| First Author | Pelengaris S | Year | 2002 |
| Journal | Cell | Volume | 109 |
| Issue | 3 | Pages | 321-34 |
| PubMed ID | 12015982 | Mgi Jnum | J:76473 |
| Mgi Id | MGI:2179563 | Doi | 10.1016/s0092-8674(02)00738-9 |
| Citation | Pelengaris S, et al. (2002) Suppression of Myc-induced apoptosis in beta cells exposes multiple oncogenic properties of Myc and triggers carcinogenic progression. Cell 109(3):321-34 |
| abstractText | To explore the role of c-Myc in carcinogenesis, we have developed a reversible transgenic model of pancreatic beta cell oncogenesis using a switchable form of the c-Myc protein. Activation of c-Myc in adult, mature beta cells induces uniform beta cell proliferation but is accompanied by overwhelming apoptosis that rapidly erodes beta cell mass. Thus, the oncogenic potential of c-Myc in beta cells is masked by apoptosis. Upon suppression of c-Myc-induced beta cell apoptosis by coexpression of Bcl-x(L), c-Myc triggers rapid and uniform progression into angiogenic, invasive tumors. Subsequent c-Myc deactivation induces rapid regression associated with vascular degeneration and beta cell apoptosis. Our data indicate that highly complex neoplastic lesions can be both induced and maintained in vivo by a simple combination of two interlocking molecular lesions. |
