pathway was interrogated using an AdenoCre-driven mouse model of SCLC harboring inactivated Rb and p53. Inactivation of one allele of PTEN in Rb/p53-deleted mice led to accelerated SCLC with frequent metastasis to the liver. In contrast with the high mutation burden reported in human SCLC, exome analyses revealed a low number of protein-altering mutations in mouse SCLC. Inactivation of both alleles of PTEN in the Rb/p53-deleted system led to nonmetastatic adenocarcinoma with neuroendocrine differentiation. This study reveals a critical role for the PTEN/PI3K pathway in both SCLC and lung adenocarcinoma and provides an ideal system to test the phosphoinositide 3-kinase (PI3K) pathway inhibitors as targeted therapy for subsets of patients with SCLC. Implications: The ability of PTEN inactivation to accelerate SCLC in a genetic mouse model suggests that targeting the PTEN pathway is a therapeutic option for a subset of human patients with SCLC. Visual Overview: http://mcr.aacrjournals.org/content/early/2014/04/28/1541-7786.MCR-13-0554/F1.lar ge.jpg. Mol Cancer Res; 12(5); 654-9. (c)2014 AACR. |
