| First Author | Rakhra K | Year | 2010 |
| Journal | Cancer Cell | Volume | 18 |
| Issue | 5 | Pages | 485-98 |
| PubMed ID | 21035406 | Mgi Jnum | J:166716 |
| Mgi Id | MGI:4849346 | Doi | 10.1016/j.ccr.2010.10.002 |
| Citation | Rakhra K, et al. (2010) CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation. Cancer Cell 18(5):485-98 |
| abstractText | Oncogene addiction is thought to occur cell autonomously. Immune effectors are implicated in the initiation and restraint of tumorigenesis, but their role in oncogene inactivation-mediated tumor regression is unclear. Here, we show that an intact immune system, specifically CD4(+) T cells, is required for the induction of cellular senescence, shutdown of angiogenesis, and chemokine expression resulting in sustained tumor regression upon inactivation of the MYC or BCR-ABL oncogenes in mouse models of T cell acute lymphoblastic lymphoma and pro-B cell leukemia, respectively. Moreover, immune effectors knocked out for thrombospondins failed to induce sustained tumor regression. Hence, CD4(+) T cells are required for the remodeling of the tumor microenvironment through the expression of chemokines, such as thrombospondins, in order to elicit oncogene addiction. |
