| First Author | Gilmore TD | Year | 2004 |
| Journal | Oncogene | Volume | 23 |
| Issue | 13 | Pages | 2275-86 |
| PubMed ID | 14755244 | Mgi Jnum | J:89745 |
| Mgi Id | MGI:3041354 | Doi | 10.1038/sj.onc.1207410 |
| Citation | Gilmore TD, et al. (2004) The c-Rel transcription factor and B-cell proliferation: a deal with the devil. Oncogene 23(13):2275-86 |
| abstractText | Activation of the Rel/NF-kappaB signal transduction pathway has been associated with a variety of animal and human malignancies. However, among the Rel/NF-kappaB family members, only c-Rel has been consistently shown to be able to malignantly transform cells in culture. In addition, c-rel has been activated by a retroviral promoter insertion in an avian B-cell lymphoma, and amplifications of REL (human c-rel) are frequently seen in Hodgkin's lymphomas and diffuse large B-cell lymphomas, and in some follicular and mediastinal B-cell lymphomas. Phenotypic analysis of c-rel knockout mice demonstrates that c-Rel has a normal role in B-cell proliferation and survival; moreover, c-Rel nuclear activity is required for B-cell development. Few mammalian model systems are available to study the role of c-Rel in oncogenesis, and it is still not clear what features of c-Rel endow it with its unique oncogenic activity among the Rel/NF-kappaB family. In any event, REL may provide an appropriate therapeutic target for certain human lymphoid cell malignancies. |
