![[feed]](/style/images/feed-icon-14x14.png){kind=icon}
Tools
Tools
![[thumbnail of 3462oa.pdf]](https://edoc.mdc-berlin.de/style/images/fileicons/application_pdf.png) |
PDF
- Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
469kB |
| Item Type: | Article |
|---|---|
| Title: | Constitutive nuclear factor-kappaB-RelA activation is required for proliferation and survival of Hodgkin's disease tumor cells |
| Creators Name: | Bargou, R.C., Emmerich, F., Krappmann, D., Bommert, K., Mapara, M.Y., Arnold, W., Royer, H.D., Grinstein, E., Greiner, A., Scheidereit, C. and Doerken, B. |
| Abstract: | The pathogenesis and etiology of Hodgkin's disease, a common human malignant lymphoma, is still unresolved. As a unique characteristic, we have identified constitutive activation of the transcription factor nuclear factor (NF)-kappaB p50-RelA in Hodgkin/Reed-Sternberg (H/RS) cells, which discriminates these neoplastic cells from most cell types studied to date. In contrast to other lymphoid and nonlymphoid cell lines tested, proliferation of H/RS cells depended on activated NF-kappaB. Furthermore, constitutive NF-kappaB p50-RelA prevented Hodgkin's lymphoma cells from undergoing apoptosis under stress conditions. Consistent with this dual function, Hodgkin's lymphoma cells depleted of constitutive nuclear NF-kappaB revealed strongly impaired tumor growth in severe combined immunodeficient mice. Our findings identify NF-kappaB as an important component for understanding the pathogenesis of Hodgkin's disease and for developing new therapeutic strategies against it. |
| Keywords: | Apoptosis, Cell Division, Cell Line, Cell Survival, Cultured Tumor Cells, Hodgkin Disease, NF-kappa B, NF-kappa B p50 Subunit, Transcription Factor RelA, Animals, Mice |
| Source: | Journal of Clinical Investigation |
| ISSN: | 0021-9738 |
| Publisher: | American Society for Clinical Investigation |
| Volume: | 100 |
| Number: | 12 |
| Page Range: | 2961-2969 |
| Date: | 15 December 1997 |
| Official Publication: | https://doi.org/10.1172/JCI119849 |
| PubMed: | View item in PubMed |
Repository Staff Only: item control page
