| First Author | Stairs DB | Year | 2011 |
| Journal | Cancer Cell | Volume | 19 |
| Issue | 4 | Pages | 470-83 |
| PubMed ID | 21481789 | Mgi Jnum | J:170980 |
| Mgi Id | MGI:4948166 | Doi | 10.1016/j.ccr.2011.02.007 |
| Citation | Stairs DB, et al. (2011) Deletion of p120-Catenin Results in a Tumor Microenvironment with Inflammation and Cancer that Establishes It as a Tumor Suppressor Gene. Cancer Cell 19(4):470-83 |
| abstractText | p120-catenin (p120ctn) interacts with E-cadherin, but to our knowledge, no formal proof that p120ctn functions as a bona fide tumor suppressor gene has emerged to date. We report herein that p120ctn loss leads to tumor development in mice. We have generated a conditional knockout model of p120ctn whereby mice develop preneoplastic and neoplastic lesions in the oral cavity, esophagus, and squamous forestomach. Tumor-derived cells secrete granulocyte macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF), monocyte chemotactic protein-1 (MCP-1), and tumor necrosis factor-alpha (TNFalpha). The tumors contain significant desmoplasia and immune cell infiltration. Immature myeloid cells comprise a significant percentage of the immune cells present and likely participate in fostering a favorable tumor microenvironment, including the activation of fibroblasts. |
