| First Author | Maitra A | Year | 2005 |
| Journal | Cancer Cell | Volume | 8 |
| Issue | 3 | Pages | 171-2 |
| PubMed ID | 16169459 | Mgi Jnum | J:103549 |
| Mgi Id | MGI:3610283 | Doi | 10.1016/j.ccr.2005.08.007 |
| Citation | Maitra A, et al. (2005) A new mouse model of pancreatic cancer: PTEN gets its Akt together. Cancer Cell 8(3):171-2 |
| abstractText | PTEN (phosphatase and tensin homolog deleted on chromosome 10) is a negative regulator of the oncogenic PI3-K/Akt signaling pathway. Loss-of-function mutations of PTEN are seen in several human solid cancers. A murine model of conditional Pten inactivation in the pancreas is described that leads to acquisition of a profound metaplastic ductal phenotype accompanied by loss of differentiated acinar units. Evidence is presented for a centroacinar cell origin of the metaplastic 'neoductules.' These mice also develop invasive pancreatic adenocarcinomas at a low frequency, and provide a unique in vivo platform for exploring the role of PI3-K/Akt signaling in pancreatic neoplasia. |
