Abstract
Recent studies have shown that the interactions between tumour and dendritic cells (DCs) promote clonogenic growth of lymphoproliferative tumours, particularly myeloma. The present study showed that the proteasome inhibitor, bortezomib, disrupts this interaction. Targeting the drug to DCs was required for optimal suppression of tumour growth, including primary myeloma tumour progenitors in clonogenic assays. Bortezomib lead to dose-dependent induction of apoptosis in both myeloid and plasmacytoid DCs, and the sensitivity of DCs to bortezomib was comparable with that of tumour cells. These data suggest that disruption of tumour-DC interactions may contribute to the clinical effects of bortezomib.
| Original language | English |
|---|---|
| Pages (from-to) | 106-110 |
| Number of pages | 5 |
| Journal | British Journal of Haematology |
| Volume | 136 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 2007 |
| Externally published | Yes |
Keywords
- Lymphoma
- Myeloid dendritic cells
- Myeloma
- Plasmacytoid dendritic cells
- Tumour microenvironment
Fingerprint
Dive into the research topics of 'Bortezomib disrupts tumour-dendritic cell interactions in myeloma and lymphoma: Therapeutic implications'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver